Ophthalmology: Uvea Glaucoma Lens Flashcards

1
Q
  1. What makes up the anterior uvea?
  2. What is the posterior uvea?
A
  1. Iris and ciliary body
  2. Choroid

Uvea is the most vascular, most pigmented and most immunologically reactvie tissue in the eye

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2
Q
  1. What is the purpose of the iris?
  2. What is ‘wall-eye’?
  3. What controls the dilator/constrictor muscle of the iris?
  4. What is the purpose of the ciliary body?
  5. What inervated the ciliary muscle?
A
  1. Variable diaphragm controlling the amount of light entering the eye
  2. Lack of pigment of the posterior epithelium of iris (white)
  3. Dilator- sympathetic, constrict- parasympathetic
  4. Accomodation of the lens via the action of ciliary muscle
  5. Parasympathetic fibres of nerve III

Zonule attaches to ciliary body and produced aqueous

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3
Q

What is a persistent pupillary membrane remnant?

A
  • Mesodermal membrane remnants that cover pupil in vitro
  • No treatment necessary
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4
Q
  1. What is anterior uveitis?
  2. What are the clinical signs?
A
  1. Inflammation of the iris and ciliary body
  2. Clinical signs
    * Pain- blephrospasm
    * Aqueous flare- aqueous not clear (proteins)
    * Miosis
    * Hypotonia- eye soft (reduced aqueous)
    * Hypoyon- inflam cells and exudate in anterior chamber
    * Keratic precipitates- focal accumulations of inflammatory cells on the deep corneal surface in sub-central area
    * Iris- swollen and dull
    * Corneal oedema
    * Loss of sision- variable
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5
Q

Without treatment of anterior uveitis what secondary and permanent changed can occur?

A
  • Synechiae- adhesion of inflammed iris to anterior lens or cornea to drainage angle
  • Iris rests- patches of pigment on anterior lens
  • Iris- may darken
  • Glaucoma- occlusion of drainage angle or circumferential posterior synechiae occluding the pupil
  • Cataract
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6
Q

What are causes of anterior uveitis?

How is it treated?

A
  • Corneal injury and ulceration
  • Blunt and penetrating trauma
  • Release of antigenic lens protein
  • Intra-ocular infection
  • Septicaemia
  • Intra-ocular neoplasia
  • Pyometra
  • Some idiopathic/immune mediated

Other than eliminating primary problem symptomatic
* Mydratics- atropine
* Anti-inflammaties- topical steroids- dexameth/pred acetate

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7
Q

What are the differentials for anterior uvea masses?

A

Order of frequency
* Uveal cysts
* Naevi
* Melanoma
* Ciliary body adenoma
* Metastasis

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8
Q

How can the following be differentiated?
1. Uveal cysts
2. Anterior uveal melanoma
3. Limbal melanoma
4. Ciliary body adenomas
5. Metastatic tumours

A
  1. May arise from posterior iris or ciliary body, break free to anterior chamber, pigmented but spherical, not solid, transilluminate
  2. Most common intra-ocular neoplasm- solid mass in iris or ciliary body, usually heavily pigmented- enucleation curative
  3. Heavily pigmented arising within the wall of the eye at the limbus
  4. Second most common- pink masses protruding into the pupil
  5. Lymphoma most common- check for mammary tumours
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9
Q

What is glaucoma?

A
  • Abnormal rise in intra-ocular pressure
  • Problem of drainage
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10
Q

Describe the normal process of aqueous (not glaucoma)

A
  • Produced in ciliary body
  • Passes through pupil into anterior chamber
  • Drains at irido-corneal angle
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11
Q

What are clinical signs of acute glaucoma?

A
  • Red eye
  • Severe pain and general lethargy
  • Mild corneal odema- steamy
  • Unresponsive mid-dilated pupil
  • Blindness
  • Palpably hard globe
  • Normal globe size
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12
Q

What are the clinical signs of chronic glaucoma?

A
  • Enlarged eye
  • Blindness
  • No response to light
  • Tears in descemets membrane
  • Variable corneal opacity, vascularisation, pigmentation
  • Lens sub (luxation)
  • Visible retinal degeneration and optic disc cupping
  • Variable degree of pain
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13
Q

What breeds are predisposed to primary cause of glaucoma?

