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Year 4 Neuro and Special Senses > Opthalmology Conditions > Flashcards

Opthalmology Conditions Flashcards

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

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2
Q

Define Glaucoma

A

Progressive optic neuropathy in which raised intraocular pressure is a key factor

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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)

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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

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5
Q

Name 5 risk factors for Acute Angle Closure Glaucoma

A

Increased Age,
Asian Ethnicity,
FH,
Hyperopia,
Anticholinergic meds

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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

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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)

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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

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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

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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

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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

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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

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13
Q

Define Endopthalmitis

A

Severe inflammation of anterior and/or posterior chamber (can be sterile but normally due to infection)

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14
Q

Give 5 causes of Endopthalmitis

A

Trauma,
Eye Surgery,
VEGF injections,
Endogenous seeding,
Extension of Corneal infection

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15
Q

Describe the likely pathogens of Endopthalmitis with each cause

A

Surgery - Coag neg Staph (epidermis),
Trauma - bacillus cereus,
Endogenous - S.Aureus,Klebsiella

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16
Q

How does Endopthalmitis present?

A

Acute eye pain,
Reduced vision,
Hypopyon ,
?swollen eyelid

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17
Q

Name four risk factors for Endopthalmitis

A

Poor surgical technique,
Contaminated lens,
Contact lens wear,
Immunosupression

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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)

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19
Q

How does Endopthalmitis present?

A

Acute eye pain,
Reduced vision,
Swollen eyelid,
Hypopyon

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20
Q

Name two differentials for Endopthalmitis

A

Retained lens material,
Raised IOP as a result of procedure

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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

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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

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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

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24
Q

Name five sources of infection for Orbital Cellulitis

A

Extension from periorbital structures

Extension from presentation structures

Direct Inoculation

Post Surgery

Haematogenous

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25
Q

Name four common pathogens and one rare for Orbital Cellulitis

A

Common - H.Influenza, Strep Pneumoniae, S.Aureus, S.Pyogenes

Rare - mucormycosis (rare fungal associated with DKA and Neutropenic Sepsis)

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26
Q

Name two anterior, two orbital and two systemic features of Orbital Cellulitis

A

Anterior - unilateral lid swelling, conjunctival chemosis

Orbital - external eye muscle painful opthamoplegia and blurred vision

Systemic - fever, Malaise

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27
Q

Orbital Cellulitis is generally a clinical diagnosis. What investigations could you do, and what would they show?

A

FBC - leukocytosis

Blood cultures - negative

LP (if focal signs)

Swabs

CT sinus and orbit - extension

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28
Q

Orbital Cellulitis is an emergency and requires urgent antibiotics and four hourly monitoring. What are the Abx of choice?

A

1) Co Amoxiclav
If pen allergic - Clindamycin and Metronidazole

MRSA - Vancomycin

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29
Q

When would you consider surgery in Orbital Cellulitis?

A

Resistant to antibiotics

Reduced visual acuity

CT evidence of orbital collection

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30
Q

Name four complications of Orbital Cellulitis

A

Endopthalmitis
Meningitis
Orbital Abscess
Subperiosteal Abscess

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31
Q

Corneal injuries can be physical, chemical or environmental. What makes a corneal abrasion (partial thickness) more likely?

A

If the eye doesn’t shut properly

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32
Q

Other than corneal abrasions, what other corneal injuries are common?

A

Superficial Keratitis
Foreign Bodies

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33
Q

If there is no clear mechanism of injury but you suspect damage to the cornea, what should you cosncier

A

HSV infection

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34
Q

How does a superficial corneal abrasion present?

A

Redness
Pain
Watering
Foreign Body Sensation
Photophobia

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35
Q

How does a penetration corneal injury present?

A

Distorted globe
Hyphaema
Conjunctival laceration
Red and watering

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36
Q

Name some functional and general features you are looking for on observation of corneal injury

A

Functional - Diplopia, Abnormal visual fields, RAPD
General - raised IOP, infection

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37
Q

How can the Cornea be examined in suspected corneal injury?

A

Seidles Test - 10% Fluorescine and slit lamp to look for corneal leak (yellow/orange)

Abrasion with dilute fluorosciene

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38
Q

Name three red flags for corneal injury

A

Deep lid laceration
Subconjunctival haemorrhage
Pupils/Iris/Fundus abnormality

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39
Q

How would you manage a Corneal Abrasion?

A

Pain relief (topical NSAIDs or Oral Abx)

Topical chloramphenicol to prevent secondary infection

Tetanus prophylaxis where necessary

Avoid contact lenses for 2 weeks

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40
Q

How are Corneal Foreign Bodies managed?

A

Topical anaesthetic

Eye irrigation and removal with damp cotton bud

After removal treat as corneal abrasion

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41
Q

How can rust rings be removed?

A

A sterile rotating burr

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42
Q

How should a penetrating corneal injury be managed?

A

Cover with rigid eye patch and refer immediately for emergency surgery

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43
Q

Give two examples of how chemical corneal injuries can be managed?

A

CA gas - blown off the eye using a hairdryer

Pepper spray and chlorine gas - copiously irrigated

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44
Q

Define Hyphaema

A

When blood enters anterior chamber between cornea and iris

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45
Q

How does a Hyphaema present?

A

Decrease/ Loss of vision (may improve as gravity pulls the blood down)
Red tinge to eye

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46
Q

Name 5 causes of a Hyphaema

A

Intraocular Surgery
Blunt trauma
Lacerating Trauma
Leukaemia
Retinoblastoma

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47
Q

How are Hyphaemas managed?

