Vascular Tunic: Iris, Ciliary Body, Choroid Flashcards

1
Q

What is Uveal tract?

A
  • Uveal tract is made up of the iris, ciliary body and choroid
  • This is a highly vascular and densely pigmented layer of eyeball between sclera and retina
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2
Q

What are causes of Uveitis?

A
  • Autoimmune: common in IBD, SLE, MS, Behcets, juvenile idiopathic arthritis, rheumatoid disease
  • Infections: associated with Herpes zoster virus, CMV
  • Iatrogenic/Drug induced: rifabutin, cidofovir, bisphosphonates
  • Traumatic: Sympathetic ophthalmia (uveal tissue exposed due to penetrative injury, causes inflammation in good eye)
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3
Q

How is Uveitis classified?

A
  • Keratitic precipitates
    • Granulomatous
    • Non-granulomatous
  • Chronicity
    • Acute
    • Recurrent: more than 3 months apart
    • Chronic: frequent but with less than 3 months apart
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4
Q

What are symptoms of Anterior Uveitis?

A
  • Progressive and usually unilateral, painful, redness with blurred vision and photophobia. Loss of vision over hours/days
  • Eye pain often worse when trying to read
  • Excess tear production
  • Headache
  • Photophobia
  • Ocular discomfort & pain (may increase with use)
  • Lacrimaton
  • Visual acuity initially normal → impaired
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5
Q

What are signs of anterior uveitis?

A
  • Small, fixed oval (or irregular) pupil
    • stuck to lens because of posterior synechiae which are adhesions between posterior surface of iris and anterior surface of lens capsule
    • Remember this usually occurs in late stages of the condition so a normal pupil doesn’t totally exclude anterior uveitis
  • Ciliary flush
  • Flare and cells seen in slit lamp - imagine in cinemas beam of light with the white things floating)
  • Keratitic precipitates - deposits at back of cornea
  • Hypopyon - describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
  • Red eye
  • Blurred Vision
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6
Q

How is anterior uveitis managed?

A

Immediate specialist urgent referral required in suspected uveitis

  • Topical steroids/subconjunctival steroids – reduce inflammation
  • Cycloplegics (eg cyclopentolate, atropine) - relax the spasm of ciliary body, reduce the pain, and relieve photophobia
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7
Q

What are symptoms and signs of intermediate uveitis (affecting viteous and posterior ciliary body)?

A

Symptoms:

  • Blurring of vision
  • Floaters
  • May not have pain

Signs:

  • Cells in vitreous
  • Snow balls - clumps of cells in vitreous
  • Snowbanking - on retina
  • Sheathing of blood vessels
  • Macular oedema
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8
Q

What is the management of Intermediate Uveitis?

A
  • Local: Periocular steroids or Intravitreal steroid implants
  • Systemic: Pulse therapy, Oral steroids, Immunosuppression, Aetiology-specific drugs
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9
Q

What are symptoms and signs of Posterior Uveitis (inflammation of choroid)?

A

Symptoms

  • Gradual, normally bilateral, visual loss, often with associated floaters
  • Occasional photophobia, little or no discomfort or redness

Signs

  • Inflammatory lesions/granulomas may be seen on retina or choroid
  • Inflammation of retinal blood vessels may occur
  • Associated with TB, Sarcoidosis, CMV
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10
Q

What are investigations for Posterior Uveitis?

A

Imaging may be useful:

  • OCT
  • Fundus fluorescein angiography
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11
Q

What are the general investigation and management for Uveitis?

A
  • Immediate specialist referral required in suspected uveitis
  • Classify based on cause and treat: infectious vs non-infectious?
    • If suspecting infection: sample of vitreous for PCR
  • Investigate and treat secondary causes as necessary
    • Autoimmune: Sarcoid ACE, anti dsDNA for SLE, MRI for MS, HLA for Behcets, HLAB27 for ankylosing spondylitis, psoriasis
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12
Q

What are complications of Uveitis?

A
  • Hypotony (low IOP)
  • Glaucoma
  • Cataracts
  • Posterior synechiae
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13
Q

What are complications of treatment for Uveitis?