A
  • English and welsh springer
  • Cockers
  • Bassett
  • Dandie dinmont
  • Flat-coated retriever
  • Great dane
  • Golden retriver
  • Minature poodle
  • Welsh terrier
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14
Q

What causes primary glaucoma?

A

Dysplastic drainage angles with sudden decompensation

Primary should be referred

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15
Q

What are secondary causes of glaucoma?

A
  • Lens luxation
  • Anterior uveitis
  • Hyphaema
  • Intumescent and hypermature cataracts
  • Tumours
  • Retinal detachement
  • Trauma and perforated ulcers
  • Chronic retinal detachment
  • Intraocular haemorrhage
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16
Q

What are the two main topical treatments for glaucoma?

A
  • Carbonic anhydrase inhibitors
  • Prostoglandin analogues

Or both

Prophylaxis in the good eye

17
Q

How can glaucoma be surgically treated?

A

Numerous procesures
* Laser
* Shunts

None amazing- specialist

18
Q

Describe the anatomy of the lens?

A
  • Transparent avascular structure
  • Lens fibres enclosed in elastic capsule
  • Supported by ciliary body via zonular fibres
  • Lens protein is antigenic- incited inflammatory response if capsule ruptured
19
Q

What are the different causes of lens luxation?

A
  • Primary
  • Secondary to chronic glaucoma
  • Trauma
  • Hypermature inflexible cataracts
20
Q

What are the stages of primary lens luxation?

A
  • Anterior lens luxation
  • Posterior luxation/subluxation
21
Q

What are the clinical signs of anterior lens luxation?

A
  • Sudden onset poor vision
  • Glaucoma
  • Some anterior uveitis
  • Glaucoma from obstruction of pupil
22
Q

What are the clinical signs of posterior luxation/subluxation?

A
  • Doesn’t cause glaucoma
  • Iridodonesis (trembling of iris)

Susceptible breeds- bilateral buyt not simultaneous

23
Q

How is lens luxation managed?

A
  • Can be removed surgically- not done
  • Can relocate- specialist
  • Subluxation- prostoglandin analogues to prevent anterior luxation

Prognosis guarded

24
Q

What is a cataract?

A
  • Any opacity of the lens
  • Disruption of fibre arrangment
  • Due to acumulation of osmotically active substances
  • Does not impair PLR
25
Q

What are the different classifications of cataracts?

A
  • Hereditary
  • Congenital
  • Diabeteic
  • Secondary to uveitis
  • Truama
  • Spontaneous/idopathic
26
Q

What are the different stages of development of cataracts?

A
  • Incipient- small opacities
  • Immature- more extensive, good tapetal reflex
  • Intumescent- rapidly developing, can obstruct drainage- diabetes
  • Mature- total opacity no fundic reflex
  • Hypermature- lens with irregular wrinkles surface
27
Q

How is nuclear scelerosis distinguished from cataract?

A
  • Affects the nucleus only
  • Does not noticibly affect vision
  • No opacity on distant direct ophthalmoscopy

Requires no treatment

28
Q
  1. How do diabetic cataracts often progress
  2. What can it lead to?
  3. How can they be treated?
A
  1. Sudden onset blindness- total cataracts in few days
  2. Lens takes in water- leakes causes lens-induced uveitis
  3. Surgery- extraction
29
Q

How can cataracts be managed?

A
  • Medical is of no avail
  • Specialist- phacoemulsification
  • Surgery- specialist

Desirable conditions for surgery
* Significantly impaired vision
* Easily handled
* Good PLR
* No history of impaired vision

30
Q

What is vitreous?

A
  • Soft gel, some collagen anf hyaluronic acid
  • Fills posterior part of eye
31
Q

What different conditions can affect the vitreous?

A
  • Persistent hyaloid remnants- no significance
  • PHPV
  • Asteroid hyalosis- older dogs (white specs)
  • Other vitreous opacities- incidental finding

PHPV- persistent hyperplastic primary vitreous