Opthalmology Conditions Flashcards
(297 cards)
1
Q
Name 8 causes of a Red Eye Presentation
A
Acute Angle Closure Glaucoma,
Endopthalmitis,
Orbital Cellulitis,
Corneal Abrasion,
Hyphaema,
Anterior uveitis,
Keratitis,
Scleritis
2
Q
Define Glaucoma
A
Progressive optic neuropathy in which raised intraocular pressure is a key factor
3
Q
What are the three types of Glaucoma
A
Open Angle,
Closed Angle,
Ocular HTN (elevated IOP without the other changes seen in Glaucoma)
4
Q
Angle Closure Glaucoma can be acute or chronic, what is the difference?
A
Acute - severe eye pain, visual loss, headache and is an Opthalmic emergency
Chronic - Normally asymptomatic and picked up on routine screening , vision preserved until late stage
5
Q
Name 5 risk factors for Acute Angle Closure Glaucoma
A
Increased Age,
Asian Ethnicity,
FH,
Hyperopia,
Anticholinergic meds
6
Q
Describe Primary Angle Closure Glaucoma
A
Anatomically predisposed
Lens sits forward and pushes against iris
Pressure increases in posterior chamber causing forwards compression
Scar tissue forms in trabecular meshwork reducing drainage
Can be acute, subacute or chronic
7
Q
Describe Secondary Angle Closure Glaucoma
A
Results from other eye pathologies
Push the iris/ciliary body in (eg SOL)
Pull the iris (iris neovascularisation)
8
Q
Chronic Angle Closure Glaucoma is normally asymptomatic, how does Acute present?
A
Severe eye pain,
Redness,
Visual loss,
Nausea and Vomiting,
Semi dilated and fixed pupil
9
Q
Name three investigations for suspected AACG
A
Tonometry (measures intraocular pressure)
Gonioscopy (allows visualisation of anterior chamber and drainage system)
Slit lamp/Opthalmascope - Optic disc cupping
10
Q
Describe the opportunistic testing for Glaucoma via NICE guidelines
A
Every 2y from 60-70y,
Annually from 70y,
From age of 40 if affected first degree relative,
African heritage >40
11
Q
Glaucoma cannot be cured, just managed. Describe the initial management options for AACG
A
Carbonic Anhydrase Inhibitors,
Beta Blockers,
Pilocarpine,
Mannitol,
If fails - anterior chamber paracentesis
12
Q
Describe the definitive treatment of AACG
A
Inital IV Acetazolamide and Drops (eg Pilocarpine)
Followed by laser peripheral iridotomy (creates opening in iris, allowing equalisation of flow)
Definitive treatment is advised prophylactically for other eye
13
Q
Define Endopthalmitis
A
Severe inflammation of anterior and/or posterior chamber (can be sterile but normally due to infection)
14
Q
Give 5 causes of Endopthalmitis
A
Trauma,
Eye Surgery,
VEGF injections,
Endogenous seeding,
Extension of Corneal infection
15
Q
Describe the likely pathogens of Endopthalmitis with each cause
A
Surgery - Coag neg Staph (epidermis),
Trauma - bacillus cereus,
Endogenous - S.Aureus,Klebsiella
16
Q
How does Endopthalmitis present?
A
Acute eye pain,
Reduced vision,
Hypopyon ,
?swollen eyelid
17
Q
Name four risk factors for Endopthalmitis
A
Poor surgical technique,
Contaminated lens,
Contact lens wear,
Immunosupression
18
Q
What are the three subtypes of Post Op Endopthalmitis?
A
Acute (one to several days post surgery)
Delayed (up to 9m later, minimal or no pain)
Bleb Associated (after trabeculotomy for Glaucoma)
19
Q
How does Endopthalmitis present?
A
Acute eye pain,
Reduced vision,
Swollen eyelid,
Hypopyon
20
Q
Name two differentials for Endopthalmitis
A
Retained lens material,
Raised IOP as a result of procedure
21
Q
How would you investigate Endopthalmitis?
A
Slit Lamp - Vitreous infiltrates
Vitreous sample for microbiology (Abx cover)
Endogenous - full infection screen
USS eye if unsure
22
Q
Endopthalmitis is an emergency, depending on the aetiology how is it managed?
A
Bacterial - Direct Abx injection into Vitreous, if severe then Vitrectomy
Fungal - Vitrectomy and Intravitreal Amphoterecin
Systemic - Systemic Abx
Non Infectious - Steroids
23
Q
Define Orbital Cellulitis
A
Sight threatening Opthalmic emergency characterised by infections of the soft tissue behind the septum
Most commonly seen in Children, spreading from local infection
24
Q
Name five sources of infection for Orbital Cellulitis
A
Extension from periorbital structures
Extension from presentation structures
Direct Inoculation
Post Surgery
Haematogenous
25
Name four common pathogens and one rare for Orbital Cellulitis
Common - H.Influenza, Strep Pneumoniae, S.Aureus, S.Pyogenes
Rare - mucormycosis (rare fungal associated with DKA and Neutropenic Sepsis)
26
Name two anterior, two orbital and two systemic features of Orbital Cellulitis
Anterior - unilateral lid swelling, conjunctival chemosis
Orbital - external eye muscle painful opthamoplegia and blurred vision
Systemic - fever, Malaise
27
Orbital Cellulitis is generally a clinical diagnosis. What investigations could you do, and what would they show?
FBC - leukocytosis
Blood cultures - negative
LP (if focal signs)
Swabs
CT sinus and orbit - extension
28
Orbital Cellulitis is an emergency and requires urgent antibiotics and four hourly monitoring. What are the Abx of choice?
1) Co Amoxiclav
If pen allergic - Clindamycin and Metronidazole
MRSA - Vancomycin
29
When would you consider surgery in Orbital Cellulitis?
Resistant to antibiotics
Reduced visual acuity
CT evidence of orbital collection
30
Name four complications of Orbital Cellulitis
Endopthalmitis
Meningitis
Orbital Abscess
Subperiosteal Abscess
31
Corneal injuries can be physical, chemical or environmental. What makes a corneal abrasion (partial thickness) more likely?
