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Finals > Opthalmology > Flashcards

Opthalmology Flashcards

1
Q

What is glaucoma and what are the two types?

A

Optic nerve damage caused by a significant rise in intraocular pressure
The raised intraocular pressure is caused by a blockage in aqueous humour trying to leave the eye

Open angle glaucoma and closed angle glaucoma

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2
Q

Describe the two chambers of the eye

A

Vitrous chamber - contains vitreous humour

Anterior chamber - between cornea and iris

Posterior humour - between lens and iris

Both anterior and posterior chambers contain aqueous humour which is produced by the ciliary bodies

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3
Q

What is the function of the aqueous humour

A

Supply nutrients to the cornea

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4
Q

Describe the journey of the aqueous humour from production to exiting the eye

A

Produced in the ciliary body
Flows around the lens and under the iris through the anterior chamber, through the trabecular meshwork and into the canal of schlemm m from the canal of schlemm it eventually enters the general circulation

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5
Q

What is the normal introcular pressure

A

10-21mmHg

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6
Q

What causes increased intraocular pressure in open angle glaucoma

A

Gradual increased resistance to flow through the trabecular meshwork into the canal of schlemm

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7
Q

What happens in acute angle closure glaucoma

A

The iris bulges forward and seals off the trabecular meshwork from the anterior chamber and prevents aqueous humour being able to drain away
This leads to a continual build up of pressure especially in the posterior chamber which causes pressure behind the iris and worsens the closure of the angle

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8
Q

What is seen on fundoscopy in cases of increased intraocular pressure

A

Cupping of the optic disc

Optic cup greater than 0.5 the size of the optic disc is abnormal

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9
Q

List some risk factors for open angle glaucoma

A

Increasing age
Black
Myopia - near sightedness
FH

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10
Q

How does open angle glaucoma present

A

Asymptomatic
Peripheral vision loss - tunnel vision
Fluctuating pain, headaches, blurred vision
Haloes around lights at night time

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11
Q

How is open angle glaucoma diagnosed

A

Non-contact tonometry - puff of air, not much response is positive for glaucoma

Goldmann applanation tonometry - gold standard, machine with slit lamp that apples different pressures to cornea

Fundoscopy - cupping

Visual field assessment - peripheral field loss

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12
Q

How is open angle glaucoma managed

A

Reduced IO pressure

Prostaglandin analogue eye drops (latanoprost) - increase uveoscleral outflow

Beta blockers (timolol) - reduce the production of aqueous humour

Carbonic anhydrase inhibitors (dorzolamide) - reduce production of aqueous humour

Sympathomimetics (brimonidine) - reduce the production of aqueous humour and increase uveoscleral outflow

Trabeculectomy - create a new channel from anterior chamber through the sclera to a location under the conjunctiva it causes a bleb and the conjunctiva where the aqueous humour drains and is then reabsorbed into general circulation

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13
Q

Give the side effects of prostaglandin analogue eye drops such as latanoprost

A

Eyelash growth, eyelid pigmentation and iris pigmentation (browning)

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14
Q

What are some risk factors of acute angle closure glaucoma

A

Increasing age
Females (4X more often than males)
FH
Chinese and east Asian ethnic origin
Shallow anterior chamber - long sightedness
Medication - adrenergic (noradrenalin), anticholinergic (oxybutynin and Solifenacin), tricyclic antidepressants (amitriptyline)

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15
Q

How do patients with acute angle closure glaucoma present

A

Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea and vomiting

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16
Q

Describe the examination of acute angle closure glaucoma

A 
Red eye 
Teary
Hazy cornea
Decreased visual acuity 
Dilation of the affected pupil 
Fixed pupil size
Firm eyeball on palpation
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17
Q

Describe the management of acute angle closure glaucoma

A

Lie patient on back without pillow
Pilocarpine eye drops
Acetazolamide 500mg PO
Give analgesia and antiemetic if required
Hyperosmotic agents - glycerol and mannitol
Timolol (beta blocker) - reduce production of aqueous humour
Brimonidine
Laser iridotomy - definitive treatment - laser to make a hole in the iris and allow the aqueous humour to flow from the posterior chamber into the anterior chamber - relieves pressure that was pushing the iris against the cornea and allows the humour to drain

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18
Q

How does pilocarpine work

A

Acts on antimuscarinic receptors in the sphincter muscles in the iris and causes constriction of the pupil - Miotic agent
Causes ciliary muscle contraction
Cause pathway for flow of aqueous humour from ciliary body around iris and into trabecular meshwork to open up.

