Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CVSOH 4 > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

Define exophthalmos.

A

Abnormal protrusion of the eye from the orbit (not larger globe)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define enophthalmos.

A

Abnormal recession of the eye in the orbit (not smaller globe)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define lagophthalmos.

A

Incomplete eye closure and globe coverage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define strabismus.

A

Eyes are not aligned towards the same object

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define episcleral.

A

Vessels and tissue exterior to sclera and under conjunctiva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define photophobia.

A

Ocular discomfort induced by bright light

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define blepharospasm.

A

Spasms of orbicularis oculi muscle resulting in eyelid closure. Caused by ocular pain and is a protective method against this pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define buphthalmos.

A

Enlargement of the globe due to glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define macroblepharon.

A

Long palpebral fissure/excessive eyelid length. Horizontally enlarged palpebral fissure due to excessive eyelid length, with/without lagophthalmos/inability to complete blink.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Distinguish entropian and ectropian.

A

Entropian – introversion of eyelid (rolling in)

Ectropian – eversion of the eyelid (rolling out)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define trichiasis.

A

Hairs on normal skin reach and irritate eye. Growing in normal place, abnormal skin position or hair direction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define distichiasis.

A

Cilia emerge from meibomian gland orifice on the eyelid margin, likely to cause corneo-conjunctival irritation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define ectopic cilium.

A

Cilia protrude through conjunctiva. - Usually abrade the cornea causing pain and ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Outline the steps of an ophthalmic consultation.

A
  1. History and general clinical examination
  2. Distance hands off exam
  3. Subjective hands on exam
  4. Schirmer tear test and neuro-ophthalmic examination
  5. Close direct – adnexa and anterior segment examination
  6. Sampling
  7. Intraocular pressure measurement, apply mydriatic
  8. Posterior segment examination
  9. Vital stain application, such as fluorescein – done last as it may affect the other tests
  10. Addition diagnostics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is normal canine ocular conformation?

A
  • Mesocephalic skull – muzzle length roughly the same length as their skull
  • Almond shaped eyes
  • No scleral show
  • No discharge
  • Just see 3rd eyelid
  • Sharp corneal reflection from the surface of the eye – light bouncing off tear film
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name and describe the ophthalmology techniques.

A

Direct observation with light source – illumination improves the image, Purkinje light reflex

Distant direct ophthalmology - looking through ophthalmoscope

Close direct ophthalmology – anterior (+5D to +20D), posterior (+0D)

Distant indirect ophthalmoscopy - indirect fundoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why does close direct ophthalmology of posterior require no magnification?

A

As both yours and the animals retina will have light focussed on it so should be straight line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is distance examination used to look for orbital diseases?

A
  • Behaviour – attitude, ability to navigate
  • Face – symmetry, ocular discharge
  • Palpebral fissure – space between upper and lower eyelids
  • Eyelid – length, colour, swelling
  • Globe – position, size, direction, movements, retropulsion
  • Pupils – symmetry, size, shape
  • Retroillumination – distant direct ophthalmoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is looked for using an ophthalmoscope using retroillumination?

A

Pupil sizes
Pupil direction
Symmetry
Reflectivity
Shadows
Obstructions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the nerves and neuro-ophthalmic reflexes?

A
  • Vision = CNII
  • Palpebral reflex
  • Corneal reflex = CNV
  • Pupillary light reflex – direct and consensual = CNII and CNIII
  • Dazzle reflex
  • Oculo-cephalic reflex – globe movement with skull
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the steps of an exophthalmos examination?

A
  1. Visual axis
  2. Position in orbit
  3. Size of globe
  4. Retropulsion – can you push this back into the orbit, does this hurt
  5. Inspect oral cavity
  6. Inspect nasal/sinus cavities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the clinical signs of exophthalmos?

A
  • Signs of ocular pain – blepharospasm, epiphora, photophobia
  • Protrusion of 3rd eyelid
  • Reduced ocular motility
  • Change in tear production
  • Episcleral injection – impaired venous return
  • Strabismus
  • Lagophthalmos and exposure keratitis/inflammation of the cornea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What may be the causes of orbital space occupying lesions?

A

Inflammatory:
- Abscess
- Cellulitis
- Myositis – extraocular muscles, masticatory muscles

Neoplasia:
- Primary orbital
- Extension from adjacent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the typical clinical signs of orbital space occupying lesions?

A
  • Unilateral exophthalmos
  • Serous to mucopurulent discharge
  • Very painful
  • Unable to open mouth fully
  • Acute onset
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the common causes of exophthalmos?