If the eye doesn’t shut properly
32
Other than corneal abrasions, what other corneal injuries are common?
Superficial Keratitis
Foreign Bodies
33
If there is no clear mechanism of injury but you suspect damage to the cornea, what should you cosncier
HSV infection
34
How does a superficial corneal abrasion present?
Redness
Pain
Watering
Foreign Body Sensation
Photophobia
35
How does a penetration corneal injury present?
Distorted globe
Hyphaema
Conjunctival laceration
Red and watering
36
Name some functional and general features you are looking for on observation of corneal injury
Functional - Diplopia, Abnormal visual fields, RAPD
General - raised IOP, infection
37
How can the Cornea be examined in suspected corneal injury?
Seidles Test - 10% Fluorescine and slit lamp to look for corneal leak (yellow/orange)
Abrasion with dilute fluorosciene
38
Name three red flags for corneal injury
Deep lid laceration
Subconjunctival haemorrhage
Pupils/Iris/Fundus abnormality
39
How would you manage a Corneal Abrasion?
Pain relief (topical NSAIDs or Oral Abx)
Topical chloramphenicol to prevent secondary infection
Tetanus prophylaxis where necessary
Avoid contact lenses for 2 weeks
40
How are Corneal Foreign Bodies managed?
Topical anaesthetic
Eye irrigation and removal with damp cotton bud
After removal treat as corneal abrasion
41
How can rust rings be removed?
A sterile rotating burr
42
How should a penetrating corneal injury be managed?
Cover with rigid eye patch and refer immediately for emergency surgery
43
Give two examples of how chemical corneal injuries can be managed?
CA gas - blown off the eye using a hairdryer
Pepper spray and chlorine gas - copiously irrigated
44
Define Hyphaema
When blood enters anterior chamber between cornea and iris
45
How does a Hyphaema present?
Decrease/ Loss of vision (may improve as gravity pulls the blood down)
Red tinge to eye
46
Name 5 causes of a Hyphaema
Intraocular Surgery
Blunt trauma
Lacerating Trauma
Leukaemia
Retinoblastoma
47
How are Hyphaemas managed?
Small - Outpatient basis, antifibrinolytics, corticosteroids, mitotics, asparin
Non resolving - surgical clean out
Pain relief - avoid aspirin and NSAIDs due to platelet interaction
48
Name two complications of Hyphaema
Haemosiderosis
Raised IOP
49
What is the grading system for chemical injury of the eye?
Roper Hall
50
What is the immediate management for Ocular Chemical Injury?
1) Check pH with universal indicator
2) Administer topical anaesthetic and remove contact lenses
3) 1L saline irrigation continued until pH is 7
4) Rechecked every 15 minutes
51
If the Chemical Injury of the eye was moderate or severe, how would it be managed?
Dexamethasone 1-2 hourly
Vitamin C (topically and orally)
Citrate and Tetracyclines
52
Conjunctivitis is inflammation of the conjunctiva. How does Bacterial Conjunctivitis present?
Purulent discharge
Worse in the morning
Inflamed conjunctiva
Starts in one eye and spreads to the other
53
How does Viral Conjunctivitis present?
Clear discharge
Other symptoms of viral infection (URTI)
Preauricular lymph nodes
54
What advice should you give patients with conjunctivitis?
Usually resolves without treatment in 1-2 weeks
Maintain good hygiene (avoid sharing towels, rubbing eyes)
Avoid contact lenses
Clean with cooled boiled water and cotton wool
55
How can bacterial conjunctivitis be managed?
Chloramphenicol (contraindicated if pregnant or breast feeding)
Fusidic Acid
56
How does Allergic Conjuncitivitis present?
Swelling of conjunctival sac and eyelid
Watery discharge
Itch
57
How is Allergic Conjunctivitis managed?
Antihistamines (Oral or topical)
Topical mast cell stabilisers used for several weeks if chronic symptoms
58
Name four causes of Anterior Uveitis
Autoimmune
Infection
Trauma
Ischaemia
59
Anterior Uveitis can be Acute or chronic . How do they differ ?
Chronic is more Granulomatous, less severe, longer symptom duration (often >3m)
60
Name three associations of Anterior Uveitis and Chronic Anterior Uveitis respectively
Anklyosing Spondylitis, IBD, Reactive Arthritis
Sarcoidosis, Syphilis, TB
61
How does Anterior Uveitis present?
Spontaneous unilateral symptoms
Dull aching
Red Eye
Ciliary Flush (ring of red from cornea outwards)
Reduced visual acuity
Flashers and floaters
62
What causes floaters in Anterior Uveitis?
Inflammation and immune cells in the anterior chamber
63
What is Posterior Synechiae? Give an association
Adhesions that can cause disruption to pupillary shape
Anterior Uveitis
64
If a GP suspects a sight threatening opthalmological condition, what should they do?
Same day assessment by ophthalmologist
Slit lamp examination and IOP measurement
65
How would you manage Anterior Uveitis?
Steroids
Cytoplegic/Mydriatic medication (eg Cyclopentolate)
Immunosupressants
Severe - Laser therapy, Cryotherapy
66
What is the role of Cytoplegic/Mydriatic Medication in Anterior Uveitis?
Paralyses ciliary muscles, reducing pain and the formation of Posterior Synechiae
67
Keratitis is infection of the cornea, give three causes
Trauma
Foreign Body
Infected Contact Lens
68
Describe the pathophysiology of Bacterial Keratitis
Infection of one or more layers of the Cornea, normally once the epithelial layer has been breached (eg corneal abrasion)
Risks - Diabetes, contact lens, corneal trauma
69
Name four presenting features of Keratitis
Redness
Pain
Photophobia
Reduced acuity
70
What can be seen on examination of a Keratitic eye?
Oedema
White cell infiltration
Epithelial defect
71
How is Keratitis managed?
Intensive topical antibiotics - Ofloxacin for Pseudomonas cover (with or without cycloplegics)
?Steroids
Stop contact lens use
72
Herpes Simplex Keratitis is the most common, and only normally affects epithelial layer. What could distinguish it from other causes of Keratitis?
