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EOY4 > Opthalmology > Flashcards

Opthalmology Flashcards

1
Q

What is the physiology of maintaining pressure within the eye?

A

1) AH produced by capillary networks in ciliary body
2) flows up between the iris and anterior lens and through the pupil
3) Flows out the drainage angle of the eye
4) flows into the trabecular meshwork and then the Canal of Schlemm
5) However, some aqueous has a novel route and flows into the roots of the ciliary muscle/iris and into the scleral circulation

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2
Q

Which receptors can be activated to affect IOP?

A

a-2-adrenoreceptors - ↓ IOP by reducing aqueous production + ↑uveoscleral outflow

ℬ-2-adrenergic receptors = ↑ IOP by increasing aqueous production

2 because you have 2 eyes

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3
Q

What is intra-ocular pressure?

A

Intra-Ocular Pressure is the force needed to flatten the corneal surface. Usually measured using Tonometry.

The normal range of IOP is 11-21mmHg.

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4
Q

What is Glaucoma?

A

Optic neuropathy with death of many retinal ganglion cells and their optic nerve axons.

Leads to irreversible vision loss

OP might be raised but this is not a necessity to be diagnosed with Glaucoma.

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5
Q

What are the 2 types of glaucoma?

A

Primary open angle

Acute closed angle

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6
Q

What is primary open angle glaucoma?

A

Angle between cornea and iris is open but the trabecular meshwork slowly clogs

Leads to a gradual increase in IOP and initial atrophy of the outer rim of CNII

Gradual ↓ in peripheral vision then central vision

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7
Q

What is acute closed angle glaucoma?

A

Ophthalmic emergency!

Angle between cornea and iris becomes too small due to lens being pushed against iris

Rapid ↑ in pressure

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8
Q

How does acute closed angle glaucoma normally present?

A

eye -Sudden onset, severe eye pain, eye is RED, haloes

pupil - non-reactive and mid-dilated

N&V

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9
Q

What are the non-modifiable and modifiable risk factors for POAG?

A

Non-modifiable
Age >40
Family History (genetics)
Ethnicity (afro-carribean)

Modifiable
Diabetes
Thyroid Eye Disease
Hypertension
Drugs (Corticosteroids, Pilocarpine/atropine, Tricyclic antidepressants)
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10
Q

What are the non-modifiable and modifiable risk factors for AACG?

A

Non-modifiable
Ethnicity - eastern asian/south eastern asian
Age
Female

Modifiable
Hypermetropia (long eye and shallow anterior chamber)
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11
Q

What investigations should be done to investigate Glaucoma?

A

Visual fields - loss of peripheral vision

Dilated eye exam on slit lamp
Cupping of the optic disc - loss of disc substance makes the cup look larger

Tonometry

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12
Q

What is the conservative management of POAG?

A

Advice on driving, drop usage (emphasise importance and lifetime treatment)

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13
Q

What is the medical management of POAG?

A

Prostaglandin Analogue e.g. Latanoprost

B-Blocker - Timalol

⍺ agonists e.g. Brimonidine also used (reduced production and small increase in drainage) but less so I think

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14
Q

What is the management of AACG?

A

Urgent referral to eye casualty

Medication - CBA
Acetazolamide
B-Blocker
Alpha agonist - Brimonidine

+/- Pilocarpine +/- latanoprost
Surgery - laser iridotomy

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15
Q

What is the role of a B-blocker in AACG?

A

REDUCE AH PRODUCTION

inhibits adrenergic stimulation (B2 adrenoceptors) to produce AH

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16
Q

What is the role of Acetazolamide in AACG?

A

REDUCE AH PRODUCTION

carbonic anhydrase inhibitor

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17
Q

What is the role of Pilocarpine in AACG?

A

Anti-muscarinic

INCREASE AH DRAINAGE

pupillary constriction to increase angle

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18
Q

What is presbyopia?

A

Reduction in ability of lens to accommodate as ageing happens.

↓ lens elasticity + ciliary body atrophy

This can be overcome by prescribing convex lenses for near work.

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19
Q

What is a cataract? What is the pathophysiology?

A

Any opacity within the lens

Protein denaturation is involved but largely unknown

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20
Q

What is a cortical cataract?