A
  • Foreign body
  • Infection from oral cavity
  • Infection from sino-nasal
  • Trauma
  • Haematogenous infection
  • Dental – did elevator instrument slip
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the causes of enophthalmos?

A
  • Decreased orbital content
  • Ocular pain
  • Breed related in dolichocephalic
  • Damage sympathetic innervation – Horner’s syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Why may orbital content decrease?

A
  • Muscular atrophy
  • Dehydration
  • Reduced orbital fat – starvation, cachexia, geriatric
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the 4 clinical signs of Horner’s syndrome?

A

Miosis
3rd eyelid protrusion
Enophthalmos
Ptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the 3 ophthalmic techniques used to assess the eyelid?

A
  • Direct observation
  • Distant direct ophthalmoscopy
  • Close direct ophthalmoscopy (+10D to +20D)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the 5 functions of eyelids?

A
  • Mechanical protection
  • Produce 2/3 tear film components: mucin from goblet cells in conjunctiva, lipid from meibomian glands
  • Spread tear film
  • Aid removal of tear film
  • Part of the surface lacrimal unit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How are the eyelids assessed?

A
  • Length – do they fit the globe?
  • Shape
  • Position – resting on globe?
  • Canthi – level and firm?
  • Assess when head down too
  • Evert the lids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the causes of entropian?

A

Can be primary (most cases) or secondary to trauma or eyelid surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the consequences of ectropian?

A
  • Reduced protection
  • Frequent conjunctivitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How is ectropian treated?

A

Eyelid shortening
Wedge resection
With/without lateral canthus stabilisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is trichiasis associated with?

A

Nasal fold
Hairy caruncle
Fluffy haircoat
Curly haircoat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How is trichiasis treated?

A

Treat the cause – keep hair short or surgical corrections to change position or remove these bits of skin

Treat any corneal complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is chalazion?

A

Blocked and infected meibomian glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the common eyelid tumours in dogs?

A
  • Meibomian gland mass - epithelioma, adenoma, adenocarcinoma
  • Melanoma
  • Squamous papilloma
  • Mast cell tumour
  • Lymphoma
  • Histiocytoma
  • Squamous cell carcinoma
  • Sarcoid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Define epiphora.

A

Excessive tear production and/or tear overflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Define hyperaemia.

A

Increased blood flow to a tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Define chemosis.

A

Conjunctival oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Define episcleral.

A

Vessels and tissue exterior to sclera and under conjunctiva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Define conjunctiva.

A

Ocular mucus membrane lining eyelids to limbus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the functions of a normal ocular surface?

A

Acts as physical and chemical barrier to debris and infectious agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What does a normal ocular surface require to function?

A
  • Normal eyelids for tear-film distribution
  • Normal tear film to stimulate functional glands and ducts
  • Corneal epithelium
  • Functional tear drainage – patent punctae and ducts
  • Conjunctival Associated Lymphoid Tissue (CALT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the function of conjunctival associated lymphoid tissue?

A
  • Recruit immune cells with chemical mediators
  • Activate the complement cascade and promote clearance
  • Identify and remove foreign substances by white blood cells
  • Activate the adaptive immune system through antigen presentation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Name the 3 layers of the pre-corneal tear film.

A
  • Deep mucin layer
  • Intermediate aqueous layer
  • Superficial lipid layer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What makes up the secretory system of the eye?

A
  • Meibomian glands (lipid phase)
  • Conjunctival goblet cells (mucus layer)
  • Orbital lacrimal gland (aqueous phase)
  • Nictitans lacrimal gland (aqueous phase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe the anatomy of the nasolacrimal ducts.

A
  • Upper and lower puncta open just inside the lid margin
  • Lacrimal sac = dacryocyst
  • Nasolacrimal duct emerges in nasal cavity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the functions of the lipid layer of the tear film?

A
  • Prevents evaporation
  • Aids distribution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the functions of the aqueous layer of the tear film?

A
  • Supplies nutrition to avascular cornea (dissolved O2 etc)
  • Antibacterial properties
  • Removal and remodelling - proteases and antiproteases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the functions of the mucus layer of the tear film?

A
  • Lubrication
  • Refractive properties
  • Anchors aqueous layer to cornea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Which techniques are used to view the ocular surface?

A
  • Direct observation with/without a light source
  • Distant direct ophthalmoscopy
  • Close direct ophthalmoscopy +10D
  • Close direct ophthalmoscopy +0D
  • Distant indirect ophthalmoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the local anaesthetic used to examine the conjunctiva?