A

Small - Outpatient basis, antifibrinolytics, corticosteroids, mitotics, asparin

Non resolving - surgical clean out

Pain relief - avoid aspirin and NSAIDs due to platelet interaction

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48
Q

Name two complications of Hyphaema

A

Haemosiderosis

Raised IOP

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49
Q

What is the grading system for chemical injury of the eye?

A

Roper Hall

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50
Q

What is the immediate management for Ocular Chemical Injury?

A

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

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51
Q

If the Chemical Injury of the eye was moderate or severe, how would it be managed?

A

Dexamethasone 1-2 hourly
Vitamin C (topically and orally)
Citrate and Tetracyclines

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52
Q

Conjunctivitis is inflammation of the conjunctiva. How does Bacterial Conjunctivitis present?

A

Purulent discharge
Worse in the morning
Inflamed conjunctiva
Starts in one eye and spreads to the other

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53
Q

How does Viral Conjunctivitis present?

A

Clear discharge
Other symptoms of viral infection (URTI)
Preauricular lymph nodes

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54
Q

What advice should you give patients with conjunctivitis?

A

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

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55
Q

How can bacterial conjunctivitis be managed?

A

Chloramphenicol (contraindicated if pregnant or breast feeding)
Fusidic Acid

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56
Q

How does Allergic Conjuncitivitis present?

A

Swelling of conjunctival sac and eyelid
Watery discharge
Itch

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57
Q

How is Allergic Conjunctivitis managed?

A

Antihistamines (Oral or topical)

Topical mast cell stabilisers used for several weeks if chronic symptoms

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58
Q

Name four causes of Anterior Uveitis

A

Autoimmune
Infection
Trauma
Ischaemia

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59
Q

Anterior Uveitis can be Acute or chronic . How do they differ ?

A

Chronic is more Granulomatous, less severe, longer symptom duration (often >3m)

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60
Q

Name three associations of Anterior Uveitis and Chronic Anterior Uveitis respectively

A

Anklyosing Spondylitis, IBD, Reactive Arthritis

Sarcoidosis, Syphilis, TB

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61
Q

How does Anterior Uveitis present?

A

Spontaneous unilateral symptoms
Dull aching
Red Eye
Ciliary Flush (ring of red from cornea outwards)
Reduced visual acuity
Flashers and floaters

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62
Q

What causes floaters in Anterior Uveitis?

A

Inflammation and immune cells in the anterior chamber

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63
Q

What is Posterior Synechiae? Give an association

A

Adhesions that can cause disruption to pupillary shape

Anterior Uveitis

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64
Q

If a GP suspects a sight threatening opthalmological condition, what should they do?

A

Same day assessment by ophthalmologist

Slit lamp examination and IOP measurement

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65
Q

How would you manage Anterior Uveitis?

A

Steroids
Cytoplegic/Mydriatic medication (eg Cyclopentolate)
Immunosupressants

Severe - Laser therapy, Cryotherapy

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66
Q

What is the role of Cytoplegic/Mydriatic Medication in Anterior Uveitis?

A

Paralyses ciliary muscles, reducing pain and the formation of Posterior Synechiae

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67
Q

Keratitis is infection of the cornea, give three causes

A

Trauma
Foreign Body
Infected Contact Lens

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68
Q

Describe the pathophysiology of Bacterial Keratitis

A

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

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69
Q

Name four presenting features of Keratitis

A

Redness
Pain
Photophobia
Reduced acuity

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70
Q

What can be seen on examination of a Keratitic eye?

A

Oedema
White cell infiltration
Epithelial defect

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71
Q

How is Keratitis managed?

A

Intensive topical antibiotics - Ofloxacin for Pseudomonas cover (with or without cycloplegics)

?Steroids

Stop contact lens use

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72
Q

Herpes Simplex Keratitis is the most common, and only normally affects epithelial layer. What could distinguish it from other causes of Keratitis?

A

Vesicles around the eye

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73
Q

What would Fluorescein staining of a HSV Keratitis eye show?

A

Dendritic corneal ulcer (branching and spreading)

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74
Q

How is HSV Keratitis managed?

A

Acyclovir (topical or oral)
Ganciclovir eye gel
Topical steroids

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75
Q

Define Scleritis

A

Inflammation of full thickness of the sclera

Normally not caused by infection

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76
Q

What is the most severe form of Scleritis?

A

Necrotising Scleritis

Visual impairment but not pain
Can lead to Scleral perforation

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77
Q

Name four associated conditions with scleritis

A

SLE
IBD
RA
Sarcoidosis

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78
Q

How does Scleritis present?

A

50% bilateral

Pain (especially on eye movement)
Photophobia
Reduced acuity
Abnormal pupillary response

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79
Q

How is Scleritis managed?

A

Underlying condition

NSAIDs and Steroids

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80
Q

Name five causes of Gradual Visual Deterioration

A

Cataracts
Open Angle Glaucoma
ARMD
Diabetic Retinopathy
Presbyopia

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81
Q

What are Cataracts?

A

Opacification of the Lens

Major cause of treatable blindness worldwide

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82
Q

Cataracts can be age related or non age related. Give three causes of non age related

A

Trauma
Steroids
Uveitis

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83
Q

What are the three classifications of Paediatric Cataracts

A

1/3 Inherited (Autosomal Dominant)
1/3 Systemic (Rubella, Fabrys)
1/3 Idiopathic

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84
Q

Cataracts can be classified depending on the location of lens affected. What are the three classifications

A

Nuclear
Cortical
Posterior Subcapsular

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85
Q

How do Nuclear Cataracts present?