A

Cortex of lens involved

Astigmatic changes

More problems in the dark when pupil dilates = more cataract exposure

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21
Q

What is a nuclear cataract?

A

Lens Nucleus becomes yellowish-brown due to pigment deposition

Myopic changes due to increased refractive index

Reduced saturation of colours

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22
Q

What is a posterior capsular cataract?

A

Subcapsular

Grandular or plaque like

Near vision affected more

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23
Q

What are the causes of cataracts?

A

SPELLS CATARACTS

C ongenital (infection e.g. rubella, familial e.g. Wilson’s

A ge >65
T rauma
A fter cataract (post intraocular surgery)
R adiation
A vitaminosis
C hemical/ Metabolic
T oxic (smoking, alcohol)
S ystemic (DM, neurofibromatosis type 2)
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24
Q

Which drugs can cause cataracts? (Chemical)

A 
Allopurinol
Amiodarone
Corticosteroids
Myotics
Antipsychotics (chlorpromazine)
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25
Q

Which metabolic conditions can cause cataracts?

A

DM

Galactosaemia

Hypocalcaemia

Wilson’s

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26
Q

What are the visual changes associated with cataracts?

A

Visual changes
Blurred vision/ ↓ in visual acuity

Unilateral - often asymptomatic

Bilateral - gradual, painless + frequent prescription changes. +/- monocular diplopia

Faded colours

↓ night vision

Glare from lights +/- halo

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27
Q

What are the eye investigations to diagnose cataracts?

A

Visual tests
Snellen’s
Keeler’s
Stereotest - may have loss of stereopsis (distance judgement)

Tonometry

Dilated eye exam (fundoscopy)

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28
Q

What is the management of cataracts?

A

Only definitive management is surgery really (phacoemulsification)

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29
Q

When should cataract surgery be offered?

A

Gets to <6/12 is when surgery is usually offered

Patient choice/ affecting QOL. Ask about reading, driving, watching telly, hobbies, faces

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30
Q

When should the DVLA be informed in a cataract patient?

A

Only if bilateral

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31
Q

What is the pre-op management of cataracts?

A

Optical biometry to measure axial length of eye

Keratometry to measure curvature of cornea

Corneal topography if cornea is abnormal

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32
Q

What is the post-op management of cataracts?

A

Can drive again when can read a number plate 20m away with both eyes open

Can usually go back to normal daily activities within a day but everyone is different

Abx and NSAID drops for 3-6 weeks

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33
Q

What are the general surgical complications of cataract surgery?

A

Infection - endopthalmitis

Bleeding - vitreous haemorrhage

Damage to other structures - Retinal Detachment

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34
Q

What are the surgical complications that are specific to a phaco?

A

Secondary Glaucoma

Post capsule thickening

Post op eye irritation

Crystoid macular oedema

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35
Q

What is the retina?

A

Innermost layer of the eye and is comprised of 2 layers: an outer, pigmented layer and an inner, neural layer.

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36
Q

What is the RPE?

A

retinal pigment epithelium

outer layer of the pigment layer

nutrition and structure

has melanin to prevent reflection in the eyeball

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37
Q

what is the RPE attached to?

A

The choroid via Bruch’s membrane (significant for ARMD)

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38
Q

What is the inner neural layer of the retina made up of?

A

Several types of photoreceptors but mainly Rods and Cones:

Rods = For vision in dim light but no colour perception

Cones = Colour perception in normal light conditions

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39
Q

Describe the distribution of rods and cones throughout the retina

A

Rods are the predominant cell type throughout the Retina EXCEPT FOR at the Fovea

@ fovea = highest concentration of cones therefore giving the area of highest visual acuity.

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40
Q

what is the blood supply to the retina?

A

Inner 2/3 = Central Retinal Artery
Outer 1/3 = Choroidal Blood Supply
(end arteries)

Macula is dense with capillaries whereas the Fovea is a capillary free zone

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41
Q

How do you present fundoscopy?

A

1) Surface Anatomy
2) Red Reflex
3) Present the Optic Disc
- Colour (pink-grey is normal)
- Swelling/Clear margins?
- Cup:disc ratio (normal is 0.3-0.5 so cup should be roughly half of the disc area)

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42
Q

What is age related macular degeneration?