A

Proxymetacaine 0.5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the characteristics of hyperaemia?

A
  • Branching, bright red vessels
  • Increased vascular contents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Where is follicular hyperplasia located?

A

Inner aspect TEL, upper fornix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the ocular surface responses?

A
  • Epiphora – increase in tearing to flush out debris and pathogens, sign of pain
  • Mucoid discharge – increase in mucus to bind up particulates
  • Purulent discharge – increase in cellular content, purulent
  • Blepharospasm – increase flow of tears, response to pain
  • Conjunctival Hyperaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What constitutes surface ocular health?

A

Inherent ocular defences
Innate immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the clinical signs of naso-lacrimal obstruction?

A
  • Dry nostril on affected side(s)
  • Ocular or nasal discharge
  • Conjunctival hyperaemia
  • Swelling of the ventral aspect of the medial canthus
  • Epiphora
  • Foreign bodies exiting from the punctum
  • Purulent fistula at the ventral aspect of the medial canthus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How can you test for naso-lacrimal obstructions?

A
  • Jones test
  • Examine the lacrimal punctum
  • Nasolacrimal flushing
  • Imaging
  • Cytology
  • Culture and sensitivity
  • Dacryocystorhinography (contrast x-ray study)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How is a Jones test conducted?

A
  1. Apply fluorescein in both eyes
  2. Observed after several minutes at the level of the nostrils
  3. Normal response in 5 mins
  4. Brachycephalic – check mouth/pharynx for dye
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the clinical signs of keratoconjunctivitis sicca?

A
  • Conjunctivital hyperaemia
  • Ocular pain/blepharospasm
  • Mucoid strings
  • Corneal pigmentation
  • Corneal vascularisation
  • Decreased vision
  • Low STT reading
  • Poor Purkinje light reflex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is quantitative keratoconjunctivitis?

A

Majority of cases are immune mediated adenitis of lacrimal glands, which is a deficiency of aqueous tear with insidious onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the iatrogenic causes of keratoconjunctivitis sicca?

A

Anaesthetics
Atropine
Drug toxicity (trimethoprim/sulfonamide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the neurogenic causes of keratoconjunctivitis sicca?

A

By lack of stimulation to the facial nerve (CN VII), trigeminal nerve (CN V), and autonomic system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are some other causes of keratoconjunctivitis sicca?

A
  • Excision 3rd eyelid gland
  • Other trauma to lids and 3rd eyelid
  • ‘Congenital’ lacrimal gland hypoplasia or aplasia (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How is keratoconjunctivitis sicca diagnosed?

A

Schirmer Tear Test and concurrent clinical signs. Check patients back after eye problem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the Schirmer tear test guidelines?

A

15-25 mm/min = normal range
10-14 mm/min = early/suspicion of KCS
6-10 mm/min = moderate KCS
0-5 mm/min = severe KCS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is qualitative keratoconjunctivitis sicca?

A

Tear-film instability. Inflammation of the meibomian glands (meibomitis, blepharoconjunctivitis). Abnormal quantity or quality of goblet cells (conjunctivitis, FHV-1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

How is qualitative keratoconjunctivitis sicca diagnosed?

A
  • Close examination – lid margins, palpebral conjunctiva, corneal epithelial erosions
  • Tear-film Break Up time low (Fluorescein test, n>5s)
  • Conjunctival biopsy and analysis of goblet cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the treatment basics of qualitative keratoconjunctivitis sicca?

A
  • Treat cause
  • Tear missing components with tear supplements (carbomer, hyaluronate, lipid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How is an aqueous deficiency causing keratoconjunctivitis sicca treated?

A

Immunomodulating agent - cyclosporin A ointment, tacrolimus. If STT still under 10mm after 6 weeks, cyclosporin 3 times a day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

How can meibomian gland disease/blepharitis causing keratoconjunctivitis sicca be treated?

A
  • Warm compress
  • Lid hygiene
  • Broad spectrum antibiotics
  • Topical or systemic anti-inflammatory treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Describe the structure of the cornea.

A
  • Non-keratinized epithelium
  • No vessels
  • No pigments
  • Stromal collagen fibres regimentally parallel
  • Layered Collagen – almost crystalline arrangement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What causes a colour change in the cornea?

A

Any alteration in structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is required for corneal clarity?

A

A functional lacrimal unit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Describe the epithelium of the cornea.

