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Y4 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. Raised intraoccular pressure is caused by blockage in aqueous humour draining from eye.

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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

Risk factors for Acute Angle Closure Glaucoma

A

Increased Age
Asian Ethnicity
F>M
FH
Hyperopia
Shallow anterior chamber

Anticholinergic meds
Adrenergic meds
Tricyclic antidepressants

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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

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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9
Q

Chronic Angle Closure Glaucoma is normally asymptomatic, how does Acute present?

A

severely painful red eye

blurred vision

halos around lights

associated headache, nausea and vomiting

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10
Q

what is seen on examination of somone with Acute Angle-Closure Glaucoma?

A

Red-eye

Teary

Hazy cornea

Decreased visual acuity

Dilation of affected pupil

Fixed pupil size

Firm eyeball on palpation

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11
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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12
Q

How is acute angle closure glaucoma managed? (primary care)

A
  • lie on back without pillow
  • give pilocarpine eye drops
  • give acetazolamide 500mg oral
  • give analgesia and an antiemetic if required
  • REFER FOR SAME DAY OPTHALMOLOGY ASSESSMENT
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13
Q

What are the secondary care management options for AACG?

A
  • pilocarpine
  • acetazolamide iv or oral
  • hyperosmotic agesnts - glycerol or mannitol
  • timolol
  • dorzolamide
  • brimonidine
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14
Q

What is the definitive treatment of AACG?

A
  • Inital Oral Acetazolamide and Drops
  • 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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15
Q

Define Endopthalmitis

A

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

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16
Q

Give 5 causes of Endopthalmitis

A

Trauma
Eye Surgery
VEGF injections
Endogenous seeding
Extension of Corneal infection

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17
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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18
Q

How does Endopthalmitis present?

A

Acute eye pain
Reduced vision
Hypopyon
?swollen eyelid

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19
Q

Name four risk factors for Endopthalmitis

A

Poor surgical technique
Contaminated lens
Contact lens wear
Immunosupression

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20
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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21
Q

Name two differentials for Endopthalmitis

A

Retained lens material
Raised IOP as a result of procedure

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22
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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23
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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24
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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25
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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26
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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27
Q

how does orbital cellulitis present?

A
  • Redness and swelling around the eye
  • Severe ocular pain
  • Visual disturbance
  • Proptosis
  • Ophthalmoplegia/pain with eye movements
  • Eyelid oedema and ptosis
  • Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)
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28
Q

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

A

FBC - leukocytosis + raised inflammatory markers
Blood cultures - negative
LP (if focal signs)
Swabs
CT sinus and orbit with contrast - extension

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29
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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30
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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31
Q

Name four complications of Orbital Cellulitis

A

Endopthalmitis
Meningitis
Orbital Abscess
Subperiosteal Abscess

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32
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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33
Q

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

A

Superficial Keratitis
Foreign Bodies

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34
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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35
Q

How does a superficial corneal abrasion present?

A

Redness
Pain
Watering
Foreign Body Sensation
Photophobia

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36
Q

How does a penetration corneal injury present?

A

Distorted globe
Hyphaema
Conjunctival laceration
Red and watering

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37
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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38
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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39
Q

Name three red flags for corneal injury

A

Deep lid laceration
Subconjunctival haemorrhage
Pupils/Iris/Fundus abnormality

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40
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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41
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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42
Q

How can rust rings be removed?

A

A sterile rotating burr

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43
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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44
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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45
Q

Define Hyphaema

A

When blood enters anterior chamber between cornea and iris

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46
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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47
Q

Name 5 causes of a Hyphaema

A

Intraocular Surgery
Blunt trauma
Lacerating Trauma
Leukaemia
Retinoblastoma

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48
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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49
Q

Name two complications of Hyphaema

A

Haemosiderosis

Raised IOP

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50
Q

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

A

Roper Hall

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51
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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52
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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53
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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54
Q

How does Viral Conjunctivitis present?

A

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

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55
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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56
Q

How can bacterial conjunctivitis be managed?

A

Chloramphenicol (contraindicated if pregnant or breast feeding)
Fusidic Acid

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57
Q

How does Allergic Conjuncitivitis present?