A

Loss of colour vision
Slow progression

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86
Q

How do Cortical Cataracts present?

A

Less visual degradation
Slow progression

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87
Q

How to Posterior Subcapsular Cataracts present?

A

Disabling glare to bright lights
Quick progression

Links to DM and Steroids

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88
Q

Describe the pathophysiology of Cataracts

A

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

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89
Q

Give 6 presenting features of Cataracts

A

Painless loss of vision
Halls around lights
Sensitivity to light and glare
Polyopia
Myopic shift (improved near sighted)
Loss of red reflex

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90
Q

Cataracts are a clinical diagnosis. What features will be seen on Opthalmoscope/Slit Lamp?

A

Loss of red reflex
Opacification
Obscuration of ocular detail

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91
Q

Surgery is carried out for Cataracts when they have a significant impact on ADLs. What are the two techniques called?

A

Phacoemulsification
Extracapsular Cataract Extraction

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92
Q

Name two differences between the Cataract surgical techniques

A

PE - breaks up diseases lens and aspirates contents, small incision
ECE- Whole removal of diseased nucleus, larger incision

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93
Q

Name three immediate and three delayed features of Cataract Surgery

A

Immediate - Endopthalmitis, Lens Malposition, Toxic Anterior Segment Syndrome

Delayed - retinal detachment, macular degeneration, Posterior capsule opacification *

*proliferation of lens remnants, treated with laser

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94
Q

Describe the four layers of the Macula

A

Choroid
Bruch’s Membrane
Retinal Pigment Epithelium
Photoreceptors

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95
Q

ARMD is the leading cause of blindness in the UK, what are the two types?

A

Dry - 90%
Wet - 10%

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96
Q

Describe Dry ARMD

A

Progressive atrophy
Doesn’t exude

Late - Geographic Atrophy (large well demarcated sections of retina stop functioning)

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97
Q

Describe Wet ARMD

A

Worse prognosis
Development of new vessels from choroid layer into retina (via VEGF)
Vessels leak - Oedema

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98
Q

Drusen are characteristic of ARMD. What are they?

A

Yellow deposits of protein/lipids between retinal pigment epithelium and Bruchs

Can be normal
Larger and greater numbers can be an early sign

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99
Q

Give four risk factors for ARMD

A

Age
Smoking
Chinese Ethnicity
FH

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100
Q

How does ARMD present?

A

Gradually worsening central visual loss
Reduced acuity
Crooked appearance to lines
Wet - more acute and rapid

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101
Q

Name four investigations (other than Snellen) for ARMD and what you would see

A

Amsler Grid Test - Straight Line Distortion

Fundoscopy - Drusen

OCT - cross sectional retinal view (wet)

Fluorescein Angiography- Oedema and Neovascularisation

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102
Q

How is Dry ARMD managed?

A

No treatment just lifestyle means urges to slow progression (smoking cessation, BP control, Vitamins)

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103
Q

How is Wet ARMD managed?

A

Anti VEGF Vitreous injections (Ranibizumab)

Started within three months

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104
Q

Give four risk factors for Open Angle Glaucoma

A

Age
Afrocaribbean ethnicity
Diabetes
Myopia

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105
Q

Open Angle Glaucoma can be primary or secondary. What is primary?

A

Unknown aetiology

Unsure if increased production or decreased drainage

May be predisposed by microcirculatory factors and genetic damage

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106
Q

Open Angle Glaucoma can be primary or secondary. What is secondary?

A

Reduced drainage and increased IOP

5 subtypes : Neovascular (DM), Pseuodoexfoliative, Uveitis, Glucocorticoid Induced, Pigmentary

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107
Q

How does Open Angle Glaucoma present?

A

Largely asymptomatic until late stages

Central vision relatively preserved until late - tunnel vision and bumping into things

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108
Q

Name five investigations for Open Angle Glaucoma

A

-Opthalmoscope (progressive cupping)
-Humphrey visual field analyser
-Goldman Applanation Tonometry
-Gonioscopy
-Corneal thickness (contextualises IOP)

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109
Q

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

A

Latanoprost

Pregnancy and Breast Feeding

Brown Iris pigmentation and pigmentation of surrounding skin (also lash thickening, irritation)

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110
Q

What is the surgical management for Open Angle Glaucoma?

A

Lasted trabeculoplasty

Soft laser ‘wakes up meshwork’

Or Trabeculectomy

Can cause iritis and blebitis

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111
Q

Describe the pathophysiology of Diabetic Retinopathy

A

Vessels in the retina are damaged by prolonged hyperglycaemia, leading to increased vascular permeability

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112
Q

Describe 6 features of Diabetic Retinopathy as seen on an Opthalmoscope

A

Blot Haemorrhages and Hard Exudates (leakage)
Microaneurysms (weakness)
Venous Beading
Cotton Wool Spots (nerve damage)
Neovascularisation (local GF release)

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113
Q

Diabetic Retinopathy can be non proliferative, proliferative or a maculopathy. Describe non proliferative

A

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

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114
Q

Diabetic Retinopathy can be non proliferative, proliferative or a maculopathy. Describe proliferative

A

Neovascularisation
Vitreous Haemorrhage

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115
Q

Diabetic Retinopathy can be non proliferative, proliferative or a maculopathy. Describe Maculopathy

A

Macular Oedema
Ischaemic Maculopathy

Can be focal/diffuse/central involving

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116
Q

Name four complications of Diabetic Retinopathy

A

Rubeosis Iridis (new BV formation in iris)
Retinal detachment
Vitreous Haemorrhage
Cataracts

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117
Q

How is Diabetic Retinpathy managed?