Vesicles around the eye
73
What would Fluorescein staining of a HSV Keratitis eye show?
Dendritic corneal ulcer (branching and spreading)
74
How is HSV Keratitis managed?
Acyclovir (topical or oral)
Ganciclovir eye gel
Topical steroids
75
Define Scleritis
Inflammation of full thickness of the sclera
Normally not caused by infection
76
What is the most severe form of Scleritis?
Necrotising Scleritis
Visual impairment but not pain
Can lead to Scleral perforation
77
Name four associated conditions with scleritis
SLE
IBD
RA
Sarcoidosis
78
How does Scleritis present?
50% bilateral
Pain (especially on eye movement)
Photophobia
Reduced acuity
Abnormal pupillary response
79
How is Scleritis managed?
Underlying condition
NSAIDs and Steroids
80
Name five causes of Gradual Visual Deterioration
Cataracts
Open Angle Glaucoma
ARMD
Diabetic Retinopathy
Presbyopia
81
What are Cataracts?
Opacification of the Lens
Major cause of treatable blindness worldwide
82
Cataracts can be age related or non age related. Give three causes of non age related
Trauma
Steroids
Uveitis
83
What are the three classifications of Paediatric Cataracts
1/3 Inherited (Autosomal Dominant)
1/3 Systemic (Rubella, Fabrys)
1/3 Idiopathic
84
Cataracts can be classified depending on the location of lens affected. What are the three classifications
Nuclear
Cortical
Posterior Subcapsular
85
How do Nuclear Cataracts present?
Loss of colour vision
Slow progression
86
How do Cortical Cataracts present?
Less visual degradation
Slow progression
87
How to Posterior Subcapsular Cataracts present?
Disabling glare to bright lights
Quick progression
Links to DM and Steroids
88
Describe the pathophysiology of Cataracts
Lens is normally a highly organised structure to maintain transparency
Lack of blood supply and inability to shed non viable cells leaves the lens succeptible to insult
Results in loss of transparency, nodular sclerosis, inability to refract light
89
Give 6 presenting features of Cataracts
Painless loss of vision
Halls around lights
Sensitivity to light and glare
Polyopia
Myopic shift (improved near sighted)
Loss of red reflex
90
Cataracts are a clinical diagnosis. What features will be seen on Opthalmoscope/Slit Lamp?
Loss of red reflex
Opacification
Obscuration of ocular detail
91
Surgery is carried out for Cataracts when they have a significant impact on ADLs. What are the two techniques called?
Phacoemulsification
Extracapsular Cataract Extraction
92
Name two differences between the Cataract surgical techniques
PE - breaks up diseases lens and aspirates contents, small incision
ECE- Whole removal of diseased nucleus, larger incision
93
Name three immediate and three delayed features of Cataract Surgery
Immediate - Endopthalmitis, Lens Malposition, Toxic Anterior Segment Syndrome
Delayed - retinal detachment, macular degeneration, Posterior capsule opacification *
*proliferation of lens remnants, treated with laser
94
Describe the four layers of the Macula
Choroid
Bruch’s Membrane
Retinal Pigment Epithelium
Photoreceptors
95
ARMD is the leading cause of blindness in the UK, what are the two types?
Dry - 90%
Wet - 10%
96
Describe Dry ARMD
Progressive atrophy
Doesn’t exude
Late - Geographic Atrophy (large well demarcated sections of retina stop functioning)
97
Describe Wet ARMD
Worse prognosis
Development of new vessels from choroid layer into retina (via VEGF)
Vessels leak - Oedema
98
Drusen are characteristic of ARMD. What are they?
Yellow deposits of protein/lipids between retinal pigment epithelium and Bruchs
Can be normal
Larger and greater numbers can be an early sign
99
Give four risk factors for ARMD
Age
Smoking
Chinese Ethnicity
FH
100
How does ARMD present?
Gradually worsening central visual loss
Reduced acuity
Crooked appearance to lines
Wet - more acute and rapid
101
Name four investigations (other than Snellen) for ARMD and what you would see
Amsler Grid Test - Straight Line Distortion
Fundoscopy - Drusen
OCT - cross sectional retinal view (wet)
Fluorescein Angiography- Oedema and Neovascularisation
102
How is Dry ARMD managed?
No treatment just lifestyle means urges to slow progression (smoking cessation, BP control, Vitamins)
103
How is Wet ARMD managed?
Anti VEGF Vitreous injections (Ranibizumab)
Started within three months
104
Give four risk factors for Open Angle Glaucoma
Age
Afrocaribbean ethnicity
Diabetes
Myopia
105
Open Angle Glaucoma can be primary or secondary. What is primary?
Unknown aetiology
Unsure if increased production or decreased drainage
May be predisposed by microcirculatory factors and genetic damage
106
Open Angle Glaucoma can be primary or secondary. What is secondary?
Reduced drainage and increased IOP
5 subtypes : Neovascular (DM), Pseuodoexfoliative, Uveitis, Glucocorticoid Induced, Pigmentary
107
How does Open Angle Glaucoma present?
Largely asymptomatic until late stages
Central vision relatively preserved until late - tunnel vision and bumping into things
108
Name five investigations for Open Angle Glaucoma
-Opthalmoscope (progressive cupping)
-Humphrey visual field analyser
-Goldman Applanation Tonometry
-Gonioscopy
-Corneal thickness (contextualises IOP)
109
There are a variety of drug classes that act on humour production and are used to treat OAG. What is the first line? Give two contraindications and two side effects
Latanoprost
Pregnancy and Breast Feeding
Brown Iris pigmentation and pigmentation of surrounding skin (also lash thickening, irritation)
110
What is the surgical management for Open Angle Glaucoma?