A

Swelling of conjunctival sac and eyelid
Watery discharge
Itch

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58
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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59
Q

Name four causes of Anterior Uveitis

A

Autoimmune
Infection
Trauma
Ischaemia

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60
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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61
Q

Name three associations of Anterior Uveitis and Chronic Anterior Uveitis respectively

A

acute: HLA B27 related conditions - Anklyosing Spondylitis, IBD, Reactive Arthritis

Sarcoidosis, Syphilis, TB, Lyme disease, herpes virus

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62
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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63
Q

what are some signs seen on examination of anterior uveitis?

A
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64
Q

What causes floaters in Anterior Uveitis?

A

Inflammation and immune cells in the anterior chamber

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65
Q

What is Posterior Synechiae? Give an association

A

Adhesions that can cause disruption to pupillary shape

Anterior Uveitis

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66
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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67
Q

How would you manage Anterior Uveitis?

A

Steroids - oral, topical, IV
Cytoplegic (paralysing ciliary muscles) /Mydriatic (dilating pupils) medication
Immunosupressants

Severe - Laser therapy, Cryotherapy

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68
Q

What is the role of Cytoplegic/Mydriatic Medication in Anterior Uveitis? and give some examples.

A

cyclopentolate or atropine eye drops - antimuscarinic that block actions of iris sphincter muscles and ciliary body, dilate pupil and reduce pain associated with ciliary spasm by stopping action of ciliary body

cycloplegic = Paralyses ciliary muscles

mydriatic = dilate pupil

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69
Q

Keratitis is inflammation of the cornea, give some causes

A

viral - herpes simplex

bacterial - pseudomonas, staphylococcus

fungal - candida or aspergillus

caonact lens acute red eye (CLARE)

exposure keratitis - indequate eyelid coverage

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70
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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71
Q

Name four presenting features of Keratitis

A

Redness
Pain
Photophobia
Reduced acuity

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72
Q

What can be seen on examination of a Keratitic eye?

A

Oedema
White cell infiltration
Epithelial defect

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73
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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74
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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75
Q

What would Fluorescein staining of a HSV Keratitis eye show?

A

Dendritic corneal ulcer (branching and spreading)

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76
Q

How is HSV Keratitis managed?

A

Acyclovir (topical or oral)
Ganciclovir eye gel
Topical steroids

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77
Q

Define Scleritis

A

Inflammation of full thickness of the sclera

Normally not caused by infection

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78
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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79
Q

Name four associated conditions with scleritis

A

SLE
IBD
RA
Sarcoidosis

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80
Q

How does Scleritis present?

A

50% bilateral

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

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81
Q

How is Scleritis managed?

A

Underlying condition

NSAIDs and Steroids

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82
Q

Name five causes of Gradual Visual Deterioration

A

Cataracts
Open Angle Glaucoma
ARMD
Diabetic Retinopathy
Presbyopia

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83
Q

What are Cataracts?

A

Opacification of the Lens

Major cause of treatable blindness worldwide

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84
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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85
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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86
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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87
Q

How do Nuclear Cataracts present?

A

Loss of colour vision
Slow progression

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88
Q

How do Cortical Cataracts present?

A

Less visual degradation
Slow progression

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89
Q

How to Posterior Subcapsular Cataracts present?

A

Disabling glare to bright lights
Quick progression

Links to DM and Steroids

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90
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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91
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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92
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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93
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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94
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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95
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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96
Q

Describe the four layers of the Macula

A

Choroid
Bruch’s Membrane
Retinal Pigment Epithelium
Photoreceptors

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97
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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98
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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99
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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100
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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101
Q

Give four risk factors for ARMD

A

Age
Smoking
Chinese Ethnicity
FH

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102
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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103
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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104
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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105
Q

How is Wet ARMD managed?

A

Anti VEGF Vitreous injections (Ranibizumab)

Started within three months

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106
Q

Give four risk factors for Open Angle Glaucoma

A

Age
Afrocaribbean ethnicity
Diabetes
Myopia

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107
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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108
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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109
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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110
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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111
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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112
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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113
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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114
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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115
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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116
Q

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

A

Neovascularisation
Vitreous Haemorrhage

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117
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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118
Q

Name four complications of Diabetic Retinopathy

A

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

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119
Q

How is Diabetic Retinpathy managed?