A

Anti VEGF
Laser Photocoagulation
Severe - keyhole vitreoretinal Surgery

Optimise DM control

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118
Q

Name three requirements of the accommodation reflex

A

Eyes converging
Pupil size reducing
Lens changing shape and pattern

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119
Q

What is Presbyopia?

A

Gradual loss of accommodation response due to decline in elasticity, becoming apparent when amplitude is insufficient to carry out near tasks

120
Q

How does Presbyopia present?

A

Difficulty carrying out near tasks

Accommodative lag (from distance to near vice versa)

Tiring with continuous close work

121
Q

How is Presbyopia treated?

A

OTC glasses are normally sufficient

If pre-existing refractive error - prescription glasses

122
Q

If Presbyopia happens prematurely, what is the likely cause?

A

Accommodative Insufficiency (Associated with encephalitis and enclosed head trauma)

Inability to maintain binocular enlargment as object becomes closer (aka eye strain)

123
Q

Name six causes of sudden visual loss

A

CRAO
Anterior Ischaemic Optic Neuropathy
Vitreous Haemorrhage
Retinal Vein Occlusion
Retinal Detachment
Optic Neuritis

124
Q

What are the five broad causes of Central Retinal Artery Occlusion?

A

CVS Disease (carotid atherosclerosis, AF)

Vascular disease (dissection, fabrys)

Inflammatory (GCA)

Haematological

Rare (toxoplasmosis, Surgery)

125
Q

Describe the arterial division and supply to the Retina

A

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
Q

How does CRAO present?

A

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
Q

How can CRAO be confirmed?

A

Fluorosciene Angiography

Slowed flow/filling defect

128
Q

CRAO just be managed within 6 hours (if GCA - immediate steroids). What are the management options?

A

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
Q

Define Anterior Ischaemic Optic Neuropathy

A

Loss of vision as a result of damage to optic nerve from ischaemia

Involves the 1mm head of optic nerve (AKA disc)

130
Q

Anterior Ischaemic Optic Neuropathy can be Arteritic or Non Arteritic. Describe the Arteritic

A

5-10%

Inflammation and thrombosis of short posterior ciliary arteries resulting in ischaemia of optic nerve head

131
Q

How does Arteritic Anterior Ischaemic Optic Neuropathy present?

A

Rapid onset unilateral visual loss and decreased acuity

Chalky white pallor of optic disc

Amaurosis fugax?

GCA signs?

132
Q

How is Arteritic Ischaemic Optic Neuropathy investigated?

A

GCA - ESR/CRP, Temporal Artery Biopsy

MRI/USS - between Arteritic and non

OCT

133
Q

Describe the management options for Arteritic Anterior Ischaemic Optic Neuropathy

A

IV Methylpred for 3 days (switch to oral and taper)

MAB against IL6 (Tocilizumab)

Methotrexate

134
Q

Anterior Ischaemic Optic Neuropathy can be Arteritic or Non Arteritic. Describe the Non Arteritic

A

Majority idiopathic reduces blood flow
Crowded optic disc

Associated with - sleep apnoea, sildenafil, drusen

135
Q

How does Non Arteritic AION present?

A

Acute painless visual loss
RAPD

Optic disc oedema and peripapillary splinter haemorrhages

136
Q

How is Non Arteritic AION managed?

A

Exclude arteritic

Large doses of steroid

137
Q

Vitreous haemorrhage is one of the most common causes of sudden painless visual loss. Describe the possible aetiologies

A

Proliferative diabetic retinopathy (fragile vessels)
Posterior vitreous detachment
Ocular Trauma

138
Q

How does Vitreous Haemorrhage present?

A

-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
Q

Name four investigations for Vitreous Haemorrhage

A

IOP
Slit Lamp - Red Cells in anterior vitreous
Rule out retinal detachment
USS

140
Q

Describe the general management of Vitreous Haemorrhage

A

Exclude retinal detachment

Rest with head elevated and re- evaluate in 3-7 days for source

141
Q

Name four definitive treatment options for Vitreous Haemorrhage

A

Laser Photocoagulation (for proliferative vasculopathies)

Anterior Retinal Cryotherapy

Vitrectomy

VEGF

142
Q

Name three complications of Vitreous Haemorrhage

A

Haemosiderosis Bulbi
Retinal Detachment
Ghost cell glaucoma (rigid cells with denatured Hb)

143
Q

Describe the pathophysiology of Retinal Vein Occlusion

A

-Thrombus forms in retinal veins and blocks drainage
-Pooling of blood in retina
-Leakage causing macula oedema and retinal haemorrhages
-VEGF release

144
Q

How does Retinal Vein Occlusion present?

A

Sudden painless loss of vision

145
Q

Name four features of fundoscopy for Retinal Vein Occlusion

A

Flame Haemorrhages
Blot Haemorrhages
Optic Disc Oedema
Macula Oedema

146
Q

Name three bloods you would like to do in Retinal Vein Occlusion

A

FBC - Leukaemia
ESR - inflammatory disorders
Glucose - Diabetes

147
Q

How is Retinal Vein Occlusion managed?

A

Laser Photocoagulation
Intravitreal Steroids
Anti VEGF therapies

148
Q

Retinal detachment is where the neuro sensory layer separates from the pigmented. What are the two classifications?

A

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
Q

Myopia is a risk factor for all classifications of retinal detachment (longer and thinner). Give two risk factors for each classification

A

Rhegmatogenous - Age, Marfans
Tractional - Diabetic Retinopathy, Retinal Vein Occlusion
Exudative - inflammatory, vascular disease

150
Q

How does Retinal Detachment present?