A

Eye condition that occurs where the Retinal Pigment Epithelium attaches to Bruch’s Junction at the macula

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43
Q

What are the 2 types of ARMD?

A

Dry
Unknown pathophysiology
No new vascular growth

Wet
Angiogenesis into Bruch’s epithelium + sub-retinal fluid or haemorrhage

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44
Q

What are the non-modifiable risk factors for ARMD?

A

Age >65

Sex (female)

Ethnicity - more common in caucasian and eastern asian population

Family history/genetics

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45
Q

What are the modifiable risk factors for ARMD?

A

Smoking

Cardiovascular risk factors e.g. hypertension, T2DM

Hypermetropia

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46
Q

What are the visual changes associated with ARMD

A

Central blurring of vision. Peripheral vision is normal.

Can manifest in difficulty reading or recognising faces. Also get problems with night vision and changing light conditions

PAINLESS

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47
Q

How do the visual changes differ between wet and dry ARMD?

A

Dry = gradual i.e. over years.

Wet = sudden + wiggly distortion

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48
Q

How do wet and dry ARMD differ on fundoscopy?

A

Dry = Drusen’s seen

Wet = new blood vessels and exudate

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49
Q

What are the Ix for ARMD?

A

OCT - see intraretinal fluid and disruption of the RPE

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50
Q

What is the treatment of dry ARMD?

A

No cure so have to focus on conservative measures/prevention

Stop smoking

Green, leafy vegetables (vitamin A, E, zinc)

Signpost to registering as blind to get full support

Using big text/magnifiying glass

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51
Q

What is the treatment for wet ARMD?

A

Medical = intravitreal injections of VEGF inhibitors - stops angiogenesis. Have to keep redoing

Surgical = Photodynamic/laser photocoagulation. Not that effective. More for chronic.

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52
Q

What are the complications of ARMD?

A

Wet = retinal detachment and blindness

Charles Bonnet syndrome

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53
Q

Why are central retinal arteries bad?

A

Is an end artery so there is no collateral blood supply to preserve tissues.

Vision loss can be irreversible in around 1-2 hours.

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54
Q

What are the main symptoms of central retinal vein/artery occlusion?

A

Sudden loss of central vision

Painless

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55
Q

How does central retinal artery/vein occlusion normally present on fundoscopy?

A

Artery = Retina becomes pale and oedematous (macular oedema)
Fovea remains bright red due to choriocapillary supply (cherry red spot)

Vein = Haemorrhages seen

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56
Q

What are the investigations for CRVO/CRAO?

A

Mainly clinical but can also use OCT and Fluoresceine Angiography

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57
Q

What is the management of central retinal vein/artery occlusion?

A

Vein - Intravitreous VEGF inhibitor injections

Artery - ↓IOP, anticoagulation?

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58
Q

What is a retinal detachment?

A

A hole or tear in the Retina allowing fluid to accumulate between the Retinal Pigment Epithelium and Vitreous humour

(rhegmatogenous = most common)

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59
Q

How does retinal detachment normally present?

A

4 Fs + painless

Flashes
Stimulation of the neural layer

Floaters

Field Loss
Loss of peripheral vision
Moves centrally like a curtain
Macula on = more of an emergency as can still save sight but gravity can pull down a superior tear more

Fall in acuity

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60
Q

What are the investigations for retinal detachment?

A

Dilated eye exam

See a grey, opalescent retina that balloons forward

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61
Q

What is the management of retinal detachment?

A

Treat lying flat

Refer to eye casualty/ to specialist surgery (Vitrectomy, Laser photocoagulation, Gas Tamponade)

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62
Q

What are the borders of the orbit?

A 
Roof = frontal bone
medial = nasal, lacrimal and ethmoidal bones
lateral = sphenoid bone
floor = maxillary bone
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63
Q

what lies directly behind the orbit?

A

ICA, cavernous sinus & brainstem

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64
Q

What is scleritis?

A

vasculitis of the sclera.

Occurs throughout the entire thickness

non-infective and granulomatous = associated with inflammatory conditions

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65
Q

How does scleritis normally present?

A

Red eye

REALLY PAINFUL ESP ON EYE MOVEMENT (DEEP BORING PAIN)

Associated watering and photophobia

Gradual decrease in vision

Elderly, associated with systemic disease

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66
Q

How does episcleritis present?