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19
Q

What is age related macular degeneration and give the two types

A

Degeneration of the macula causing a progressive deterioration in vision
Most common cause of blindness in the UK
Wet and dry AMD

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20
Q

Which AMD has the worse prognosis

A

Wet

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21
Q

Describe the layers of the macular

A

Photoreceptors at top
Retinal pigment epithelium
Bruchs membrane
Choroid layer - blood vessels

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22
Q

Give some features seen in both wet and dry AMD

A

Drusen - yellow deposits of protein and lipids that appear between the retinal pigment epithelium and Bruchs membrane
Atrophy of the retinal pigment epithelium
Degeneration of photoreceptors

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23
Q

What is a key feature of wet AMD

A

New vessel growing from choroid layer into the retina

The vessels can cause oedema and more rapid vision loss

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24
Q

Which chemical stimulates development of new blood vessels

A

Vascular endothelial growth factor (VEGF)

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25
Q

List some risk factors for age related macular degeneration

A 
Age
Smoking
White or Chinese 
FH
CVD
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26
Q

Describe the presentation of AMD

A

Gradual worsening central visual field loss
Reduced visual acuity
Crooked or wavy appearance to straight lines
Wet AMD presents more acutely - loss of vision over days

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27
Q

What is seen on examination in AMD

A

Reduced acuity on Snellen chart

Scotoma - central patch vision loss

Amsler grid test - wavy lines

Fundoscopy - drusen

Slit lamp fundus examination

Optic coherence tomography (OCT) - layers of the retina - wet AMD

Fluorescein angiography - fluorescein contrast and photographing the retina to look in detail at the blood supply to the retina - oedema and neovascularisation - used second line to diagnose wet AMD if OCT does not exclude it

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28
Q

How is dry age related macular degeneration managed

A

No specific treatment - lifestyle
Stop smoking
Reduce BP
Vitamin supplementation

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29
Q

How is wet age related macular degeneration managed

A

Anti-VEGF medication
Ranibizumab, bevacizumab and pegaptanib
Injected into vitreous chamber once a month
Typically need to be started within 3 months to be beneficial

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30
Q

What is the pathophysiology of diabetic retinopathy

A

Hyperglycaemia leads to damage to retinal small vessels and endothelial cells.

Leakage from vessels causes blot haemorrhages and formation of hard exudates

Damage to blood vessel walls leads to microaneurysms and venous beading

Damage to nerve fibres in the retina cause cotton wool spots

Intraretinal microvascular abnormalities (IMA) shunt between arterial and venous vessels in the retina

Neovascularisation - growth factors into the retina causing development of new blood vessels

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31
Q

Describe the classification of diabetic retinopathy

A

Non-proliferative diabetic retinopathy

Proliferative diabetic retinopathy

Diabetic maculopathy

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32
Q

Describe non-proliferative (pre-proliferative/background) diabetic retinopathy

A

Mild - microaneurysms

Moderate - microaneurysms, blot haemorrhages, hard exudates, cotton wool spots and venous beading

Severe - blot haemorrhages plus microaneurysms in 4 quadrants, venous beading in 2 quadrants or Intraretinal microvascular abnormality in any quadrant

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33
Q

Describe proliferative retinopathy

A

Neovascularisation

Vitreous haemorrhage

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34
Q

Describe diabetic maculopathy

A

Macular oedema

Ischaemic maculopathy

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35
Q

List the complications of diabetic retinopathy

A 
Retinal detachment
Vitreous haemorrhage
Rebeosis iridis - vessel development in iris
Optic neuropathy
Cataracts
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36
Q

How is diabetic retinopathy managed

A

Laser photocoagulation
Anti-VEGF medication - ranibizumab and bevacizumab
Vitreoretinal surgery

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37
Q

Describe hypertensive retinopathy and its features

A

Damage to the retina as a result of hypertension (either chronic or malignant)