A

Painless
Peripheral vision loss (shadow coming across vision)
Flashes and floaters

151
Q

How would you examine suspected retinal detachment?

A

-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
Q

How are Retinal Tears managed?

A

Laser therapy or Cryotherapy

Created adhesions between retina and choroid to prevent detachment

153
Q

How is retinal detachment managed?

A

-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
Q

Define Optic Neuritis

A

Inflammation of optic nerve characterised by the triad: reduced vision, eye pain and impaired colour vision

155
Q

There are many causes of Optic Neuritis. Name 6

A

GCA
Autoimmune diseases
Post infectious
TB
B12 Deficiency
Drugs (Ethambutol, Isoniazid)

156
Q

Give three signs on examination of Optic Neuritis

A

RAPD
Altitudinal field defects
Scotoma

157
Q

How could you consider managing Optic Neuritis?

A

IV Methylpred to speed healing

158
Q

What is Devics Disease?

A

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
Q

What is Acute Demyelinating Optic Neuritis?

A

Demyelination and atonal loss likely secondary to inflammatory process and delayed hypersensitivity

160
Q

Name three presenting features of Acute Demyelinating Optic Neuritis

A

Photopsia
Uhthoff Phenomenon - increase in symptoms with increase in body temp
Pulfrichs Phenomenon - objects moving straight appear curved

161
Q

Diplopia can be monocular or binocular, what is the difference?

A

Monocular - doesn’t disappear with one eye closed, likely opthalmological aetiology

Binocular - with one eye closed it disappears, likely neurological aetiology

162
Q

Describe the anatomical course of CNIII

A

Emerges from midbrain
Travels close to PCA
Pierces dura near tentorium cerebelli
Lateral cavernous sinus
Superior orbital fissure

163
Q

Name four causes of Oculomotor nerve lesions

A

Diabetes
GCA
Raised ICP
PCA Aneurysm

164
Q

How do Oculomotor nerve lesions present?

A

Fixed dilated pupil that doesn’t accommodate

Ptosis

Unopposed lateral deviation

Intortion on looking down

Microvascular - pupil sparing

165
Q

How do Oculomotor nerve lesions present (sympathetics involved)?

A

Pupil will be fixed but not dilated

166
Q

Trochlear Nerve lesions are rare, give three causes

A

Orbital trauma
Diabetes
Infarction secondary to hypertension

167
Q

Name 6 causes of Diplopia

A

CNIII lesion
CNIV lesion
CNVI lesion
Orbital Blow Out #
Thyroid Eye Disease
MG

168
Q

How do Trochlear Nerve Lesions present?

A

Vertical Diplopia

Weakness of downward and intortion

Compensatory head tilt away from affected side

169
Q

How does a CNVI lesion appear?

A

Inability to look laterally

170
Q

Give three causes of a CNVI lesion

A

MS
Pontine Cerebrovascular incident
Raised ICP (due to long course)

171
Q

Describe the pathophysiology of an Orbital Blow Out Fracture

A

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
Q

Name five clinical features of Orbital Blow Out Fractures

A

Periorbital bruising
Surgical Emphysema
Vertical Diplopia (worse on looking up)
Endopthalmos
Infraorbital Paraesthesia

173
Q

What investigations should you do for a suspected Orbital Blow Out?

A

Plain XRay - Facial, Occipitomental, Submentovertical (droplet sign in maxillary sinus)

CT

174
Q

How are Orbital Blow Out Fractures managed?

A

Don’t blow nose for 10 days

Some can be managed with just broad spec abx

Surgery

175
Q

What Orbital Blow Out Fractures require surgery?

A

-White eye blow out
-Symptomatic Exopthalmos of >2mm
->50% orbital floor involved
-Non resolving Diplopia after 2-3 weeks

176
Q

What is Thyroid Eye Disease?

A

Most common extrathyroidal manifestation of Graves

Can also be hypothyroid or euthyroid

Due to cross reactivityof autoantibodies

177
Q

The onset of Thyroid Eye Disease is normally within 18 months of diagnosis. Describe the pathophysiology

A

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
Q

What are the important receptors in Thyroid Eye Disease?

A

TSH
IGF1

179
Q

Name four risk factors for Thyroid Eye Disease

A

Current smoker
Female
Middle Aged
Radioiodine therapy

180
Q

How does Thyroid Eye Disease present?

A

Ocular irritation
Ache behind eye
Lid oedema and lateral flare
Circumferential white eye
Lid lag

Progressive optic neuropathy - blurred vision, reduced acuity

181
Q

How would you investigate Thyroid Eye Disease?

A

Thyroid levels
CT (soft tissue)/MRI (bone view pre op)
Visual acuity
CXR and TPMT (pre med)

182
Q

How is Thyroid Eye Disease staged?

A

Clinical activity scoring and severity

Dolor, Rubor, Calor, Tumor, Functio Laesa

(Mourits)

183
Q

Describe some general management points for Thyroid Eye Disease

A

Joint endocrine ophthalmology clinic
Smoking cessation
Maintain Euthyroid State
Prescribe ocular lubricants

184
Q

Describe the more definite management of Thyroid Eye Disease

A

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
Q

When does Thyroid Eye Disease require management?

A

Mourits>4
DON/RAPD/Field Defect

186
Q

What is Myasthenia Gravis?