A

Red eye (acute onset)

Foreign Body sensation

Watering

Normal acuity

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67
Q

What conditions are associated with scleritis?

A

Uveitis

Retinal detachment
Cataracts
Glaucoma

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68
Q

What conditions are associated with episcleritis?

A

anterior uveitis (10% of cases)

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69
Q

How should scleritis and episcleritis be investigated?

A

Examination - Retract the lids and slit lamp. Phenylephrine drops - episcleritis will blanch but scleritis will not

Bloods - all the normal ones + rheumatoid + syphyllis

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70
Q

What serology should be done for [epi]scleritis?

A

RA = rheumatoid factor + anti CCP

SLE = ANA, anti-dsDNA

Wegners = c-ANCA

Reactive arthritis = HLA-B27

Churg-Strauss = p-ANCA

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71
Q

What is the conservative management of scleritis?

A

Refer to ophthalmology

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72
Q

What is the medical management of scleritis?

A

Oral NSAIDS&raquo_space; Oral Prednisolone

? immunosuppressants if ineffective

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73
Q

What are the complications of scleritis?

A

Scleral thinning (scleromalacia)

Anterior segment ischaemia

Raised IOP

Retinal detachement

Cataracts

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74
Q

How can squints be classified?

A

Where the eye deviates to

the nose: esotropia (ESOOOO = NOSE)

temporally: exotropia
superiorly: hypertropia
inferiorly: hypotropia

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75
Q

What is the usual pathophysiology of a squint?

A

Imbalance in the extra ocular muscles

76
Q

How is a squint detected?

A

Corneal light reflection test

Hold the light up to the eye (about 30cm away) and see if it reflects equally in both eyes

77
Q

Which medication can be used to differentiate scleritis and episcleritis?

A

phenylephrine drops may be used to differentiate between episcleritis and scleritis.

Blanches the conjunctival and episcleral vessels but not the scleral vessels.

78
Q

What is the cornea?

A

Transparent, AVASCULAR structure

Separates the tear film from the anterior chamber

Has a rich nerve supply from the ophthalmic branch of the trigeminal nerve

79
Q

What are the layers of the cornea? (5)

A

ABCDE

Anterior corneal epithelium
Bowman's Layer
Corneal Stroma
Descemet's Membrane
Endothelium
80
Q

What are the 3 types of corneal injury?

A

Partial thickness e.g. minor trauma due to grit etc

Superficial keratitis e.g. UV/chemical injury

Full thickness - high velocity injury

81
Q

How does injury to the cornea normally present?

A

White eye

Pain

Lacrimation

Blurred vision

Foreign body sensation

82
Q

What are the investigations for corneal foreign bodies?

A

Slit lamp exam

Fluoresceine dye

83
Q

How should corneal foreign bodies be managed?

A

Remove under slit lamp

+ topical anaesthetic + topical chloramphenicol

84
Q

How do corneal abrasions differ in presentation from FB?

A

Have photophobia in addition to pain and lacrimation

85
Q

What are the complications of corneal abrasions?

A

Keratitis

Recurrent erosions

86
Q

What is the pathophysiology of a corneal ulcer + keratitis?

A

Loss of epithelium exposes nerve endings = severe pain

Inflammation = increase in peri-corneal vascularity = red and discharges

87
Q

What are the risk factors for corneal ulcer?

A

Non-modifiable onlu

Contact lens
Immunocompromised
Diabetes

88
Q

What are the most common types of keratitis?

A

Bacterial - Coagulase negative Staph, pseudomonas

Viral - HSV or VZV

89
Q

How does bacterial keratitis present?

A

Red eye

Pain + photophobia + FB

Reduced acuity

Epiphoria

Hypopyon?

90
Q

What is the management of bacterial keratitis?

A

Conservative - don’t wear contact lenses

Medical - intensive abx (avascular so no WCC clearance)

91
Q

What is the pathophysiology of ophthalmic shingles (herpes simplex opthalmicus)?

A

Primary VZV infection = chickenpox

Virus then lies dormant in Dorsal Root Ganglion

Reactivates in the sensory ganglion leading to HSV/shingles in a specific dermatome

92
Q

What are the clinical features of opthalmic shingles?