A

Anti VEGF
Laser Photocoagulation
Severe - keyhole vitreoretinal Surgery

Optimise DM control

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120
Q

Name three requirements of the accommodation reflex

A

Eyes converging
Pupil size reducing
Lens changing shape and pattern

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121
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

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122
Q

How does Presbyopia present?

A

Difficulty carrying out near tasks

Accommodative lag (from distance to near vice versa)

Tiring with continuous close work

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123
Q

How is Presbyopia treated?

A

OTC glasses are normally sufficient

If pre-existing refractive error - prescription glasses

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124
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)

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125
Q

Name six causes of sudden visual loss

A

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

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126
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)

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127
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

128
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)

129
Q

How can CRAO be confirmed?

A

Fluorosciene Angiography

Slowed flow/filling defect

130
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

131
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)

132
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

133
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?

134
Q

How is Arteritic Ischaemic Optic Neuropathy investigated?

A

GCA - ESR/CRP, Temporal Artery Biopsy

MRI/USS - between Arteritic and non

OCT

135
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

136
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

137
Q

How does Non Arteritic AION present?

A

Acute painless visual loss
RAPD

Optic disc oedema and peripapillary splinter haemorrhages

138
Q

How is Non Arteritic AION managed?

A

Exclude arteritic

Large doses of steroid

139
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

140
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
141
Q

Name four investigations for Vitreous Haemorrhage

A

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

142
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

143
Q

Name four definitive treatment options for Vitreous Haemorrhage

A

Laser Photocoagulation (for proliferative vasculopathies)

Anterior Retinal Cryotherapy

Vitrectomy

VEGF

144
Q

Name three complications of Vitreous Haemorrhage

A

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

145
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
146
Q

How does Retinal Vein Occlusion present?

A

Sudden painless loss of vision

147
Q

Name four features of fundoscopy for Retinal Vein Occlusion

A

Flame Haemorrhages
Blot Haemorrhages
Optic Disc Oedema
Macula Oedema

148
Q

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

A

FBC - Leukaemia
ESR - inflammatory disorders
Glucose - Diabetes

149
Q

How is Retinal Vein Occlusion managed?

A

Laser Photocoagulation
Intravitreal Steroids
Anti VEGF therapies

150
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)

151
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

152
Q

How does Retinal Detachment present?

A

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

153
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

154
Q

How are Retinal Tears managed?

A

Laser therapy or Cryotherapy

Created adhesions between retina and choroid to prevent detachment

155
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)
156
Q

Define Optic Neuritis

A

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

157
Q

There are many causes of Optic Neuritis. Name 6

A

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

158
Q

Give three signs on examination of Optic Neuritis

A

RAPD
Altitudinal field defects
Scotoma

159
Q

How could you consider managing Optic Neuritis?

A

IV Methylpred to speed healing

160
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

161
Q

What is Acute Demyelinating Optic Neuritis?

A

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

162
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

163
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

164
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

165
Q

Name four causes of Oculomotor nerve lesions

A

Diabetes
GCA
Raised ICP
PCA Aneurysm

166
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

167
Q

How do Oculomotor nerve lesions present (sympathetics involved)?

A

Pupil will be fixed but not dilated

168
Q

Trochlear Nerve lesions are rare, give three causes

A

Orbital trauma
Diabetes
Infarction secondary to hypertension

169
Q

Name 6 causes of Diplopia

A

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

170
Q

How do Trochlear Nerve Lesions present?

A

Vertical Diplopia

Weakness of downward and intortion

Compensatory head tilt away from affected side

171
Q

How does a CNVI lesion appear?

A

Inability to look laterally

172
Q

Give three causes of a CNVI lesion

A

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

173
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)

174
Q

Name five clinical features of Orbital Blow Out Fractures

A

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

175
Q

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

A

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

CT

176
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

177
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
178
Q

What is Thyroid Eye Disease?

A

Most common extrathyroidal manifestation of Graves

Can also be hypothyroid or euthyroid

Due to cross reactivityof autoantibodies

179
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

180
Q

What are the important receptors in Thyroid Eye Disease?

181
Q

Name four risk factors for Thyroid Eye Disease

A

Current smoker
Female
Middle Aged
Radioiodine therapy

182
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

183
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)

184
Q

How is Thyroid Eye Disease staged?