A
  • Steroid – may lead to cataract or glaucoma
  • Immunosuppressants - side effects such as immunosuppression
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14
Q

What are features associated with Glaucoma?

A
  • Group of conditions – could be caused with or without increased pressure in the eye
  • Leads to damage to the optic nerve and loss of retinal ganglion cells forming main cause of irreversible blindness
  • Early detection and treatment is important in preventing glaucoma related blindness
  • Compliance/adherence to treatment is important
  • Affects 0.5% of people over the age of 40
  • The prevalence increases with age up to 10% over the age of 80 years. Affects males and females equally
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15
Q

What are types of Glaucoma?

A
  • Open angle – asymptomatic
    • Primary Open Angle Glaucoma
    • Normal Tension Glaucoma
  • Closed angle glaucoma
    • Acute
    • Primary Angle Closure Glaucoma
  • Primary Glaucoma
  • Secondary Glaucoma (Inflammatory, Secondary to haemorrhage, Neovascular, Steroid induced, Ocular tumour)
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16
Q

What are risk factors of Primary Open Angle Glaucoma?

A
  • Age
  • Genetics: first degree relatives of an open-angle glaucoma patient have a 16% chance of developing the disease
  • Black patients
  • Myopia
  • Hypertension
  • Diabetes mellitus
  • Corticosteroids
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17
Q

What are symptoms and signs of Primary Open Angle Glaucoma?

A
  • Symptoms
    • Characterised by a slow rise in intraocular pressure: symptomless for a long period
    • Typically present following an ocular pressure measurement during a routine examination by an optometrist
  • Signs
    • Peripheral visual field loss - nasal scotomas progressing to ‘tunnel vision’
    • Decreased visual acuity
    • Optic disc cupping
    • Increased intraocular pressure
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18
Q

What are the signs on fundoscopy on Primary Open-Angle Glaucoma?

A
  1. Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
  2. Optic disc pallor - indicating optic atrophy
  3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
  4. Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages
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19
Q

What is the process of diagnosis and case finding for Primary Open Angle Glaucoma?

A
  • Case finding and provisional diagnosis is done by an optometrist and if suspected full investigations are performed
    • optic nerve head damage visible under the slit lamp
    • visual field defect
    • IOP > 24 mmHg as measured by Goldmann-type applanation tonometry
  • Referral to the ophthalmologist is done via the GP
  • Final diagnosis is done by full set of investigations
20
Q

What are investigations for Primary Open angle glaucoma?

A
  • Automated perimetry to assess visual field
  • Slit lamp examination with pupil dilatation to assess optic neve and fundus for a baseline
  • Applanation tonometry to measure IOP
  • Central corneal thickness measurement
  • Gonioscopy to assess peripheral anterior chamber configuration and depth
  • Assess risk of future visual impairment, using risk factors such as IOP, central corneal thickness (CCT), family history, life expectancy
21
Q

How is Primary Open Angle Glaucoma managed?

A
  • Medical Treatment
    • First line: prostaglandin analogue (PGA) eyedrop
    • Second line: beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop
  • If more advanced
    • Laser
      • Selective laser trabeculoplasty (shine into angle to open it up)
      • Cylodiode: acts on ciliary body
      • Peripheral laser iridotomy: reserved for angle closure glaucoma because it works very quickly
    • Surgery
      • Trabeculectomy – creates a fistula to increase aqueous outflow. Steroids required every 2 hours post surgery for 2 weeks to prevent scarring and closure of the anastomosis
      • Artificial shunts
  • Reassessment
    • Important to exclude progression and visual field loss
    • Needs to be done more frequently if: IOP uncontrolled, the patient is high risk, or there is progression
22
Q

What are factors predisposing to acute angle closure glaucoma?

A

Rise in Intra-ocular pressure secondary to impairment of aqueous outflow

  • Hypermetropia (long-sightedness)
  • Pupillary dilatation
  • Lens growth associated with age
23
Q

What are symptoms and signs of Acute Angle Closure Glaucoma?