Think of that old lady in Dr Eames’ teaching you saw

A

Dermatomal rash - papules > vesicles > pustules > scab. affected top quarter of face and just stopped so in CN V

Hutchinson’s sign - tip of nose indicating nasociliary nerve involvement alluding ocular complications

Viral prodrome

Pre-herpatic neuralgia (tingling or electric pain)

93
Q

What are the complications of opthalmic shingles?

A

Ocular, systemic

Basically all of the opthalmic ‘itis’es e.g conjunctivitis, scleritis etc.

Acute retinal necrosis (ARN) or Progressive outer retinal necrosis (PORN)

Systemic = strokes and Post-herpatic neuralgia

94
Q

What is the management of opthalmic shingles?

A

Start an antiviral as soon as rash appears e.g. Aciclovir PO

? steroid eye drops

Emotional complications of post-herpatic neuralgia e.g. depression - gabapentin and that

95
Q

What are the different types of discharge seen in conjunctivitis and what do they mean?

A

Purulent - Pus + morning crusty and difficult to open = BACTERIAL

Mucopurulent - pus + caught in eyelashes = BACTERIAL USUALLY CHLAMYDIAL

Watery - viral or allergic

Mucoid (stringy) - dry eye

96
Q

Why does hyperaemia of the eye occur?

A

dilated blood vessels due to inflammation

generalised - conjunctivitis, CL, scleritis
localised - episcleritis, FB, corneal abrasion
circumcorneal - keratitis, anterior uveitis

97
Q

What are papillae in the eye?

A

Vascular response

oedema surrounding a core of vessels

98
Q

When do papillae occur?

A

Conjunctivitis - bacterial and allergic (not viral)

Blepharitis

Contact lens use

99
Q

What are follicles?

A

Hyperplasia of lymphoid tissue

Occur in viral or chlamydial conjunctivitis

100
Q

What is keratoconjunctivitis sicca also known as

A

Dry eye!

loss of homeostasis of the tear film + ocular symptoms

reduced lubrication + altered tear film composition
+ hypersensitivity of pain receptors on ocular surface

101
Q

How does dry eye normally present?

A

burning + pain +/- itchy

blurred vision if cornea is involved

FB sensation

102
Q

What is the conservative management of dry eye?

A

Limit contact lense wearing

lid hygiene - warm compress + massage

Avoid using a computer for too long

103
Q

What is the medical management of dry eye?

A

artificial tears

if infection present then can use topical abx + steroids

104
Q

What is the systemic condition that can cause keratoconjunctivitis sicca ?

A

Sjorgen’s

105
Q

What are the 5 most common bacterial pathogens associated with conjunctivitis?

A

Staph epidermidis

Staph aureus

Strep pneumoniae

H influenzae

Moraxella lacunata

106
Q

When is periauricular lymphadenopathy associated with conjunctivitis?

A

If the infection is

viral

chlamydial

107
Q

When are papillae associated with conjunctivitis?

A

bacterial

allergic

108
Q

when are follicles associated with conjunctivitis?

A

viral

chlamydial

toxic e.g. oven cleaner

109
Q

how does allergic conjunctivitis normally present? (5)

A

seasonal

bilateral red eye (painless)

puffy eye lids

itchy

cobblestoning on underside (papillae)

110
Q

How does bacterial conjunctivitis normally present/

A

mucopurulent discharge

red eye (painless)

eyes stick together upon waking

unilateral (usually)

111
Q

How does viral conjunctivitis normally present?

A

lots of watery discharge

red eye (painless)

unilateral then becomes bilateral

+/- flu like symptoms

112
Q

When should conjunctivitis be investigated?

A

severe
recurrent
resists treatment
vulnerable patient

113
Q

What is the management of bacterial conjunctivitis?

A

topical abx for 1 week

chloramphenicol/sodium fusidate/ trimethoprim

don’t touch eye, don’t share towels etc.

114
Q

What are the clinical features of gonococcal conjunctivitis?

A

more common in adults and neonates

severe purulent discharge

lid is really swollen

pre-auricular lymphadenopathy

115
Q

How should gonococcal conjunctivitis be investigated?

A

conjunctival swab for gram staining, culture and sensitivities

refer to GUM + contact tracing

116
Q

What is the treatment for gonococcal conjunctivitis?