Lasted trabeculoplasty
Soft laser ‘wakes up meshwork’
Or Trabeculectomy
Can cause iritis and blebitis
111
Describe the pathophysiology of Diabetic Retinopathy
Vessels in the retina are damaged by prolonged hyperglycaemia, leading to increased vascular permeability
112
Describe 6 features of Diabetic Retinopathy as seen on an Opthalmoscope
Blot Haemorrhages and Hard Exudates (leakage)
Microaneurysms (weakness)
Venous Beading
Cotton Wool Spots (nerve damage)
Neovascularisation (local GF release)
113
Diabetic Retinopathy can be non proliferative, proliferative or a maculopathy. Describe non proliferative
Mild - Microaneurysms
Moderate - Microaneurysms, Blot Haemorrhages, Hard Exudates, Cotton Wool Spots, Venous Beading
Severe - Blot Haemorrhages and Microaneurysms in four quadrants, beading in >2 quadrants, IMRA in any quadrant
114
Diabetic Retinopathy can be non proliferative, proliferative or a maculopathy. Describe proliferative
Neovascularisation
Vitreous Haemorrhage
115
Diabetic Retinopathy can be non proliferative, proliferative or a maculopathy. Describe Maculopathy
Macular Oedema
Ischaemic Maculopathy
Can be focal/diffuse/central involving
116
Name four complications of Diabetic Retinopathy
Rubeosis Iridis (new BV formation in iris)
Retinal detachment
Vitreous Haemorrhage
Cataracts
117
How is Diabetic Retinpathy managed?
Anti VEGF
Laser Photocoagulation
Severe - keyhole vitreoretinal Surgery
Optimise DM control
118
Name three requirements of the accommodation reflex
Eyes converging
Pupil size reducing
Lens changing shape and pattern
119
What is Presbyopia?
Gradual loss of accommodation response due to decline in elasticity, becoming apparent when amplitude is insufficient to carry out near tasks
120
How does Presbyopia present?
Difficulty carrying out near tasks
Accommodative lag (from distance to near vice versa)
Tiring with continuous close work
121
How is Presbyopia treated?
OTC glasses are normally sufficient
If pre-existing refractive error - prescription glasses
122
If Presbyopia happens prematurely, what is the likely cause?
Accommodative Insufficiency (Associated with encephalitis and enclosed head trauma)
Inability to maintain binocular enlargment as object becomes closer (aka eye strain)
123
Name six causes of sudden visual loss
CRAO
Anterior Ischaemic Optic Neuropathy
Vitreous Haemorrhage
Retinal Vein Occlusion
Retinal Detachment
Optic Neuritis
124
What are the five broad causes of Central Retinal Artery Occlusion?
CVS Disease (carotid atherosclerosis, AF)
Vascular disease (dissection, fabrys)
Inflammatory (GCA)
Haematological
Rare (toxoplasmosis, Surgery)
125
Describe the arterial division and supply to the Retina
First branch of internal carotid - Opthalmic
Opthalmic gives off retinal and ciliary (supplying outer retina)
Retinal splits into superior and inferior and then temporal and nasal
126
How does CRAO present?
Sudden onset painless loss of vision
Due to potential supply from cilioretinal it can have a central area of visual sparing
RAPD
Pale Retina
Cheery Red Spot (Anastamotic supply)
127
How can CRAO be confirmed?
Fluorosciene Angiography
Slowed flow/filling defect
128
CRAO just be managed within 6 hours (if GCA - immediate steroids). What are the management options?
Intra-arterial thrombolysis - catheter directed delivery of tPA via Opthalmic Artery
Anterior Chamber Paracentesis (if not a candidate for Thrombolysis,reduces IOP to dislodge)
Ocular massage
Hyperbaric O2
Vasodilator
129
Define Anterior Ischaemic Optic Neuropathy
Loss of vision as a result of damage to optic nerve from ischaemia
Involves the 1mm head of optic nerve (AKA disc)
130
Anterior Ischaemic Optic Neuropathy can be Arteritic or Non Arteritic. Describe the Arteritic
5-10%
Inflammation and thrombosis of short posterior ciliary arteries resulting in ischaemia of optic nerve head
131
How does Arteritic Anterior Ischaemic Optic Neuropathy present?
Rapid onset unilateral visual loss and decreased acuity
Chalky white pallor of optic disc
Amaurosis fugax?
GCA signs?
132
How is Arteritic Ischaemic Optic Neuropathy investigated?
GCA - ESR/CRP, Temporal Artery Biopsy
MRI/USS - between Arteritic and non
OCT
133
Describe the management options for Arteritic Anterior Ischaemic Optic Neuropathy
IV Methylpred for 3 days (switch to oral and taper)
MAB against IL6 (Tocilizumab)
Methotrexate
134
Anterior Ischaemic Optic Neuropathy can be Arteritic or Non Arteritic. Describe the Non Arteritic
Majority idiopathic reduces blood flow
Crowded optic disc
Associated with - sleep apnoea, sildenafil, drusen
135
How does Non Arteritic AION present?
Acute painless visual loss
RAPD
Optic disc oedema and peripapillary splinter haemorrhages
136
How is Non Arteritic AION managed?
Exclude arteritic
Large doses of steroid
137
Vitreous haemorrhage is one of the most common causes of sudden painless visual loss. Describe the possible aetiologies
Proliferative diabetic retinopathy (fragile vessels)
Posterior vitreous detachment
Ocular Trauma
138
How does Vitreous Haemorrhage present?
-Sudden painless visual loss
-Red Hue (may turn green after breakdown)
-New onset floaters/cobwebs
- May be worse in the morning if blood settles during sleep
139
Name four investigations for Vitreous Haemorrhage
IOP
Slit Lamp - Red Cells in anterior vitreous
Rule out retinal detachment
USS
140
Describe the general management of Vitreous Haemorrhage
Exclude retinal detachment
Rest with head elevated and re- evaluate in 3-7 days for source
141
Name four definitive treatment options for Vitreous Haemorrhage
Laser Photocoagulation (for proliferative vasculopathies)
Anterior Retinal Cryotherapy
Vitrectomy
VEGF
142
Name three complications of Vitreous Haemorrhage
Haemosiderosis Bulbi
Retinal Detachment
Ghost cell glaucoma (rigid cells with denatured Hb)
143
Describe the pathophysiology of Retinal Vein Occlusion
-Thrombus forms in retinal veins and blocks drainage
-Pooling of blood in retina
-Leakage causing macula oedema and retinal haemorrhages
-VEGF release
144
How does Retinal Vein Occlusion present?