A

Clinical activity scoring and severity

Dolor, Rubor, Calor, Tumor, Functio Laesa

(Mourits)

185
Q

Describe some general management points for Thyroid Eye Disease

A

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

186
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

187
Q

When does Thyroid Eye Disease require management?

A

Mourits>4
DON/RAPD/Field Defect

188
Q

What is Myasthenia Gravis?

A

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

189
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
190
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

191
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

192
Q

Name two laboratory tests for MG

A

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

193
Q

What is the main differential for MG?

A

Lambert Eaton Syndrome

Improvement of symptoms with repeated stimulation

194
Q

Describe the management of MG

A

Med - Steroids, Pyridostigmine, Immunomodulators (if refractory)

Surgery - Removal of thymus

195
Q

Give three causes of Transient Visual Symptoms

A

Amaurosis Fugax
Papilledema
Migraine

196
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

197
Q

Other than carotid pathology, give three causes of Amaurosis Fugax

A

GCA
Retinal Migraine
Papilledema

198
Q

How does Amaurosis Fugax present?

A

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

199
Q

How is Amaurosis Fugax investigated?

A

Inflammatory markers
Carotid imaging and cardiac evaluation
MRI/MRA

200
Q

How is Amaurosis Fugax managed?

A

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

201
Q

What is Papilledema?

A

Optic disc swelling secondary to raised ICP

Oedema, continued pressure and optic nerve atrophy

202
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

203
Q

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

A

BP
CT/MRI
LP with opening pressure

204
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

205
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

206
Q

Name three ways Papilloedema can present

A

Asymptomatic
Signs of raised ICP
Abducens Palsy

207
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

208
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

209
Q

What is Photophobia?

A

Light sensitivity, ocular discomfort and headache exacerbated by light

Always bilateral (differentiates from trigeminal issues - unilateral)

210
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)
211
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)
212
Q

What are the symptoms of Blepharitis?

A

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

Associated - dry eye, Seborrhoeic dermatitis, rosacea

213
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

214
Q

Give three differentials of Blepharitis

A

BCC/SCC of eyelid
Contact/Atopic dermatitis
Impetigo

215
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

216
Q

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

A

Sjögren
Lacrimal gland insufficiency
Lacrimal gland obstruction
Antihistamines
TCA

217
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

218
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

219
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)

220
Q

What are some general managements for dry eyes?

A

Review medications
Smoking cessation
Regular breaks

221
Q

Name three tear substitutes

A

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

222
Q

Define Chalazion

A

Focus of granulomatous inflammation in eyelid arising from blocked meibomian

223
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

224
Q

How would you manage Chalazia

A

BD warm compress
Massage
Clean with baby shampoo

225
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)

226
Q

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

A

BCC of the eye

Older age, Male, UV exposure

227
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

228
Q

How are Periocular BCCs managed?

A

Advise on sun protection
Mohs micrographic Surgery
?Radiotherapy

229
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

230
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

231
Q

Name four investigations for Herpes Zoster Opthalmaticus

A

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

232
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

233
Q

What is a Subconjunctival Haemorrhage? Give four causes

A

Bleeding of the conjunctival vessels into subconjunctival space

Valsalva
HTN
Contact lenses
Drugs

234
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

235
Q

What advice should you give someone with Subconjunctival Haemorrhages?

A

Self limiting
Eye drops for dry eyes
Discourage Aspirin and NSAIDs

236
Q

What is Posterior Vitreous Detachment?

A

Vitreous gel comes away from retina

Very common, especially in older patients

237
Q

How does Posterior Vitreous Detachment present?

A

Painless condition

May be completely asymptomatic

Slight Vision loss, floaters, flashing lights

238
Q

How is Posterior Vitreous Detatchment managed?

A

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

239
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)

240
Q

How does Retinitis Pigmentosa present?

A

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

241
Q

What would be seen on fundoscopy of Retinitis Pigmentosa?

A

Bony spicule pigmentation (most concentrated around mid peripheral area)

242
Q

Name two diseases associated with Retinitis Pigmentosa

A 
Ushers Syndrome (+ hearing loss)
Bassen Kornzweig
243
Q

Describe the management of Retinitis Pigmentosa

A

Genetic counselling
Visual aids
Driving limitations

Slow progression - vitamins, antioxidants, anti vegf, steroids

244
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)

245
Q

Name four causes of a dilated pupil

A

Oculomotor nerve palsy
Raised ICP
Cocaine
Adie/Tonic Pupil

246
Q

What is a Tonic Pupil?