Silver/copper wiring - sclerosed and thickened arterioles
AV nipping - where arterioles cause compression of the veins where they cross - sclerosis

Cotton wool spots - ischaemia and infarction causing nerve fibre damage

Hard exudates - lipids leaking into the retina

Retinal haemorrhages- damaged vessels rupturing and releasing blood into the retina

Papilloedema - ischaemia to the optic nerve - swelling and blurring of the disc margins

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38
Q

Describe the Keith Wagener classification for hypertensive retinopathy

A

Stage 1 - mild narrowing of arterioles

Stage 2 - focal constriction and AV nipping

Stage 3 - cotton wool patches, exudates and haemorrhages

Stage 4 - papillooedema

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39
Q

How is hypertensive retinopathy managed

A

Control BP

Modify RF - smoking and blood lipids

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40
Q

What are cataracts

A

Where the lens becomes cloudy and opaque

Loss of visual acuity by reducing the light entering the eye

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41
Q

What is the function of the lens

A

To focus the light onto the retina

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42
Q

Describe the anatomy of the lens

A

Held by suspensory ligmanets attached to the ciliary body
The ciliary body contracts and relaxes to focus the lens
When the ciliary body contracts it releases tension on the suspensory ligament and the lens thickens
When the ciliary body relaxes, it increases tension on the suspensory ligaments causing the lens to narrow

The lens does not have a blood supply so it grows and develops throughout life

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43
Q

List some risk factors for cataracts

A 
Age
Smoking
Alcohol 
Diabetes
Steroids 
Hypocalcaemia
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44
Q

Describe the presentation of cataracts

A

Very slow reduction in vision
Progressive blurring of the vision
Change in colour vision with colours becoming more brown or yellow
Starbursts can appear around lights - at night time

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45
Q

What is a sign of a cataracts on examination

A

Loss of the red light reflex - lens appears grey/white

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46
Q

What causes a generalised loss of vision with starbursts around light

A

Cataracts

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47
Q

What causes a peripheral loss of vision and halos round light

A

Glaucoma

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48
Q

What causes a central loss of vision with crooked appearance to straight lines

A

Age related macular degeneration

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49
Q

Describe the management of cataracts

A

None if asymptomatic
Surgery if wanting to detect other eye pathology or patient wants the cataract removed - pseudophakia (artificial lens) implanted

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50
Q

Name one important complication of cataracts surgery and give its management and complications

A

Endophthalmitis
Inflammation of the inner contents of eye usually due to infection
Treated with Intravitreal antibiotics injected into the eye
Can lead to loss of vision or loss of the eye

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51
Q

Describe how pupil constriction and dilation occur

A

Constriction - Circular muscles of iris stimulated by acetylcholine of parasympathetic nervous system travelling along the oculomotor nerve

Dilation - dilator muscles travel from inside to outside of the iris and stimulated by adrenalin by the sympathetic nervous system

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52
Q

List some causes of abnormal pupil shape

A

Trauma to sphincter muscles - surgery
Adhesions - anterior uveitis
Vertical oval - acute angle closure glaucoma - ischaemic damage to muscles of iris
Rubeosis iridis - neovascularisation of the iris in DR
Coloboma - congenital malformation - hole in iris
Tadpole pupil - spasm in a segment of iris associated with migraines

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53
Q

List the causes of mydriasis (pupil dilation)

A 
3rd nerve palsy 
Holmes Adie syndrome 
Stimulants - cocaine 
Congenital 
Raised ICP
Trauma 
Anticholinergic drugs
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54
Q

List the causes of miosis (pupil constriction)

A 
Horner's syndrome
Cluster headache
Argyll-Robertson pupil (neurosyphilis) 
Opiates 
Nicotine
Pilocarpine
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55
Q

Describe a third nerve palsy

A

Ptosis - CN3 innervates levator palpabrae superioris

Mydriasis (dilation) and non reactive pupil -CN3 contains parasympathetic supply which normally constricts pupil so palsy causes dilatation

Divergent strabismus (squint) and Down and out position of the eye - CN3 innervates all the extraocular muscles except lateral rectus and superior oblique so palsy causes down and out as lateral rectus and superior oblique still functioning