Sudden painless loss of vision
145
Name four features of fundoscopy for Retinal Vein Occlusion
Flame Haemorrhages
Blot Haemorrhages
Optic Disc Oedema
Macula Oedema
146
Name three bloods you would like to do in Retinal Vein Occlusion
FBC - Leukaemia
ESR - inflammatory disorders
Glucose - Diabetes
147
How is Retinal Vein Occlusion managed?
Laser Photocoagulation
Intravitreal Steroids
Anti VEGF therapies
148
Retinal detachment is where the neuro sensory layer separates from the pigmented. What are the two classifications?
Rhegmatous - following retinal break, normally after posterior vitreous detachment
Non Rhegmatous - Exudative (retinal drainage fluid between subretinal space) or tractional (fibres in vitreous contract, pulling retina away)
149
Myopia is a risk factor for all classifications of retinal detachment (longer and thinner). Give two risk factors for each classification
Rhegmatogenous - Age, Marfans
Tractional - Diabetic Retinopathy, Retinal Vein Occlusion
Exudative - inflammatory, vascular disease
150
How does Retinal Detachment present?
Painless
Peripheral vision loss (shadow coming across vision)
Flashes and floaters
151
How would you examine suspected retinal detachment?
-Pupillary Reflexes (?RAPD)
-Visual Acuity and Fields
-Dilated fundal exam (if large - sheet of sensory retina towards centre of globe)
Slit lamp - cells in anterior chamber, tobacco dust
152
How are Retinal Tears managed?
Laser therapy or Cryotherapy
Created adhesions between retina and choroid to prevent detachment
153
How is retinal detachment managed?
-Vitrectomy (replacement with oil/gas)
-Scleral buckling (pressure on sclera to bring choroid in)
-Pneumatic Retinopexy (gas bubble in vitreous to push against retinal layers)
154
Define Optic Neuritis
Inflammation of optic nerve characterised by the triad: reduced vision, eye pain and impaired colour vision
155
There are many causes of Optic Neuritis. Name 6
GCA
Autoimmune diseases
Post infectious
TB
B12 Deficiency
Drugs (Ethambutol, Isoniazid)
156
Give three signs on examination of Optic Neuritis
RAPD
Altitudinal field defects
Scotoma
157
How could you consider managing Optic Neuritis?
IV Methylpred to speed healing
158
What is Devics Disease?
Inflammatory demyelinating and necrotising Disease mainly involving the spinal cord and optic nerve
Appears like MS on scans
Cause of Optic Neuritis
Treated with steroids and plasma exchange
159
What is Acute Demyelinating Optic Neuritis?
Demyelination and atonal loss likely secondary to inflammatory process and delayed hypersensitivity
160
Name three presenting features of Acute Demyelinating Optic Neuritis
Photopsia
Uhthoff Phenomenon - increase in symptoms with increase in body temp
Pulfrichs Phenomenon - objects moving straight appear curved
161
Diplopia can be monocular or binocular, what is the difference?
Monocular - doesn’t disappear with one eye closed, likely opthalmological aetiology
Binocular - with one eye closed it disappears, likely neurological aetiology
162
Describe the anatomical course of CNIII
Emerges from midbrain
Travels close to PCA
Pierces dura near tentorium cerebelli
Lateral cavernous sinus
Superior orbital fissure
163
Name four causes of Oculomotor nerve lesions
Diabetes
GCA
Raised ICP
PCA Aneurysm
164
How do Oculomotor nerve lesions present?
Fixed dilated pupil that doesn’t accommodate
Ptosis
Unopposed lateral deviation
Intortion on looking down
Microvascular - pupil sparing
165
How do Oculomotor nerve lesions present (sympathetics involved)?
Pupil will be fixed but not dilated
166
Trochlear Nerve lesions are rare, give three causes
Orbital trauma
Diabetes
Infarction secondary to hypertension
167
Name 6 causes of Diplopia
CNIII lesion
CNIV lesion
CNVI lesion
Orbital Blow Out #
Thyroid Eye Disease
MG
168
How do Trochlear Nerve Lesions present?
Vertical Diplopia
Weakness of downward and intortion
Compensatory head tilt away from affected side
169
How does a CNVI lesion appear?
Inability to look laterally
170
Give three causes of a CNVI lesion
MS
Pontine Cerebrovascular incident
Raised ICP (due to long course)
171
Describe the pathophysiology of an Orbital Blow Out Fracture
Usually from an object <5cm
Force transmits along rim and into orbital floor
Force is transmitted into three buttresses (infraorbital, displacement of zygomaticofrontal suture, fracture of zygomatic arch)
172
Name five clinical features of Orbital Blow Out Fractures
Periorbital bruising
Surgical Emphysema
Vertical Diplopia (worse on looking up)
Endopthalmos
Infraorbital Paraesthesia
173
What investigations should you do for a suspected Orbital Blow Out?
Plain XRay - Facial, Occipitomental, Submentovertical (droplet sign in maxillary sinus)
CT
174
How are Orbital Blow Out Fractures managed?
Don’t blow nose for 10 days
Some can be managed with just broad spec abx
Surgery
175
What Orbital Blow Out Fractures require surgery?
-White eye blow out
-Symptomatic Exopthalmos of >2mm
->50% orbital floor involved
-Non resolving Diplopia after 2-3 weeks
176
What is Thyroid Eye Disease?
Most common extrathyroidal manifestation of Graves
Can also be hypothyroid or euthyroid
Due to cross reactivityof autoantibodies
177
The onset of Thyroid Eye Disease is normally within 18 months of diagnosis. Describe the pathophysiology
Initial inflammatory phase lasting 6-24 months (expansion of extraocular muscles and orbital fat resulting in proptosis and optic neuropathy)
Followed by inactive fibrotic phase
Infiltration of lymphocytes stimulate cytokine release and polysaccharide release from fibroblasts - leads to oedema
178
What are the important receptors in Thyroid Eye Disease?