A

Symptoms

  • Severe pain: may be ocular or headache
  • Systemic malaise
  • Nausea and vomiting
  • Decreased visual acuity
  • Symptoms worse with mydriasis (e.g. watching TV in a dark room)
  • Blurred vision when loking at lights and haloes around lights

Signs

  • Semi-dilated non-reacting pupil
  • Corneal oedema results in dull or hazy cornea
  • Systemic upset may be seen, such as nausea and vomiting and even abdominal pain
  • Hard, red-eye with hazy cornea. Minimally or non light reactve mid-dilated pupil
24
Q

What is the management of Acute Angle Closure Glaucoma?

A
  • Urgent referral to an ophthalmologist
  • Medical management options includes:
    • Reducing aqueous secretions with acetazolamide
    • Inducing pupillary constriction with topical pilocarpine and phenylephrine in patients with artificial lens
    • Beta blockers - topical timolol
    • Steroids – prednisolone 15mg every 15 minutes for an hour, then hourly
    • Sympathomimetic topically – apraclonidine or brimonidine
    • Preventative treatment in other eye too
    • Not in patients with sulfonamide allergy or sickle cell disease/trait
    • Analgesia and antiemetics as necessary
  • Surgical Management
    • Peripheral iridotomy – allows for free flow of aqueous to leave and therefore to reduce the pressure (small hole made in the iris)
    • Surgical iridectomy – similar procedure but more invasive and prone to complications
    • Lensectomy – remove lens in cataractous cause of acute angle closure
25
Q

What is the pathophysiology for glaucoma?

A

2 theories

  1. Drain blocks at iridocorneal angle
    • Aqueous humour produced by ciliary body can’t drain out through trabecular mesh work into Schlemm’s canal and hence pressure builds up
    • Patients’ eyesight gradually declines with loss of peripheral visual fields
    • Pressure is not always raised - some patients may develop normal pressure glaucoma (optic nerve damage without raised intraocular pressure)
  2. Poor blood supply to optic nerve
26
Q

What is the pathophysiology of open angle glaucoma?

A
  • More likely to be a chronic condition, more common than closed angle. Patients often asymptomatic for a long time as they do not notice the losses to their peripheral vision in early disease
  • Usually only present once severe, irreversible damage has occurred - up to 90% of the optic nerve fibres may have been damaged
  • Aqueous fluid does not drain well out of the eye, increasing the pressure in the eye. It is thought that the trabecular meshwork becomes blocked, preventing this drainage
27
Q

What are examination and investigations for Acute Angle Glaucoma?

A
  • RAPD on swinging flashlight test due to optic nerve damage
  • Hardness of the eyeball on palpation due to raised IOP
  • Slit lamp: may show corneal oedema, change in pupil shape and iris atrophy
  • IOP >21mmHg (better to not spend too much time investigating)
28
Q

How is primary open-angle glaucoma classified?

A

Classified based on :

  • Whether the peripheral iris is covering the trabecular meshwork, which is important in the drainage of aqueous humour from the anterior chamber of the eye.
  • In open-angle glaucoma, the iris is clear of the meshwork. The trabecular network functionally offers an increased resistance to aqueous outflow, causing increased IOP. It is now recognised that a minority of patients with raised IOP do not have glaucoma and vice versa.
29
Q

How is Hyphema managed?

A
  • Hyphema is blood in the anterior chamber of the eye
  • In context of trauma, referral to opthalmic specialist for assessment and management.
    • Main risk to sight comes from raised intraocular pressure developing from blockage of angle and trabecular meshwork with eythrocytes.
    • Strict bed rest required as excessive movement can redisperse blood that had previously settled therefore high risk cases are often admitted
  • Isolated hyphema will also require dailly opthalmic review and pressure check initially as an outpatient.
30
Q

What are features of Horner’s Syndrome?

A
  • Miosis (small pupil)
  • Ptosis
  • Enophthalmos* (sunken eye)
  • Anhidrosis (loss of sweating one side)
31
Q

How does anhidrosis help to distinguish between different causes of Horner’s Syndrome?