A

Autoimmune disease where antibodies destroy neuromuscular connections
Affects voluntary muscles of the body

187
Q

Describe the pathophysiology of Myasthenia Gravis

A

-Receptor sites at NMJ are destroyed
-Not enough stimulation to trigger action potential
- Increased fatiguability with use (reduced ACh) and improvement with rest

188
Q

Name some signs of Myasthenia Gravis

A

Ptosis
Cogan Lid Twitch (down gaze followed by up gaze, eye saccades and lid overshoots)
Incomitant strabismus
Raised eyebrows

Pupils never involved

189
Q

Name three diagnostic tests for MG

A

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
Q

Name two laboratory tests for MG

A

Serum Anti ACh Receptor Titre
Serum Anti Muscle Specific Kinase AB titre

191
Q

What is the main differential for MG?

A

Lambert Eaton Syndrome

Improvement of symptoms with repeated stimulation

192
Q

Describe the management of MG

A

Med - Steroids, Pyridostigmine, Immunomodulators (if refractory)

Surgery - Removal of thymus

193
Q

Give three causes of Transient Visual Symptoms

A

Amaurosis Fugax
Papilledema
Migraine

194
Q

What is Amaurosis Fugax?

A

Hypoperfusion of optic nerve, normally secondary to carotid artery atherosclerosis and secondary thromboemboli

Precedes stroke so urgent investigations required

195
Q

Other than carotid pathology, give three causes of Amaurosis Fugax

A

GCA
Retinal Migraine
Papilledema

196
Q

How does Amaurosis Fugax present?

A

Curtain descending down over vision
If provoked by gaze - optical lesion

197
Q

How is Amaurosis Fugax investigated?

A

Inflammatory markers
Carotid imaging and cardiac evaluation
MRI/MRA

198
Q

How is Amaurosis Fugax managed?

A

TIA - stroke work up
GCA - Emperic steroids and temporal artery biopsy
Antiplatelets/Anticoag

199
Q

What is Papilledema?

A

Optic disc swelling secondary to raised ICP

Oedema, continued pressure and optic nerve atrophy

200
Q

Name five causes of raised ICP

A

Skull is too small for brain
Brain volume is too large
Obstruction of CSF flow
Increased CSF production
Decreased CSF drainage

201
Q

Name three investigations you would do to define the underlying cause of Papilledema

A

BP
CT/MRI
LP with opening pressure

202
Q

What is the Dandy Criteria for Idiopathic Intracranial Hypertension?

A

Papilledema
Normal neuro exam
Normal MRI imaging
Normal CSF composition
Elevated LP opening pressure

203
Q

The fundoscopy of Papilloedema is graded by the Frisen scale. What is this?

A

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
Q

Name three ways Papilloedema can present

A

Asymptomatic
Signs of raised ICP
Abducens Palsy

205
Q

The gold standard management for Papilloedema is to treat underlying cause and reduced ICP. How should IIH be managed?

A

Weight reduction
Acetazolamide

?CSF Shunt, Duran Venous Stenting

206
Q

Define Migraine

A

Primary headache disorder characterised by severe unilateral throbbing pain, associated with nausea, photophobia, phonophobia and preceding aura
Typically lasting 4-72hrs

207
Q

What is Photophobia?

A

Light sensitivity, ocular discomfort and headache exacerbated by light

Always bilateral (differentiates from trigeminal issues - unilateral)

208
Q

What are the five types of migraine with neuro- opthalmological symptoms

A

-Aura without headache (eg TIA)
-Basilar Type (dizziness, ataxia, tinnitus)
-Retinal (headache, scotoma, scintillation#)
-Migraine with binocular blindness
-Migrainous infarction (ischaemic brain lesions)

209
Q

Blepharitis is inflammation of the eyelid margin, and can be anterior or posterior. What are the three main aetiologies?

A

Staph Infection
Seborrhoeic Dermatitis (ant)
Meibomian Gland Dysfunction (post)

210
Q

What are the symptoms of Blepharitis?

A

Gritty/Itching/Burning
Bilateral symptoms
Lids stuck together upon waking

Associated - dry eye, Seborrhoeic dermatitis, rosacea

211
Q

What are the signs of each of the underlying causes of Blepharitis?

A

Staph - Telangiectasia, eyelash deformity

Seborrhoeic- greasy lid margin, eyelashes stuck together

Meibomian - oil globules, Chalazia

212
Q

Give three differentials of Blepharitis

A

BCC/SCC of eyelid
Contact/Atopic dermatitis
Impetigo

213
Q

How should you manage Blepharitis?

A

Inform it’s a chronic condition but can be managed

Avoid contact lenses

Warm compress/lid massage/ cleansing

Chloramphenicol is infection

214
Q

Dry eyes can be hyposecretive or evaporative. Give some causes of hyposecretion

A

Sjögren
Lacrimal gland insufficiency
Lacrimal gland obstruction
Antihistamines
TCA

215
Q

Dry eyes can be hyposecretive or evaporative. Give some causes of evaporation

A

Meibomian gland dysfunction (Blepharitis)
Blink disorder (Parkinson’s
Thyroid
Allergies
Prolonged computer use

216
Q

Dry eyes can cause a gritty, foreign body sensation worse at the end of the day. What are some red flags?

A

Severe eye pain
Significant visual loss
Photophobia

217
Q

Name three investigations for dry eyes

A

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
Q

What are some general managements for dry eyes?

A

Review medications
Smoking cessation
Regular breaks

219
Q

Name three tear substitutes

A

Drops (Hypermellose)
Gels (Viscotears, less frequent application)
Ointments (Coat cornea and reduce evaporation)

220
Q

Define Chalazion

A

Focus of granulomatous inflammation in eyelid arising from blocked meibomian

221
Q

How do Meibomian Cysts/Chalazions present?