A

adults - topical abx (ofloxacin every 2 hours), irrigate

neonates - cefotaxime + frequent irrigation + refer mam and partner to GUM

117
Q

How does neonatal chlamydial conjunctivitis differ to gonococcal?

A

see papillae due to delayed development of lymphoid tissue (i.e. not follicles)

118
Q

How is neonatal chlamydial conjunctivitis managed?

A

Erythromycin for 2 weeks

refer mam and partner to gum

119
Q

What are the common viral agents that cause conjunctivitis? (3)

A

Adenovirus

Molluscum Contagiosum

Herpes Simplex

120
Q

What is the management of viral conjunctivitis?

A

Conservative - cool compress, artificial tears, wash hands frequently, take time off school (red = contagious)

Medical - need abx if there is a secondary bacterial infection

121
Q

What are the 5 main types of allergic conjunctivitis?

A

Seasonal e.g. grass/tree pollen (spring and summer)

Perennial e.g. house dust mites (peaks in autumn)

Vernal (spring)

Atopic

Giant papillary

122
Q

How can allergic conjunctivitis be investigated?

A

Essentially try and find the allergy - skin prick testing/IgE

123
Q

What is the conservative management of allergic conjunctivitis?

A

Identify and avoid allergen

Don’t rub eyes

Cold compress

Ocular surface lubricants

124
Q

What is the medical management of allergic conjunctivitis?

A

Mild = artificial tears to dilute allergen

moderate = mast cell stabiliser/ antihistamines

severe = short course of a mild topical steroid

125
Q

What is the uvea?

A

structure consisting of the iris, ciliary body and choroid

pigmented and vascular

126
Q

What is the iris?

A

Pigmented structure that divides the anterior and posterior chamber

Attached to the lens and controls the amount of light entering the eye

changes size of pupil

127
Q

What class of medication are the following and how do they affect the pupil?

Tropicamide
Phenylephrine
Pilocarpine

A

Tropicamide = antimuscarinic = mydriasis (dilated)

Phenylephrine = sympathomimetic = mydriasis

Pilocarpine = muscarinic agonist = miosis (constriction)

128
Q

How does sympathetic and parasympathetic stimulation affect the iris and pupil size?

A

parasympathetic e.g. due to bright light = constriction of the pupil (miosis)

sympathetic e.g. due to low light = dilation of the pupil (mydriasis)

129
Q

What is the ciliary body?

A

Pigmented structure for accommodation, aqueous humour production and suspensory ligament attachment

130
Q

What is the choroid?

A

Covers posterior eye and divides retina from sclera

Prevents reflection within the eye and nutrition to retina

Attaches to retina via Bruch’s membrane

131
Q

What is uveitis?

A

Inflammation of the uveal tract i.e. iris, choroid and ciliary body

132
Q

What is anterior uveitis?

A

Inflammation of the anterior uveal tract i.e. iris and ciliary body

133
Q

What is posterior uveitis?

A

Inflammation of the posterior uveal tract i.e. choroid, optic nerve head and retina

134
Q

What is the triad of symptoms seen with anterior uveitis?

A

Red eye

Pain

Photophobia

(also watery, normal vision etc)

135
Q

What are the associated conditions with anterior uveitis? (5)

A

PAIR seronegative conditions (HLA-B27) - Psoriasis, Ank Spons, IBD, Reactive arthritis

IBD
Sarcoidosis
Behcet’s (eye casualty man)
infection - TB, Syphyllis, CMV, Toxoplasmosis

136
Q

What is the management of anterior uveitis?

A

Refer to opthalmology

Topical antimuscarinics to dilate the pupil and prevent posterior synechiae

Topical steroids

essentially want to reduce inflammation

137
Q

How does posterior uveitis normally present?

A

Painless and blurred vision

Floaters

Blind spots

Can progress to vision loss

138
Q

How is posterior uveitis normally managed?

A

Oral/ injected steroids

immunosuppressants if this doesn’t work

139
Q

What is the vitreous?

A

Fluidy kind of stuff that is behind the lens and supports the eye

140
Q

How does the vitreous change with age?