A

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

247
Q

Name four causes of a constricted pupil

A

Horners
Argyll Robertson (Neurosyphilis)
Opiates
Pilocarpine

248
Q

Describe the features of Horners Syndrome

A

Ptosis
Miosis
Anhidrosis
Enopthalmos
Light and Accomodation reflexes unaffected

249
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

250
Q

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

A

Tumour
Trauma
Thyroidectomy
Top Rib

Anhidrosis of race

251
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

252
Q

What is associated with Congenital Horners?

A

Heterochromia

253
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

254
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

255
Q

Name three risk factors for Choroidal Melanoma

A

Light iris
Sunlight exposure
Positive FH

256
Q

How does Choroidal Melanoma present?

A

Tends to be asymptomatic

May have blurred vision, paracentral scotoma, floaters and flashes

257
Q

How does a Choroidal Melnaoma appear on Fundoscopy?

A

Nodular dome shaped lesion

258
Q

Name two non surgical and two surgical managements of Choroidal Melanoma

A

Laser Photocoagulation, Sterotactic Radiotherapy

Block excision, Enucleation

259
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)

260
Q

Name three common causes of Amblyopia

A

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

261
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

262
Q

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

A

Two or more Snellen/LogMAR differences

263
Q

How can Amblyopia be managed?

A

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

264
Q

Define Strabismus

A

Misalignment of the Eyes resulting in non corresponding retinal images

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

265
Q

What is the terminology for Strabismus?

A

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

266
Q

How can Strabismus be classified?

A

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

267
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

268
Q

How does Esotropia present?

A

Inward turning squint
Can be on accommodation

269
Q

How does Exotropia present?

A

Outward squint
Begins intermittently with daydreaming/tiredness and progresses

270
Q

How does Hyper/Hypotropia present?

A

Vertical Strabismus
Changes in head posture
SO paresis

271
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

272
Q

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

A

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

273
Q

How is Strabismus managed?

A

Correcting refractive errors
Prisms

?Surgical intervention
?Chemodenervation

274
Q

What is Paralytic Strabismus?

A

Damag to extraocular muscles/nerves

275
Q

What is Myopia?

A

Near sighted

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

276
Q

Name three risk factors for Myopia

A

FH
Close up work
Marfans

277
Q

Define Hypermetropia

A

Long sightedness

Insufficient power for axonal length

Light is focussed beyond retina

278
Q

Name three risk factors for Hypermetropia

A

Corneal Dystrophy
Congenital Cataracts
Micropthalmia

279
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

280
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

281
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

282
Q

How can a LogMAR score be calculated from Snellen?

A

Snellen 6/10

Log10(10/6)

283
Q

How can a LogMAR score be calculated?

A

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

284
Q

Name three causes of generalised blurring

A

Presbyopia
Dry Eyes
Cataracts

285
Q

Name two causes of central blurring

A

Diabetic Maculopathy
Macular Degeneration

286
Q

Name two causes of black spots/blobs

A

Does it move with eye?

Y - Vitreous Disease
N - Retinal Detachment

287
Q

Name two causes of Photopsia

A

Detached Retina
Migraine with Aura

288
Q

Name three uses for Mydriatic/Cycloplegic drops

A

Dilation for retinal visualisation
Amblyopia
Refraction for children with glasses

289
Q

Name three Mydriatic/Cycloplegic drops

A

Anticholinergic - Atropine, Cyclopentolate
Sympathetic - Phenylephrine

290
Q

Name three side effects of Mydriatic/a Cycloplegic drops

A

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

291
Q

Name a side effect of Fluoroscein

292
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)

293
Q

What are the two types of Retinoblastoma

A

Sporadic (usually unilateral)

Hereditary (normally bilateral and associated with other malignancies)

294
Q

Describe the aetiology of Heritable Retinoblastoma

A

Two hit hypothesis of Rb gene

Autosomal Dominant inheritance

295
Q

How do Retinoblastomas present?

