Seminar: The Red Eye Flashcards

1
Q

3 steps to thinking through ophthalmology cases

A
  1. Where, What and HOW (pathophysiology)
  2. Work up
  3. Treatment Plan
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2
Q

3 areas to think about with possible pathophysiology? Other things to think about?

A
  1. tissue affected
  2. its parts
  3. its relationship to other tissues
    - anything related but not directly visualised involved?
    - occular v systemic disease
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3
Q

What are the 3 steps of the workup?

A
  1. diagnositcs
  2. Ddx
  3. further diagnostics necessary
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4
Q

3 steps of treatment plan in general practice?

A
  1. diagnostics and advice
  2. treat what you feel confident about
  3. refer to the right specialist
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5
Q

Where can redness be seen?

A
  • eyelids
  • conjunctiva/episclera/sclera
  • TE
  • cornea
  • anterior chamber
  • anterior uvea
  • posterior uvea/retina and retrobulbar area not directly visualised
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6
Q

What is the uvea?

A
  • “grape”
  • a mesh of blood vessels, heavily pigmented
  • iris, ciliary body and choroid
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7
Q

What can leaky vessels d/t inflammation lead to?

A

flare

  • keratic precipitates
  • hypophema
  • posterior synechia
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8
Q

How can eyelids be affected -> redness? What may occour 2* to eyelid damage?

A
  • skin, meibomian glands and conjunctiva
  • dermatitis
  • meibomian glands
  • > 2* cornea and tear film affected as intimately associated (loss of protection/loss of oily part of tear film/contact problem)
  • > ulcers and epiphora, hyperaemia and vascularisation
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9
Q

Which layers of blood vessels may be seen as hyperaemic?

A

> conjunctival (dichotomous branching, v senstivie to surface irritation -> hyperaemia and oedema (chemosis))
- line eyelids, sclera and 3rd eyelid, ends at limbus where white meets cornea (stem cells stop conjunctiva taking over cornea)
episcleral (thick, chunky, meandering, connective tissue under conjunctiva)
- only line sclera on eyeball
- may be inflamed 2* to very severe surface disease or more commonly INTRAOCULAR disease (uveitis/glacuoma)

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10
Q

How do vascular patterns in cats differ from dogs?

A

less aggressive looking and red and angry, more subtle

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11
Q

What does the sclera consist of ?

A

white of the eye

  • fibrous tunic continuous with cornea via limbus
  • collagen fibres, fibroblasts and emisaria (holes for BVs and nerves)
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12
Q

How may the TE be affected by inflammation?

A

> lymphoid folicles on bulbar side + some on palpebral side
- v. prominent young animals and allergies
T shaped cartilagenous core
- can curl and cause outward fold
contains a lacrimal gland
- 30% aqueous tear production
- can prolapse and become inflamed (Cherry eye)

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13
Q

What are the 4 layers of the cornea?

A
  • epithelium (protective barrier, hydrophobic, no BVs if healthy, has unmyelinated nerves)
  • stroma (hydrophilic, stays dehydrated d/t epithelium and endothelium [actively pumps fluid back into AC])
  • Descement’s membrane
  • endothelium (may be damaged d/t uveitis, 1* inflame/infection, glaucoma)
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14
Q

What happens if protection of storm is lost or damaged? 3 causes

A
  • overhydration = corneal oedema

- d/t epithelial damage, endothelial damage or vascularisation of the cornea

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15
Q

What structures define the AC?

A
  • corneal endothelium
  • anterior surface of iris and lens
  • irial corneal angle (outflow of aqueous humour)
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16
Q

Where is aqueous formed and where does it travel?

A
  • ciliary body
  • posterior chamber to anterior chamber through pupil
  • exits via iridial corneal angle
17
Q

What 2 diseases affectt the AC?

A
  • glaucoma (ICA closure/clogging - ^ IOP)

- uveitis (^ uveoscleral outflow - v IOP, if chronic -> clogged 2* glaucoma)

18
Q

What sections make up the uvea?

A
  • anterior uvea (ciliary body, iris; muscles (constrictor and dilator, CB musculature) anterior blood ocular barrier)
  • posterior uvea (choroid; tapetum lucidum)
19
Q

What can uveitis result in?

A
  • mioisis (iris spasm and pain)
  • mydriasis (opposite of miosis)
  • endothelial cell separation -> leakage of blood components into the AC (keratin precipitates, hypopion, hyphema, protein) and around the lens (“snow banking”)
  • posterior synechia (adhesion of iris to anterior lens)
  • development of PIFMs (preiridial fibroaxillar membranes)
    > grow over iris (rubiosus iridis)
    > may cause bleeding (hyphema)
    > blockage of ICA (2* glaucoma)
20
Q

When may rubiosus iridis be seen?

A

FIP/FIV/FeLV

21
Q

What is the cause of anterior synechia?

A
  • sudden decompression -> iris prolapse and adherence to cornea
22
Q

Which parts of the eye cannot be seen directly? What may occur d/t damage to these?

A

> posterior uvea
- continuous with anterior urea so often both affected (panuveitis)
- retinal detachement
- hyphema if in anterior chamber too
retrobulbar area
- inflam/infection (dentals, trauma [carnivores and pigs have incomplete orbit] idiopathic, middle ear abscess, haematogenous, parasites, conjunctival FBs migrating… )
- neoplasia (muscle sarcomas, haemoagniosarcoma, nerve gliomas etc., osteosarcomas, lacrimal ducts and salivary glands)
sinuses
something else important look up

23
Q

What do retrobulbar problems lead to?

A
  • altered position of eye within orbit and relationship w/ eyelids
  • ^ pressure around eye
  • swelling/infection of surrounding tissues (eg. conjunctiva)
    > these may all cause redness of the eye
  • vision loss (ON)
  • pupillary problems
  • restricted ocular movement
24
Q

Ddx remembering thingy

A

DAMNIT (C)

  • developmental, degenerative
  • autoimmune, acquired
  • metabolic
  • neoplastic, nutritional, neurological
  • immune, infection, inflammation, iatrogenic, inherited
  • trauma, toxins
  • congenital