56
Q

Which nerve innervates lateral rectus

A

Abducens (6)

57
Q

Which nerve innervates superior oblique

A

Trochlear (4)

58
Q

What does a third nerve palsy with pupil sparing suggest

A

Sparing of parasympathetic fibres so the cause is microvascular

  • DM
  • HTN
  • Ischaemia
59
Q

List the causes of a full third nerve palsy

A

Compression of the nerve including parasympathetic fibres - surgical third

  • Idiopathic
  • Trauma
  • Tumour
  • Cavernous sinus thrombosis
  • Posterior communicating artery aneurysm
  • Raised ICP
60
Q

Which two brain structures does the third cranial nerve travel close to

A

Cavernous sinus

Posterior communicating artery

61
Q

Describe Horner’s syndrome

A

Ptosis
Miosis
Anhidrosis (loss of sweating)

May have enopthalmos - sunken eye

62
Q

What causes Horner’s syndrome

A

Damage to the sympathetic nerves supplying the face

Congenital - heterochromia (difference in eye colour on affected eye)

Central

  • Stroke
  • MS
  • Swelling/tumour
  • Syringomyelia (cysts in the spinal cord)

Pre-ganglionic

  • Tumour - Pancoasts tumour
  • Trauma
  • Thyroidectomy
  • Cervical rib

Post-ganglionic

  • Carotid artery dissection
  • Cavernous sinus thrombosis
  • Cluster headache
63
Q

Describe the journey of the sympathetic nerves to the head

A

Arise from spinal cord in the chest (pre-ganglionic nerves)

They enter the sympathetic ganglion on at the base of the neck and exit as post ganglionic nerves

They then travel to head alongside internal carotid artery

64
Q

How can the location of the Horner syndrome be determined

A

If there is anhidrosis

Central lesions cause anhidrosis of the arm and trunk and face

Pre-ganglionic lesions cause anhidrosis of the face

Post-ganglionic lesions do not cause anhidrosis

65
Q

What affect do cocaine eye drops have on a pupil in Horner’s syndrome

A

No affect

66
Q

What affect do adrenaline eye drops have on a Horner’s syndrome pupil

A

Dilation

67
Q

Describe a Holme’s-Adie pupil

A

Unilateral dilated pupil which is sluggish to react to light with slow dilation after constriction
Damage to post-ganglionic parasympathetic fibres probably viral

68
Q

What is Holmes-Adie syndrome

A

Holmes Adie pupil with absent ankle and knee reflexes

69
Q

What causes an Argyll Robertson pupil

A

Neurosyphilis

70
Q

Describe argyll-robertson pupil

A

Irregularly shaped
Constricted pupil
Accommodates but does not react

71
Q

Describe blepharitis

A

Inflammation of eyelid margins
Causes dry, itchy, gritty sensation
Dysfunction of Meibomian glands (secrete oil onto eye) leading to styes and chalazions

72
Q

How is blepharitis managed

A

Hot compress
Gentle cleaning of eye - baby shampoo and sterile water

Lubricating eye drops - hypromellose, polyvinyl alcohol (start with these - middle viscous) and carbomer (most viscous lasting 30-60 mins)

73
Q

Describe styes and their management

A

Hordeolum externum - infection of glands of zeis (sebaceous glands ) and glands of moll (sweat glands) at base of eyelashes

Tender red lump that may contain pus

Hordeolum internum - infection of Meibomian glands, deeper and more painful and may point inwards under the eyelid

Managed with hot compress and analgesia, may require topical antibiotic (chloramphenicol) if associated conjunctivitis or persistent

74
Q

What are chalazions and how are they managed

A

Blocked Meibomian glands - cyst, typically non-tender but can be
Managed with hot compress and possible topical antibiotics
May require drainage

75
Q

What is entropion and its treatment

A

Eyelid inward with lashes against eyeball
Lashes may cause corneal ulceration and damage
Initial management - taping down of eyelid and regular lubricating eye drops
Definitive management - surgery

76
Q

What is ectropion and its treatment

A

Eyelid turned outward with inner aspect of eyelid exposed
Exposure keratopathy
Management - if mild no treatment, lubricating drops, more severe require surgery

77
Q

What is periorbital cellulitis and its management

A

Infection in front of the orbital septum - swelling, redness and hot skin around eyelid