A

Leukocoria
Strabismus

296
Q

How is suspected Retinoblastoma investigated?

A

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

297
Q

How should Retinoblastomas be managed?

A

Salvageable - Cryotherapy, Brachytherapy, Chemotherapy

Non Salvagable - Enucleation

298
Q

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

A

Endopthalmitis - prophylactic abx

Posterior Capsule Rupture

Floppy Iris Syndrome

299
Q

Name three causes of RAPD

A

Optic Neuritis
Retinal Detachment
CMV

300
Q

What is Pilocarpine and how does it work?

A
  • muscarinic cholinergic agonist
  • causes
    • constriction of the pupil - mitotic
    • ciliary muscle contraction
  • both of which open up pathway to trabecular meshwork
301
Q

What are Acetazolamide and Dorzolamide and how do they work?

A
  • Carbonic anhydrase inhibitor
  • reduces production of aqueous humour = reduces IOP
302
Q

How do hyperosmotic agents such as glycerol and mannitol work?

A

increase the osmotic gradient between the blood and fluid in the eye

303
Q

What is Timolol and how does it work?

A
  • Beta blocker
  • reduces production of aqueous humour
304
Q

What is Brimonidine and how does it work?

A

sympathomimetic that reduces the production of aqueous fluid and increase uveoscleral outflow

305
Q

What is open-angle glaucome?

A

gradual increase in resistance through the trabecular meshwork making it more difficult for aqueous humour to flow through the meshwork and exit the eye. Therefore the pressure slowly builds within the eye and this gives a slow and chronic onset of glaucoma

306
Q

what happens to the optic disc when IOP is raised?

A
  • Cupping of the optic disc
  • small indent in the optic disc becomes larger as the pressure in the eye puts pressure on the indent making it wider and deeper
  • >0.5 the size of the optic disc is abnormal
307
Q

what are some risk factors for OAG?

A
  • increasing age
  • FHx
  • black ethnic origin
  • Nearsightedness (myopia)
308
Q

how does OAG present?

A
  • often asymptomatic for a long time
  • diagnosed by routien screening
  • affects peripheral vision first which closes in until the pt experinces tunnel vision
  • gradual onset of fluctuating pain, headaches, blurred vision and halos aroud lights (more at night)
309
Q

what are the 2 ways intraocular pressure can be measured?

A

non-contact tonometry - shooting a puff of air at the cornea and mesauring the corneal response to the air - less accurate

goldmann applanation tonometry - gold standard, device mounted on a slit lamp that makes contact with cornea and applies different pressures to front of the cornea to get accurate measurement of the intraocular pressure

310
Q

how is OAG diagnosed

A
  • goldmann applanation tonometry - check pressure
  • fundoscopy - optic disc cupping and optic nerve health
  • visual field assessment - peripheral vision loss
311
Q

What is the management of OAG? And when is treatment usually initiated?

A
  • 1st line = latanoprost (prostaglandin analogue which increases uveoscleral outflow)
  • other options: timolol, dorzolamide, brimonidine
  • trabeculectomy surgery can be performed when eyedrops are inefective
312
Q

what are the 3 main side effects of latanoprost?

A
  • eyelash growth
  • eyelid pigmentation
  • iris pigmentation / browning
313
Q

what is trabeculectomy surgery and what is it used for?

A

used in OAG when eyedrops ineffective

new channel created from the naterior chamber through the sclera to a location under conjunctiva. causes a bleb under the conjunctiva where the aqueous humour drains. resbsorbed into the general circulation from the bleb

314
Q

what is preseptal/periorbital cellulitis? what commonly causes it?

A

an infection anterior to the orbital septum

commonly caused by an infection in adjacent structures, dacryocystitis, insect bites, hordeolum, trauma

315
Q

how does preseptal/periorbital cellulitis present?

A

inflammed eyelids but with white eyes and normal visual acuity

painless eye movements

no diplopia

316
Q

how is periorbital/preseptal cellulitis managed?

A

Flucloxacillin 500mg QDS 7 days

317
Q

how is preseptal/periorbital cellulitis differentiated from orbbital cellulitis?

A

reduced visual acuity, proptosis, ophthalmoplegia/painful eye movements not associated with preseptal cellulitis

Y4 Neuro and Special Senses (9 decks)

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