A

Gradually enlarging round firm lesion

Generally painless once inflammation has settled

Blurred vision if compressing cornea

Yellowish swelling on underside of lid

222
Q

How would you manage Chalazia

A

BD warm compress
Massage
Clean with baby shampoo

223
Q

You would only investigate chalazia if it was recurrent or atypical. When would you refer?

A

Large and persistent
Visual problems
Low threshold in young children (amblyopia)

224
Q

What is the most common periocular malignancy? Give three risk factors

A

BCC of the eye

Older age, Male, UV exposure

225
Q

How does Periocular BCC present?

A

Slow developing non resolving lesion of the eyelid
On lower lid or medial canthus most commonly
May lose eyelashes

226
Q

How are Periocular BCCs managed?

A

Advise on sun protection
Mohs micrographic Surgery
?Radiotherapy

227
Q

What is Herpes Zoster Opthalmaticus (ie Shingles of Eye)?

A

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
Q

How does Herpes Zoster Opthalmaticus present?

A

Prodrome
Acute painful vesicular rash

Hutchinsons Sign - lesions at side/root of nose which is a strong predictor of ocular inflammation

229
Q

Name four investigations for Herpes Zoster Opthalmaticus

A

Test corneal sensation
Culture for VZV specific IgM
Slit lamp
Fluorosciene (Rule out corneal damage)

230
Q

How is Herpes Zoster Opthalmaticus managed?

A

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
Q

What is a Subconjunctival Haemorrhage? Give four causes

A

Bleeding of the conjunctival vessels into subconjunctival space

Valsalva
HTN
Contact lenses
Drugs

232
Q

How do Subconjunctival Haemorrhages present?

A

Unilateral red eye

Red patch with sharply defined edges
Otherwise normal eye exam

If no posterior margin - intracranial bleed

233
Q

What advice should you give someone with Subconjunctival Haemorrhages?

A

Self limiting
Eye drops for dry eyes
Discourage Aspirin and NSAIDs

234
Q

What is Posterior Vitreous Detachment?

A

Vitreous gel comes away from retina

Very common, especially in older patients

235
Q

How does Posterior Vitreous Detachment present?

A

Painless condition

May be completely asymptomatic

Slight Vision loss, floaters, flashing lights

236
Q

How is Posterior Vitreous Detatchment managed?

A

No treatment necessary, over time brain adjusts
Can predispose to retinal tears/detachment so monitor

237
Q

What is Retinitis Pigmentosa?

A

Congenital inherited condition where there is degeneration of rods and cones

Rods degenerate more than cones (night time blindness)

238
Q

How does Retinitis Pigmentosa present?

A

Symptoms usually start in childhood
Night blindness
Peripheral vision lost before central

239
Q

What would be seen on fundoscopy of Retinitis Pigmentosa?

A

Bony spicule pigmentation (most concentrated around mid peripheral area)

240
Q

Name two diseases associated with Retinitis Pigmentosa

A

Ushers Syndrome (+ hearing loss)
Bassen Kornzweig

241
Q

Describe the management of Retinitis Pigmentosa

A

Genetic counselling
Visual aids
Driving limitations

Slow progression - vitamins, antioxidants, anti vegf, steroids

242
Q

Give five causes of an abnormally shaped pupil

A

Trauma to muscles
Anterior uveitis (scar tissue)
AACG (Ischaemic damage - oval)
Coloboma (holes in iris)
Tadpole (spasm in part of pupil, migraines)

243
Q

Name four causes of a dilated pupil

A

Oculomotor nerve palsy
Raised ICP
Cocaine
Adie/Tonic Pupil

244
Q

What is a Tonic Pupil?

A

Damage to post ganglion parasympathetic
May be viral
Dilated and sluggish to light

245
Q

Name four causes of a constricted pupil

A

Horners
Argyll Robertson (Neurosyphilis)
Opiates
Pilocarpine

246
Q

Describe the features of Horners Syndrome

A

Ptosis
Miosis
Anhidrosis
Enopthalmos
Light and Accomodation reflexes unaffected

247
Q

Name the four central lesions that can cause Horners Syndrome (4S’s). What is characteristic?

A

Stroke
Multiple Sclerosis
Swelling
Syringomyelia

Anhidrosis of arm and trunk as well as face

248
Q

Name the four preganglionic lesions that can cause Horners Syndrome (4Ts). What is characteristic?

A

Tumour
Trauma
Thyroidectomy
Top Rib

Anhidrosis of race

249
Q

Name the four post ganglionic lesions that can cause Horners Syndrome (4Cs). What is characteristic?

A

Carotid aneurysm
Carotid artery dissection
Cavernous sinus thrombosis
Cluster headache

No anhidrosis

250
Q

What is associated with Congenital Horners?

A

Heterochromia

251
Q

Name two ways Horner’s Syndrome can be diagnosed

A

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
Q

Name five features on fundoscopy of Hypertensive Retinopathy

A

Silver/copper wiring (thickened and sclerosed)
AV nipping (sclerosis where they cross)
Cotton wool spots
Hard exudate
Retinal haemorrhages

253
Q

Name three risk factors for Choroidal Melanoma

A

Light iris
Sunlight exposure
Positive FH

254
Q

How does Choroidal Melanoma present?

A

Tends to be asymptomatic

May have blurred vision, paracentral scotoma, floaters and flashes

255
Q

How does a Choroidal Melnaoma appear on Fundoscopy?