CT to differentiate from orbital cellulitis

Treat with systemic antibiotics as risk of developing orbital cellulitis

78
Q

What is orbital cellulitis and its management

A

Infection around eyeball involving tissues behind orbital septum

Pain on eye movement, change in vision, abnormal pupil reaction, forward movement of eyeball
Medical emergency - admission and IV antibiotics - may require surgical drainage if an abscess forms

79
Q

What is conjunctivitis

A

Inflammation of the conjunctiva - thin layer of tissue that covers the inside of the eyelids and the sclera of the eye

80
Q

List and describe the three types of conjunctivitis

A

Bacterial - purulent discharge
Viral - clear discharge and other signs of viral infection such as dry cough, sore throat, blocked nose and tender periauricular lymph nodes
Allergic - lots of watery discharge

81
Q

What are the symptoms of conjunctivitis

A

Discharge
Itch
Gritty sensation
Red eye
Not painful or photophobia or reduced visual acuity
Blurring may be due to discharge but resolves when discharge clears
Unilateral/bilateral

82
Q

What is the differential for an acutely red painful eye

A 
Glaucoma 
Anterior uveitis
Corneal abrasions/ulcers
Scleritis
Keratitis
Foreign body 
Traumatic or chemical injury
83
Q

What is the differential for an acutely red painless eye

A

Conjunctivitis
Episcleritis
Subconjunctival haemorrhage

84
Q

How is conjunctivitis managed

A

Usually resolves without treatment within 1-2weeks

Good hygiene to avoid spreading and avoid the use of contact lenses. Clean the eyes with cooled boiled water and cotton wool to help clear the discharge

Bacterial conjunctivitis - topical antibiotic eye drops - chloramphenicol and fusidic acid

Allergic conjunctivitis - antihistamines (topical or oral) and topical mast cell stabilisers in patients with chronic seasonal symptoms - preventing mast cells releasing histamine - require use for several weeks before showing benefit

85
Q

What is anterior uveitis

A

Inflammation in the anterior part of the uvea
Uvea involves the iris, ciliary body and choroid (layer between the retina and sclera)

Inflammation and immune cells in the anterior part of the eye - becomes infiltrated by neutrophils, lymphocytes and macrophages

Can be acute or chronic

86
Q

What is acute anterior uveitis associated with

A

HLAB27 related conditions
Ankylosing spondylitis
Inflammatory bowel disease
Reactive arthritis

87
Q

What is chronic anterior uveitis associated with

A 
More granulomatous diseases
Sarcoidosis
TB
Lyme disease
Herpes virus 
Syphylis
88
Q

Describe chronic anterior uveitis

A

> 3 months

Less severe

89
Q

Describe the presentation of anterior uveitis

A

Unilateral symptoms that start spontaenously without history of trauma/precipitating event

May occur with a flare of the associated disease

Dull, aching, painful red eye
Ciliary flush - red ring spreading from the cornea outward

Reduced visual acuity
Floaters and flashes

Sphincter muscle contraction - miosis
Photophobia due to ciliary muscle spasm
Pain on movement
Excess tear production
Abnormally shaped pupil - posterior synechiae (adhesions)
Hypopyon - collection of white cells in anterior chamber - yellowish fluid settled in front of the lower iris

90
Q

Describe the management of anterior uveitis

A

Urgent ophthalmology review - slit lamp and intraocular pressure assessment

Steroids - oral, topical, IV
Cycloplegic-mydriatic medication - cyclopentolate or atropine - dilates the pupils and relaxes the ciliary bodies to reduce pain associated with ciliary body spasm
Immunosuppressants - DMARDs and TNF inhibitors
Laser therapy, cryotherapy or surgery

91
Q

What is episcleritis

A

Inflammation of the episclera (layer under the conjunctiva)
Common in young and middle aged adults
Associated with IBD and RA

92
Q

How does episcleritis present

A 
Not painful
Segmental redness - lateral sclera
Foreign body sensation
Dilated episcleral vessels 
Watering of the eye 
No discharge
93
Q