A

Fluid fills space between vitreous and retina

Vitreous also shrinks = flashes as v pulls on retina = stimulation of nerves

opacities can form which drift around = floaters

141
Q

What are the differentials for painless sudden loss of vision? (5)

A

CRAO: cherry red spot

CRVO: stormy sunset

Retinal Detachment: curtain folding

Vitreous haemorrhage: can see haemorrhage

Papilloedema : swelling of optic disc

142
Q

What are the key questions to assess sudden loss of vision?

A

HELLP

Headache: GCA
Eye movements painful: optic neuritis
Lights before: RD
Like a curtain: amaurosis fugax, GCA, RD
Poorly controlled DM: vit haemorrhage
143
Q

What is the pathophysiology of a vitreous haemorrhage?

A

3 possible mechanisms

  • bleeding from diseased retinal vessels (fluid in)
  • Abnormal new vessels
  • bleeding into vitreous from outside (fluid out)
144
Q

What are the 3 most common causes of vitreous haemorrhage?

A

Proliferative diabetic retinopathy

Posterior vitreous detachment

Ocular trauma

145
Q

How does Proliferative diabetic retinopathy lead to a vit haemorrhage?

A

Ischaemia = VEGF expression and angiogenesis

BUT new vessels are fragile

146
Q

How does vitreous haemorrhage normally present?

A

Sudden, painless loss of vision

Red hue

Floaters

in the morning

147
Q

How should vit haemorrhage be investigated?

A

Dilated eye exam - can see haemorrhage + RBCs in anterior vitreous

Tonometry - asses IOP

OCT

Fluorescin angiography

148
Q

What is the conservative management of vitreous haemorrhage?

A

Avoid strenuous activity

Elevate head of bed

Aspirin?

149
Q

What is the surgical management of vitreous haemorrhage?

A

laser photocoagulation if proliferative retinopathy

Vitrectomy

150
Q

What are the complications of vitreous haemorrhage?

A

Proliferative vitreoretinopathy

Ghost cell/haemolytic glaucoma

151
Q

What are the differentials of painful loss of vision?

A
  • Optic neuritis
  • Episcleritis
  • Closed angle glaucoma
  • Anterior uveitis
152
Q

What is the deal with screening and diabetic eye disease?

A

Should be screened annually

Photograph the fundus

Any abnormality found = opthalmology referral

153
Q

What is the pathophysiology of cataract formation in diabetic eye disease?

A

Hyperglycaemia = increase uptake of glucose into the lens

Increased sorbitol production in the lens

Depletes the eye of NADPH = reduces glutathione = more susceptible to oxidative stress

Also causes a water influx = opacity and damage

154
Q

What are the risk factors for diabetic eye disease/

A

non-modifiable - race and family hx, age

modifiable - DM, HTN, steroids, no protective factors e.g. oestrogen

155
Q

What is diabetic retinopathy?

A

Obstruction of the microvascular structures within the retina

Essentially hyperglycaemia damages the pericytes - weaker and leaky walls

Micro-aneurysms and lipid leakage

Abnormal vessel formation

156
Q

Define Keratitis

A

Inflammation and damage to the corneal epithelium, stroma, or endothelium.

Characterised by a white area on the cornea indicating a collection of white cells in the corneal tissue

157
Q

Define corneal abrasion

A

A breach of the corneal epithelium causing pain, photophobia +/- reduction in vision

158
Q

What is the management a corneal abrasion?

A

Ix = Fluorescin drops + blue light on slit lamp = green staining

Tx = Topical local anaesthetic. Should heal within 48hr

159
Q

How does a corneal ulcer normally present?

A

FB sensation, photophobia, red eye, lacrimation, ↓ visual acuity

160
Q

What are the likely causative agents of a corneal ulcer?

A

Bacterial = pseudomonas

Viral - HSV1 = dendritic ulcer

Protozoal = acanthamoeba (swimming in contacts)

Fungal = candida, aspergillus

161
Q

What is the management of a corneal ulcer?

A

Refer to eye casualty within 24hr

Chloramphenicol + ofloaxcin (covers gram +ve and -ve)

162
Q

What is the definition of the sclera and what are scleritis and episcleritis

A

The outermost, fibrous layer of the eyeball that provides attachment to the extraocular muscles.

Scleritis = Inflammation of the sclera

Episcleritis = more superficial inflammation of the sclera

163
Q

How does episcleritis normally present?