A

Central Lesions

  • Anhidrosis of the face, arm and trunk

Pre-ganglionic Lesions

  • Anhidrosis of the face

Post-ganglionic Lesions

  • No anhidrosis
32
Q

What are causes of central lesions, pre-ganglionic, and post-ganglionic leading to Horner’s syndrome?

A

Damage to the sympathetic trunk

  • Central Lesions
    • Stroke
    • Syringomyelia
    • Multiple sclerosis
    • Tumour
    • Encephalitis
  • Pre-Ganglionic Lesions
    • Pancoast’s tumour
    • Thyroidectomy
    • Trauma
    • Cervical rib
  • Post-Ganglionic Lesions
    • Carotid artery dissection
    • Carotid aneurysm
    • Cavernous sinus thrombosis
    • Cluster headache
33
Q

What is a key feature in congenital Horner’s?

A

Heterochromia (difference in iris colour) is seen in congenital Horner’s

34
Q

What is Cataracts?

A
  • Common eye condition where the lens of the eye gradually opacifies i.e. becomes cloudy. This cloudiness makes it more difficult for light to reach the back of the eye (retina), thus causing reduced/blurred vision.
  • Cataracts are the leading cause of curable blindness worldwide.
  • Cataracts are more common in women than in men
  • The incidence of cataracts increases with age. One study found that 30% of individuals aged 65 and over had a visually-impairing cataract in either one or both eyes
35
Q

What are causes of Cataracts?

A
  • Normal Ageing process is most common
  • Smoking
  • Increased alcohol consumption
  • Trauma
  • Diabetes mellitus
  • Long-term corticosteroids
  • Radiation exposure
  • Myotonic dystrophy
  • Metabolic disorders: hypocalcaemia
36
Q

What are symptoms of Cataracts?

A
  • Reduced vision
  • Faded colour vision: making it more difficult to distinguish different colours
  • Glare: lights appear brighter than usual
  • Halos around lights
37
Q

What are the signs of Cataracts?

A

Defect in the red reflex

  • Red reflex is essentially the reddish-orange reflection seen through an ophthalmoscope when a light is shone on the retina. Cataracts will prevent light from getting to the retina, hence you see a defect in the red reflex.
38
Q

What is the investigations for Cataracts?

A
  • Ophthalmoscopy: done after pupil dilation.
    • Findings: normal fundus and optic nerve
  • Slit-lamp examination
    • Findings: visible cataract
39
Q

What are classifications for Cataracts?

A
  • Nuclear: change lens refractive index, common in old age
  • Polar: localized, commonly inherited, lie in the visual axis
  • Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
  • Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy
40
Q

What are some complications following cataract surgery ?

A
  • Posterior capsule opacification: thickening of the lens capsule
  • Retinal detachment
  • Posterior capsule rupture
  • Endophthalmitis: inflammation of aqueous and/or vitreous humour
41
Q

What is the non-surgical management of cataracts?

A

In the early stages, age-related cataracts can be managed conservatively by

  • prescribing stronger glasses/contact lens,
  • encouraging the use of brighter lighting.

These options help optimise vision but do not actually slow down the progression of cataracts, therefore surgery will eventually be needed.

42
Q

What is the surgical management of Cataracts?

A
  • Surgery is the only effective treatment for cataracts which involves removing the cloudy lens and replacing this with an artificial one.
  • After cataract surgery, patients should be advised on the use of eye drops and eyewear, what to do if vision changes and the management of other ocular problems.
  • Cataract surgery has a high success rate with 85-90% of patients achieving 6/12 corrected vision (on a Snellen chart) postoperatively.
43
Q

How is Cataract surgery referral made?

A
  • NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice. Also whether both eyes are affected and the possible risks and benefits of surgery should be taken into account.
  • Prior to cataract surgery, patients should be provided with information on the refractive implications of various types of intraocular lenses
44
Q

What is Anterior Uveitis?

A
  • Anterior Uveitis describes inflammation of the anterior portion of the uvea - iris and ciliary body.
  • Associated with HLA-B27 and may be seen in association with other HLA-B27 linked conditions.
45
Q

What

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46
Q
A