Describe the management of episcleritis

A 
Self limiting - 1-4 weeks 
Cold compress 
Lubricating eye drops can help 
Simple analgesia
Safety net advice
More severe cases may benefit from systemic NSAIDs and topical steroid eye drops
94
Q

Describe scleritis

A

Inflammation of the full thickness of the sclera

95
Q

What are the complications of scleritis

A

Visual impairment - Necrotising scleritis and perforation of the sclera

96
Q

What conditions are associated with scleritis

A 
IBD
RA
SLE
Sarcoidosis
Granulomatosis with polyangitis
97
Q

Describe the presentation of scleritis

A 
Severe pain
Pain with eye movement
Photophobia
Eye watering
Reduced visual acuity 
Abnormal pupil reaction to light 
Tenderness to palpation of the eye 
50% bilateral
98
Q

How is scleritis managed

A 
Urgent ophthalmology referral - same day 
Consider underlying systemic condition 
NSAIDs
Steroids
Immunosuppression
99
Q

List some causes of corneal abrasions

A 
Contact lenses
Foreign bodies
Finger nails
Eyelashes
Entropion
100
Q

Which bacteria may infect the eye if abrasion associated with contact lenses

A

Pseudomonas

101
Q

What is an important differential to consider in corneal abrasions

A

Herpes keratitis

102
Q

Describe the presentation of corneal abrasions

A 
Painful red eye
Foreign body sensation
Watering eye
History of contact lens use
Blurring of vision
Photophobia
103
Q

How is a corneal abrasion diagnosed

A

Fluorescein stain - yellow/orange colour which collects in abrasions and ulcers
Slit lamp examination - more significant

104
Q

How are abrasions managed

A 
Slit lamp assessment 
Remove foreign bodies
Simple analgesia 
Lubricating eye drops 
Chloramphenicol
Follow up after 24hrs 
Chemical abrasions require immediate irrigation for 25-30 mins and urgent referral to ophthalmology 
Uncomplicated abrasions heal over 2-3 days
105
Q

List some causes of keratitis

A 
Viral - herpes simplex
Bacterial - pseudomonas and staphylococcus 
Fungal - candida or aspergillus
Contact lens acute red eye 
Exposure keratitis
106
Q

What is the most common cause of keratitis

A

Herpes simplex virus

107
Q

Describe herpes simplex keratitis

A

Primary or recurrent
Affects the epithelial layer of the cornea
If there is stromal inflammation risk of - stromal necrosis, vascularisation and corneal blindness

Painful red eye
Photophobia
Vesicles around the eye
Foreign body sensation
Watering eye
Reduced visual acuity
108
Q

How is herpes keratitis diagnosed

A

Fluorescein stain - dendritic (branching) corneal ulcer

Slit lamp examination

Corneal swabs or scrapings - isolate the virus using viral culture or PCR

109
Q

Describe the management of herpes keratitis

A

Aciclovir - topical or oral
Ganciclovir eye gel
Topical steroids - alongside antivirals to treat stromal keratitis
Corneal transplant - may be required after the infection has resolved to treat corneal scarring caused by stromal keratitis

110
Q

What is a subconjunctival haemorrhage, how does it present, what causes it and how is it managed?

A

Blood vessel in conjunctiva ruptures causing a patch of blood between the sclera and conjunctiva

Does not affect vision
Occurs after heavy lifting, coughing or straining af with consitpation

HTN and bleeding disorders or medications (warfarin, DOACs and antiplatelets may lead to this)

Resolves spontaneously over 2 weeks
Investigate if underlying cause suspected
If foreign body sensation - give lubricating eye drops

111
Q

What is the vitreous body

A

Gel inside the eye that maintains the eyeball structure and keeps the retina pressed on the choroid
Made of collagena and water
With age becomes less firm

112
Q

What is posterior vitreous detachment

A

When the vitreous body comes away from the retina

113
Q

How does posterior vitreous detachment present

A 
Painless 
Spots of vision loss
Floaters
Flashing lights 
Brain adjusts till asymptomatic
114
Q

What can occur as a result of posterior vitreous detachment

A

Retinal tears and detachment

115
Q

How is posterior vitreous detachment managed

A

No management - brain adjusts

Exclude retinal tear/detachment

116
Q

Describe retinal detachment

A

Retina detaches from the choroid underneath

Usually due to retinal tear which allows vitreous fluid to get under the retina and fill the space between the retina and the choroid