TSH
IGF1
179
Name four risk factors for Thyroid Eye Disease
Current smoker
Female
Middle Aged
Radioiodine therapy
180
How does Thyroid Eye Disease present?
Ocular irritation
Ache behind eye
Lid oedema and lateral flare
Circumferential white eye
Lid lag
Progressive optic neuropathy - blurred vision, reduced acuity
181
How would you investigate Thyroid Eye Disease?
Thyroid levels
CT (soft tissue)/MRI (bone view pre op)
Visual acuity
CXR and TPMT (pre med)
182
How is Thyroid Eye Disease staged?
Clinical activity scoring and severity
Dolor, Rubor, Calor, Tumor, Functio Laesa
(Mourits)
183
Describe some general management points for Thyroid Eye Disease
Joint endocrine ophthalmology clinic
Smoking cessation
Maintain Euthyroid State
Prescribe ocular lubricants
184
Describe the more definite management of Thyroid Eye Disease
Prisms to control Diplopia
Botox to reduce upper lid swelling
Pulsed IV Methylprednisolone and Azathioprine
Orbital Radiotherapy
Orbital decompression if steroids don’t work
185
When does Thyroid Eye Disease require management?
Mourits>4
DON/RAPD/Field Defect
186
What is Myasthenia Gravis?
Autoimmune disease where antibodies destroy neuromuscular connections
Affects voluntary muscles of the body
187
Describe the pathophysiology of Myasthenia Gravis
-Receptor sites at NMJ are destroyed
-Not enough stimulation to trigger action potential
- Increased fatiguability with use (reduced ACh) and improvement with rest
188
Name some signs of Myasthenia Gravis
Ptosis
Cogan Lid Twitch (down gaze followed by up gaze, eye saccades and lid overshoots)
Incomitant strabismus
Raised eyebrows
Pupils never involved
189
Name three diagnostic tests for MG
Tensilon Test (inhibits AChesterase, only useful when they have measurable findings)
Repetitive Nerve Stimulation Test (decline in compound muscle action potentials within the first 4-5 stimuli)
Single Fibre EMG
190
Name two laboratory tests for MG
Serum Anti ACh Receptor Titre
Serum Anti Muscle Specific Kinase AB titre
191
What is the main differential for MG?
Lambert Eaton Syndrome
Improvement of symptoms with repeated stimulation
192
Describe the management of MG
Med - Steroids, Pyridostigmine, Immunomodulators (if refractory)
Surgery - Removal of thymus
193
Give three causes of Transient Visual Symptoms
Amaurosis Fugax
Papilledema
Migraine
194
What is Amaurosis Fugax?
Hypoperfusion of optic nerve, normally secondary to carotid artery atherosclerosis and secondary thromboemboli
Precedes stroke so urgent investigations required
195
Other than carotid pathology, give three causes of Amaurosis Fugax
GCA
Retinal Migraine
Papilledema
196
How does Amaurosis Fugax present?
Curtain descending down over vision
If provoked by gaze - optical lesion
197
How is Amaurosis Fugax investigated?
Inflammatory markers
Carotid imaging and cardiac evaluation
MRI/MRA
198
How is Amaurosis Fugax managed?
TIA - stroke work up
GCA - Emperic steroids and temporal artery biopsy
Antiplatelets/Anticoag
199
What is Papilledema?
Optic disc swelling secondary to raised ICP
Oedema, continued pressure and optic nerve atrophy
200
Name five causes of raised ICP
Skull is too small for brain
Brain volume is too large
Obstruction of CSF flow
Increased CSF production
Decreased CSF drainage
201
Name three investigations you would do to define the underlying cause of Papilledema
BP
CT/MRI
LP with opening pressure
202
What is the Dandy Criteria for Idiopathic Intracranial Hypertension?
Papilledema
Normal neuro exam
Normal MRI imaging
Normal CSF composition
Elevated LP opening pressure
203
The fundoscopy of Papilloedema is graded by the Frisen scale. What is this?
0 - Normal Optic Disc
1 -C shaped Halo of disc oedema
2 - Circumferential halo of disc oedema
3 - Obscuration of one or more segments of major blood vessels leaving disc
4 - partial obstruction of a segment of blood vessels on disc
5 - partial or total obstruction of all vessels on disc
204
Name three ways Papilloedema can present
Asymptomatic
Signs of raised ICP
Abducens Palsy
205
The gold standard management for Papilloedema is to treat underlying cause and reduced ICP. How should IIH be managed?
Weight reduction
Acetazolamide
?CSF Shunt, Duran Venous Stenting
206
Define Migraine
Primary headache disorder characterised by severe unilateral throbbing pain, associated with nausea, photophobia, phonophobia and preceding aura
Typically lasting 4-72hrs
207
What is Photophobia?
Light sensitivity, ocular discomfort and headache exacerbated by light
Always bilateral (differentiates from trigeminal issues - unilateral)
208
What are the five types of migraine with neuro- opthalmological symptoms
-Aura without headache (eg TIA)
-Basilar Type (dizziness, ataxia, tinnitus)
-Retinal (headache, scotoma, scintillation#)
-Migraine with binocular blindness
-Migrainous infarction (ischaemic brain lesions)
209
Blepharitis is inflammation of the eyelid margin, and can be anterior or posterior. What are the three main aetiologies?
Staph Infection
Seborrhoeic Dermatitis (ant)
Meibomian Gland Dysfunction (post)
210
What are the symptoms of Blepharitis?
Gritty/Itching/Burning
Bilateral symptoms
Lids stuck together upon waking
Associated - dry eye, Seborrhoeic dermatitis, rosacea
211
What are the signs of each of the underlying causes of Blepharitis?
Staph - Telangiectasia, eyelash deformity
Seborrhoeic- greasy lid margin, eyelashes stuck together
Meibomian - oil globules, Chalazia
212
Give three differentials of Blepharitis
BCC/SCC of eyelid
Contact/Atopic dermatitis
Impetigo
213
How should you manage Blepharitis?