A

Nodular dome shaped lesion

256
Q

Name two non surgical and two surgical managements of Choroidal Melanoma

A

Laser Photocoagulation, Sterotactic Radiotherapy

Block excision, Enucleation

257
Q

What is Amblyopia?

A

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
Q

Name three common causes of Amblyopia

A

Constant Strabismus
Asymmetric refractive errors
Orbital pathology affecting growth/clarity (eg strawberry naevus)

259
Q

Describe the period in which Amblyopia can be reversed

A

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
Q

Amblyopia normally has a significant difference in acuity between eyes. How is this defined?

A

Two or more Snellen/LogMAR differences

261
Q

How can Amblyopia be managed?

A

Modifying visual input into affected eye
Correcting refractive error
Obscuring visual input to other eye(patching, drops)

262
Q

Define Strabismus

A

Misalignment of the Eyes resulting in non corresponding retinal images

Often idiopathic or secondary to hydroceph/SOL/cerebral palsy/trauma

263
Q

What is the terminology for Strabismus?

A

Eso - inward
Exo - outward
Hypo - down
Hyper - up
Manifested - tropia
Latent - Phonia

264
Q

How can Strabismus be classified?

A

Congenital or acquired
Right/Left/Alternating
Permanent or intermittent
Manifest or latent
Concomitant (non paralytic) or incomitant

265
Q

What is a non paralytic strabismus?

A

Size of deviation doesn’t vary with direction of gaze

Usually congenital
Extraocular muscles and nerves are normal
Compensatory head tilt

266
Q

How does Esotropia present?

A

Inward turning squint
Can be on accommodation

267
Q

How does Exotropia present?

A

Outward squint
Begins intermittently with daydreaming/tiredness and progresses

268
Q

How does Hyper/Hypotropia present?

A

Vertical Strabismus
Changes in head posture
SO paresis

269
Q

What is the Hirschberg test for Strabismus?

A

Hold a pen torch in front of patients eyes and observe where reflection lies

Outer margin - Esotropia
Inner Margin - Exotropia

270
Q

Other than the Hirschberg test, name three other investigations for Strabismus

A

Cover uncover - observe movement
Alternate cover - shows latent
Orthoptic Assessment

271
Q

How is Strabismus managed?

A

Correcting refractive errors
Prisms

?Surgical intervention
?Chemodenervation

272
Q

What is Paralytic Strabismus?

A

Damag to extraocular muscles/nerves

273
Q

What is Myopia?

A

Near sighted

Excess optical power for axon length, light focuses in front of retina

274
Q

Name three risk factors for Myopia

A

FH
Close up work
Marfans

275
Q

Define Hypermetropia

A

Long sightedness

Insufficient power for axonal length

Light is focussed beyond retina

276
Q

Name three risk factors for Hypermetropia

A

Corneal Dystrophy
Congenital Cataracts
Micropthalmia

277
Q

Describe registering as visually impaired

A

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
Q

Name two benefits to officially registering as blind or partially

A

Blind persons income tax allowance, 50% reduction on TV licence

Free NHS Sight Test, Glasses vouchers

279
Q

Describe the DVLA visual requirements for driving

A

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
Q

How can a LogMAR score be calculated from Snellen?

A

Snellen 6/10

Log10(10/6)

281
Q

How can a LogMAR score be calculated?

A

0.1 + score of best line read - (0.02* letters read)

282
Q

Name three causes of generalised blurring

A

Presbyopia
Dry Eyes
Cataracts

283
Q

Name two causes of central blurring

A

Diabetic Maculopathy
Macular Degeneration

284
Q

Name two causes of black spots/blobs

A

Does it move with eye?

Y - Vitreous Disease
N - Retinal Detachment

285
Q

Name two causes of Photopsia

A

Detached Retina
Migraine with Aura

286
Q

Name three uses for Mydriatic/Cycloplegic drops

A

Dilation for retinal visualisation
Amblyopia
Refraction for children with glasses

287
Q

Name three Mydriatic/Cycloplegic drops

A

Anticholinergic - Atropine, Cyclopentolate
Sympathetic - Phenylephrine

288
Q

Name three side effects of Mydriatic/a Cycloplegic drops

A

Eye whitening
Face redness/warmth
Can’t drive until worn off

289
Q

Name a side effect of Fluoroscein

A

Staining

290
Q

Define Retinoblastoma

A

Retinoblastomas are the most common primary intraocular malignancy in children. They are caused by sporadic or inherited mutations in the retinoblastoma gene (Rb)

291
Q

What are the two types of Retinoblastoma

A

Sporadic (usually unilateral)

Hereditary (normally bilateral and associated with other malignancies)

292
Q

Describe the aetiology of Heritable Retinoblastoma

A

Two hit hypothesis of Rb gene

Autosomal Dominant inheritance

293
Q

How do Retinoblastomas present?

A

Leukocoria
Strabismus

294
Q

How is suspected Retinoblastoma investigated?

A

Fundoscopy
Ultrasound of the orbit
MRI (CT radiation could induce cancer in those with germline RB mutation)

295
Q

How should Retinoblastomas be managed?

A

Salvageable - Cryotherapy, Brachytherapy, Chemotherapy

Non Salvagable - Enucleation

296
Q

Name three complications of Cataract surgery and how they’re minimised (if relevant)

A

Endopthalmitis - prophylactic abx

Posterior Capsule Rupture

Floppy Iris Syndrome

297
Q

Name three causes of RAPD

A

Optic Neuritis
Retinal Detachment
CMV

Year 4 Neuro and Special Senses (8 decks)

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