Retina relies on the choroid for its blood supply - sight threatening- emergency

117
Q

List some risk factors for retinal tears

A 
Posterior vitreous detachment
Older age
Diabetic retinopathy
Damage to the eye - trauma 
Retinal malignancy 
Family history
118
Q

How does retinal detachment present

A

Peripheral vision loss - sudden and like a shadow coming across vision
Blurred or distorted vision
Flashes and floaters
Painless

119
Q

How are retinal tears managed

A

Create adhesions between retina and choroid - laser therapy or cryotherapy

120
Q

How is retinal detachment managed

A

Vitrectomy - remove vittreous body and replace with oil/gas

Scleral buckling - silocone buckle to put pressure on outer eye and indent the eye so the choroid touches the retina

Pneumatic retinopexy - inject gas bubble into the eye and position patient so bubble creates pressure that flattens the retina against the choroid and close the detachment

121
Q

Describe retinal vein occlusion

A

Occurs when thrombus blocks the retinal veins from draining the retina
Central retinal vein runs through the optic nerve and rains blood from the retina

4 branched veins come together to form the central retinal vein, blockage of a branch leads to problems in the area drained by this branch whereas central retinal vein occlusion leads to problems in the whole retina

122
Q

What does central retinal vein occlusion cause

A

Macular oedema and retinal haemorrhages
Damage in the tissue in the retina and loss of vision
Release of VEGF which causes neovascularisation

123
Q

How does central retinal vein occlusion present

A

Painless loss of vision

Flame and blot haemorrhages, optic disc oedema and macula oedema on fundoscopy

124
Q

List the risk factors for central retinal vein occlusion

A 
HTN
High cholesterol
DM
Smoking
Glaucoma
SLE
125
Q

Describe the management of central retinal vein occlusion

A

Laser photocoagulation
Intravitreal steroids
Anti-VEGF therapy

126
Q

Describe central retinal artery occlusion

A

Blockage of flow through retinal artery caused by atherosclerosis or giant cell arteritis

127
Q

Describe the formation of the central retinal artery

A

ICA - opthalmic artery - central retinal artery

128
Q

List some risk factors for central retinal artery occlusion

A 
Older age
FH
Smoking
Alcohol
HTN
DM
Poor diet
Inactivity 
Obesity 
GCA RF - females, white, >50yo, PMR or GCA
129
Q

Describe the presentation of central retinal artery occlusion

A

Sudden painless loss of vision
Relative afferent pupillary defect
Fundoscopy - pale retina with cherry red spot

130
Q

Describe relative afferent pupillary defect

A

Pupil in affected eye constricts more when light shone into normal eye due to consensual response whereas light shone into affected eye is not detected by the affected eye/ischaemic retina

131
Q

What is the cherry red spot seen in central retinal artery occlusion on fundoscopy

A

Macula - thinner surface and shows the red coloured choroid below and contrasts with the pale retina

132
Q

Describe the management of central retinal artery occlusion

A

GCA - reversible cause - ESR and temporal artery biopsy - high dose steroids - 60mg prednisolone

Thrombus - ocular massage, inhale carbogen (5% CO2 and 95% O2), sublingual isosorbide dinitrate to dilate the artery and remove fluid from anterior chamber to reduce intraocular pressure

Long term management- modify RF

133
Q

What is retinitis pigmentosa

A

Inherited congenital condition where there is degeneration of rods and cones. The rods degenerate more than the cones
Can occur on its own or part of a disease with hearing (Ushers syndrome), neurological (Bassen-kornzweig syndrome) or skin issues (Refsums disease)

134
Q

Describe the presentation of retinitis pigmentosaq

A

Peripheral vision loss before central vision loss
Night blindness
Fundoscopy shows bone-spicule pigmentation in the mid peripheral area of the retina
Narrow arterioles
Waxy or pale optic disc

135
Q

How is retinitis pigmentosa managed

A

Ophthalmology
genetic counselling
Vision aids
Sunglasses to protect retina from accelerated damage
Driving limitation - inform DVLA
Regular follow up to assess for other conditions such as cataracts

Finals (18 decks)

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