A

Acute onset of red eye and pain (dull ache and is tender over the affected area)

Focal area of engorged vessels - Can move these with a cotton bud as are superficial + blanche with phenylephrine

Visual acuity not affected

164
Q

How does scleritis present?

A

A constant, dull but severe ‘boring’ pain that worsens on eye movement [as extra-ocular muscles attach into sclera]

Visual acuity is initially unaffected

+/- headache +/- photophobia

165
Q

How does scleritis differ from episcleritis?

A

Scleritis = Generalised inflammation of the sclera + conjunctival oedema + scleral thinning + vasculitic changes

166
Q

Which diseases are scleritis associated with?

A

Systemic ones e.g. Rheumatoid arthritis, Granulomatosis with polyangitis

167
Q

What is the management of scleritis?

A

Urgent referral to eye casualty (within 24hr)

NSAIDS or steroids

Necrotising type requires systemic therapy e.g. Rituximab

About to perforate requires surgical intervention

168
Q

Define anterior uveitis

A

inflammation affecting the iris (iritis) +/- the ciliary body (iridocyclitis)

169
Q

Define intermediate uveitis

A

inflammation of the posterior part of the ciliary body and nearby peripheral retina and choroid

170
Q

Define posterior uveitis

A

inflammation of the retina and choroid

171
Q

Define panuveitis

A

inflammation of the whole uveal tract

most associated with sight loss

172
Q

How does anterior uveitis present?

A

Onset over hours to days

Red eye

Photophobia - progressive
Pain

Reduced vision

Watery eye that may overflow (epiphora)

173
Q

Which conditions is anterior uveitis associated with?

A

HLA-B27 (PAIR)

Psoriasis
Ankylosing Spondylitis
IBD
Reactive Arthritis

174
Q

What is anterior uveitis like on examination?

A

Corneal injection @ angle of sclera and cornea

Irregular pupil/dilates irregularly - due to adhesion formation between lens and iris. These can also obstruct the passage of aqueous humour so can increase risk of glaucoma!

Slit lamp = inflammatory cells in anterior chamber

175
Q

What is the medical management of anterior uveitis?

A

Topical Prednisolone (eye drops to reduce the inflammation)

Cyclopentolate (paralyses the ciliary muscle - Muscarinic antagonist so causes pupil dilation. This reduces pain and also prevents the adhesions forming

176
Q

What is an Adie pupil?

A

Tonically dilated pupil

Slowly reactive to light

More definite accommodation response

Damage to parasympathetic innervation (infection)

Commonly seen in females + absent knee jerks

177
Q

What is a Marcus-Gunn pupil?

A

Relative afferent pupillary defect

Most commonly caused by damage to the optic nerve or severe retinal disease

178
Q

What is Hutchinson’s pupil?

A

Unilaterally dilated pupil which is unresponsive to light

Compression of the occulomotor nerve of the same side, usually due to an intracranial mass

179
Q

What is an Argyll-Robertson pupil?

A

Bilaterally small pupils that accommodate but don’t react to bright light

Neurosyphyllis and Diabetes Mellitus

‘Accommodates but doesn’t react’

180
Q

What are the stages of hypertensive retinopathy?

A

I = Arteriolar narrowing and tortuosity. Increased light reflex - silver wiring

II = Arteriovenous nipping

III = Cotton-wool exudates. Flame and blot haemorrhages

IV = Papilloedema

181
Q

What are the stages of non proliferative diabetic retinopathy?

A

Mild NPDR
1 or more microaneurysm

Moderate NPDR
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots, venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR

Severe NPDR
blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
Intraretinal microvascular abnormalities (IRMA) in at least 1 quadrant

182
Q

What are the features of proliferative diabetic retinopathy?

A

Proliferative retinopathy

retinal neovascularisation - may lead to vitrous haemorrhage

fibrous tissue forming anterior to retinal disc

More common in type 1

183
Q

What are the features of macula diabetic retinopathy?

A

Same as normal but @ the macula

More common in type 2

184
Q

How does blepharitis normally present?

A

Kind of like allergic conjunctivitis

Bilateral itchy eyes + crusting at lid margins + red + swelling
Worse first thing in the morning

185
Q

How should blepharitis be managed?

A

Good eye hygiene - warm compress, keep clean

Chloramphenicol if this doesn’t work

EOY4 (22 decks)

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