Inform it’s a chronic condition but can be managed
Avoid contact lenses
Warm compress/lid massage/ cleansing
Chloramphenicol is infection
214
Dry eyes can be hyposecretive or evaporative. Give some causes of hyposecretion
Sjögren
Lacrimal gland insufficiency
Lacrimal gland obstruction
Antihistamines
TCA
215
Dry eyes can be hyposecretive or evaporative. Give some causes of evaporation
Meibomian gland dysfunction (Blepharitis)
Blink disorder (Parkinson’s
Thyroid
Allergies
Prolonged computer use
216
Dry eyes can cause a gritty, foreign body sensation worse at the end of the day. What are some red flags?
Severe eye pain
Significant visual loss
Photophobia
217
Name three investigations for dry eyes
Slit lamp
Schirmers (measure amount of eye wetting after five minutes)
Tear break uptime (time between last blink and first appearance of fluorosciene stained tear)
218
What are some general managements for dry eyes?
Review medications
Smoking cessation
Regular breaks
219
Name three tear substitutes
Drops (Hypermellose)
Gels (Viscotears, less frequent application)
Ointments (Coat cornea and reduce evaporation)
220
Define Chalazion
Focus of granulomatous inflammation in eyelid arising from blocked meibomian
221
How do Meibomian Cysts/Chalazions present?
Gradually enlarging round firm lesion
Generally painless once inflammation has settled
Blurred vision if compressing cornea
Yellowish swelling on underside of lid
222
How would you manage Chalazia
BD warm compress
Massage
Clean with baby shampoo
223
You would only investigate chalazia if it was recurrent or atypical. When would you refer?
Large and persistent
Visual problems
Low threshold in young children (amblyopia)
224
What is the most common periocular malignancy? Give three risk factors
BCC of the eye
Older age, Male, UV exposure
225
How does Periocular BCC present?
Slow developing non resolving lesion of the eyelid
On lower lid or medial canthus most commonly
May lose eyelashes
226
How are Periocular BCCs managed?
Advise on sun protection
Mohs micrographic Surgery
?Radiotherapy
227
What is Herpes Zoster Opthalmaticus (ie Shingles of Eye)?
Viral disease characterised by painful vesicular rash in one or more dermatomal distributions by trigeminal nerve
Due to reactivation of VZV within sensory ganglion
228
How does Herpes Zoster Opthalmaticus present?
Prodrome
Acute painful vesicular rash
Hutchinsons Sign - lesions at side/root of nose which is a strong predictor of ocular inflammation
229
Name four investigations for Herpes Zoster Opthalmaticus
Test corneal sensation
Culture for VZV specific IgM
Slit lamp
Fluorosciene (Rule out corneal damage)
230
How is Herpes Zoster Opthalmaticus managed?
If skin rash is only symptom - Aciclovir and topical steroids
If any sign of intraocular pathology - systemic steroids
WHO ladder for pain relief
May require corneal transplant or glaucoma surgery in future
231
What is a Subconjunctival Haemorrhage? Give four causes
Bleeding of the conjunctival vessels into subconjunctival space
Valsalva
HTN
Contact lenses
Drugs
232
How do Subconjunctival Haemorrhages present?
Unilateral red eye
Red patch with sharply defined edges
Otherwise normal eye exam
If no posterior margin - intracranial bleed
233
What advice should you give someone with Subconjunctival Haemorrhages?
Self limiting
Eye drops for dry eyes
Discourage Aspirin and NSAIDs
234
What is Posterior Vitreous Detachment?
Vitreous gel comes away from retina
Very common, especially in older patients
235
How does Posterior Vitreous Detachment present?
Painless condition
May be completely asymptomatic
Slight Vision loss, floaters, flashing lights
236
How is Posterior Vitreous Detatchment managed?
No treatment necessary, over time brain adjusts
Can predispose to retinal tears/detachment so monitor
237
What is Retinitis Pigmentosa?
Congenital inherited condition where there is degeneration of rods and cones
Rods degenerate more than cones (night time blindness)
238
How does Retinitis Pigmentosa present?
Symptoms usually start in childhood
Night blindness
Peripheral vision lost before central
239
What would be seen on fundoscopy of Retinitis Pigmentosa?
Bony spicule pigmentation (most concentrated around mid peripheral area)
240
Name two diseases associated with Retinitis Pigmentosa
Ushers Syndrome (+ hearing loss)
Bassen Kornzweig
241
Describe the management of Retinitis Pigmentosa
Genetic counselling
Visual aids
Driving limitations
Slow progression - vitamins, antioxidants, anti vegf, steroids
242
Give five causes of an abnormally shaped pupil
Trauma to muscles
Anterior uveitis (scar tissue)
AACG (Ischaemic damage - oval)
Coloboma (holes in iris)
Tadpole (spasm in part of pupil, migraines)
243
Name four causes of a dilated pupil
Oculomotor nerve palsy
Raised ICP
Cocaine
Adie/Tonic Pupil
244
What is a Tonic Pupil?
Damage to post ganglion parasympathetic
May be viral
Dilated and sluggish to light
245
Name four causes of a constricted pupil
Horners
Argyll Robertson (Neurosyphilis)
Opiates
Pilocarpine
246
Describe the features of Horners Syndrome
Ptosis
Miosis
Anhidrosis
Enopthalmos
Light and Accomodation reflexes unaffected
247
Name the four central lesions that can cause Horners Syndrome (4S’s). What is characteristic?
Stroke
Multiple Sclerosis
Swelling
Syringomyelia
Anhidrosis of arm and trunk as well as face
248
Name the four preganglionic lesions that can cause Horners Syndrome (4Ts). What is characteristic?
Tumour
Trauma
Thyroidectomy
Top Rib
Anhidrosis of race
249
Name the four post ganglionic lesions that can cause Horners Syndrome (4Cs). What is characteristic?
Carotid aneurysm
Carotid artery dissection
Cavernous sinus thrombosis
Cluster headache
No anhidrosis
250
What is associated with Congenital Horners?
Heterochromia
251
Name two ways Horner’s Syndrome can be diagnosed
Cocaine Eye Drops - blocks NA uptake, normal eye dilated but no effect on other eye
Adrenaline Eye Drops - Won’t dilate a normal pupil but will in Horners
252
Name five features on fundoscopy of Hypertensive Retinopathy
Silver/copper wiring (thickened and sclerosed)
AV nipping (sclerosis where they cross)
Cotton wool spots
Hard exudate
Retinal haemorrhages
253
Name three risk factors for Choroidal Melanoma
Light iris
Sunlight exposure
Positive FH
254
How does Choroidal Melanoma present?
Tends to be asymptomatic
May have blurred vision, paracentral scotoma, floaters and flashes
255
How does a Choroidal Melnaoma appear on Fundoscopy?
Nodular dome shaped lesion
256
Name two non surgical and two surgical managements of Choroidal Melanoma
Laser Photocoagulation, Sterotactic Radiotherapy
Block excision, Enucleation
257
What is Amblyopia?
Decreased vision arising from dysfunctional processing of visual information
Due to degradation of retinal image during critical development
Can be functional or organic (irreversible)
258
Name three common causes of Amblyopia
Constant Strabismus
Asymmetric refractive errors
Orbital pathology affecting growth/clarity (eg strawberry naevus)
259
Describe the period in which Amblyopia can be reversed
In first 2-3 years it develops rapidly
Develops more slowly until 7/8y
If halted and then restored before the age of around 8 it can be reversed
260
Amblyopia normally has a significant difference in acuity between eyes. How is this defined?
Two or more Snellen/LogMAR differences
261
How can Amblyopia be managed?
Modifying visual input into affected eye
Correcting refractive error
Obscuring visual input to other eye(patching, drops)
262
Define Strabismus
Misalignment of the Eyes resulting in non corresponding retinal images
Often idiopathic or secondary to hydroceph/SOL/cerebral palsy/trauma
263
What is the terminology for Strabismus?
Eso - inward
Exo - outward
Hypo - down
Hyper - up
Manifested - tropia
Latent - Phonia
264
How can Strabismus be classified?
Congenital or acquired
Right/Left/Alternating
Permanent or intermittent
Manifest or latent
Concomitant (non paralytic) or incomitant
265
What is a non paralytic strabismus?
Size of deviation doesn’t vary with direction of gaze
Usually congenital
Extraocular muscles and nerves are normal
Compensatory head tilt
266
How does Esotropia present?
Inward turning squint
Can be on accommodation
267
How does Exotropia present?
Outward squint
Begins intermittently with daydreaming/tiredness and progresses
268
How does Hyper/Hypotropia present?
Vertical Strabismus
Changes in head posture
SO paresis
269
What is the Hirschberg test for Strabismus?
Hold a pen torch in front of patients eyes and observe where reflection lies
Outer margin - Esotropia
Inner Margin - Exotropia
270
Other than the Hirschberg test, name three other investigations for Strabismus
Cover uncover - observe movement
Alternate cover - shows latent
Orthoptic Assessment
271
How is Strabismus managed?
Correcting refractive errors
Prisms
?Surgical intervention
?Chemodenervation
272
What is Paralytic Strabismus?
Damag to extraocular muscles/nerves
273
What is Myopia?
Near sighted
Excess optical power for axon length, light focuses in front of retina
274
Name three risk factors for Myopia
FH
Close up work
Marfans
275
Define Hypermetropia
Long sightedness
Insufficient power for axonal length
Light is focussed beyond retina
276
Name three risk factors for Hypermetropia
Corneal Dystrophy
Congenital Cataracts
Micropthalmia
277
Describe registering as visually impaired
Two levels: Severely sight impaired/Blind
Loss of sight in one eye doesn’t qualify you unless you also have poor sight in the other
278
Name two benefits to officially registering as blind or partially
Blind persons income tax allowance, 50% reduction on TV licence
Free NHS Sight Test, Glasses vouchers
279
Describe the DVLA visual requirements for driving
Able to read a car plate made after 1st September 2001 from 20 meters
Visual Acuity of 6/12
Lorry/Bus have to have 6/7.5 Atleast in best eye
280
How can a LogMAR score be calculated from Snellen?
Snellen 6/10
Log10(10/6)
281
How can a LogMAR score be calculated?
0.1 + score of best line read - (0.02* letters read)
282
Name three causes of generalised blurring
Presbyopia
Dry Eyes
Cataracts
283
Name two causes of central blurring
Diabetic Maculopathy
Macular Degeneration
284
Name two causes of black spots/blobs
Does it move with eye?
Y - Vitreous Disease
N - Retinal Detachment
285
Name two causes of Photopsia
Detached Retina
Migraine with Aura
286
Name three uses for Mydriatic/Cycloplegic drops
Dilation for retinal visualisation
Amblyopia
Refraction for children with glasses
287
Name three Mydriatic/Cycloplegic drops
Anticholinergic - Atropine, Cyclopentolate
Sympathetic - Phenylephrine
288
Name three side effects of Mydriatic/a Cycloplegic drops
Eye whitening
Face redness/warmth
Can’t drive until worn off
289
Name a side effect of Fluoroscein
Staining
290
Define Retinoblastoma
Retinoblastomas are the most common primary intraocular malignancy in children. They are caused by sporadic or inherited mutations in the retinoblastoma gene (Rb)
291
What are the two types of Retinoblastoma
Sporadic (usually unilateral)
Hereditary (normally bilateral and associated with other malignancies)
292
Describe the aetiology of Heritable Retinoblastoma
Two hit hypothesis of Rb gene
Autosomal Dominant inheritance
293
How do Retinoblastomas present?
Leukocoria
Strabismus
294
How is suspected Retinoblastoma investigated?
Fundoscopy
Ultrasound of the orbit
MRI (CT radiation could induce cancer in those with germline RB mutation)
295
How should Retinoblastomas be managed?
Salvageable - Cryotherapy, Brachytherapy, Chemotherapy
Non Salvagable - Enucleation
296
Name three complications of Cataract surgery and how they’re minimised (if relevant)
Endopthalmitis - prophylactic abx
Posterior Capsule Rupture
Floppy Iris Syndrome
297
Name three causes of RAPD
Optic Neuritis
Retinal Detachment
CMV