A
  • Lipophilic layer 6-8 cells thick
  • Constantly regrown from basal cells
  • Basal cells replaced by centripetal migration from limbal stem cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe the endothelium of the cornea.

A
  • 1 cell thick, nutrition from aqueous
  • On Descemet’s basement membrane
  • Contain Na+/K+ ATPase physiologic pumps to constantly remove water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the ocular clinical signs of corneal lesions?

A
  • Epiphora
  • Blepharospasm
  • Conjunctival hyperaemia
  • Colour change in cornea
  • Anisocoria – asymmetry to pupil size, relative miosis on affected side, sign of ‘reflex uveitis’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What does a blue cornea indicate?

A
  • Oedema
  • Dehydrated state compromised
  • Defect of epithelial or endothelial barrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Describe the blue cornea if caused by an epithelial defect.

A

Ulceration
Diffuse
Focal
Hazy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Describe the blue cornea if caused by an endothelial defect.

A

Mottled, diffuse blue
Often more generalised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What could cause an endothelial defect causing a blue cornea?

A
  • Intraocular cause – uveitis, glaucoma, lens luxation
  • Primary endothelial degeneration (geriatrics)/inherited dystrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is a red cornea caused by?

A

Neovascularisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is superficial neovascularisation?

A
  • Surface inciting cause
  • Focal to cause
  • Branching trees of bright red, vessels
  • Extend from bulbar conjunctiva
  • Crosses the limbus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is deep neovascularisation?

A
  • Deep stromal/intraocular cause
  • Circumferential
  • Fine, short, straight vessels
  • Arise from limbus – can’t see until they start at the limbus
  • Do not cross the limbus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are 5 vascular patterns and what are the indicative of?

A
  • Superficial corneal vessels – surface corneal/ocular disease
  • Deep corneal vessels – deep corneal disease
  • Episcleral congestion – intraocular disease very likely
  • Ciliary flush/brush border – severe eye disease
  • Conjunctival hyperaemia – non-specific, most eye disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are 3 reasons for white corneal change?

A
  • Corneal fibrosis – scar
  • Metabolic infiltrates – lipids (crystalline) or minerals (fluffy)
  • Inflammatory cell infiltrates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What can cause black/brown pigmentary keratitis on the cornea?

A
  • Chronic irritation
  • Insufficient protection of the cornea
  • Part of Brachycephalic Ocular Syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

How can black/brown pigmentary keratitis be treated?

A
  • Correct the cause of irritation (excessive nasal fold, medial entropion)
  • Lubricate the eyes on a daily basis, topical immunomodulating agent (ciclosporin, tacrolimus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What are the clinical signs of pink proliferative cellular infiltrate?

A
  • Superficial vessels
  • With/without pigments
  • Pink tissue in acute phase
  • White crystalline spots
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Define panuveitis.

A

Inflammation of iris ciliary body and choroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Distinguish anterior and posterior uveitis.

A

Anterior – inflammation of the iris with/without ciliary body, iridocyclitis

Posterior – inflammation of the choroid, chorioretinitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Define phthisis bulbi.

A

End stage shrunken globe, chronic uveitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is the uvea?

A

Vascular layer of the eye composed of the iris, ciliary body and choroid. Blood aqueous barrier and blood retina barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are the functions of the uvea?

A
  • Aqueous humour secretion
  • Nutrition globe contents
  • Immune function – protects delicate cells and preserves clarity
  • Accommodation of lens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What techniques can we use to image inside the globe?

A
  • Direct observation with/without light source
  • Distant direct ophthalmoscopy
  • Close direct ophthalmoscopy +10D
  • Close direct ophthalmoscopy +0D
  • Distant indirect ophthalmoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What is cellular infiltrate of the eye?

A

White blood cells - purulent/yellow/green exudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Why does inflammation of the eye lead to possible cell death of delicate structures?

A

Globe is immune privileged site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What is iris rubeosis/rubeosis iridis?

A

Hyperaemia of the iris – vasodilation or neovascularisation. Inflammation damages vascular endothelium causing the breakdown of blood aqueous barrier and exudation into aqueous humour/anterior chamber.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is aqueous flare?

A

Unclear/cloudy/turbid due to serous exudate into the anterior chamber from a leaky blood aqueous barrier.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What are keratic precipitates?

A

Protein and WBC clump together and attach to corneal endothelium with/without focal corneal oedema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

How are keratic precipitates visualised?

A

Can look white when you shine a light on them because they affect the endothelium and can look like shadows if light is shone from the side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Define hypopyon.

A

Exudate in aqueous, white blood cells, pus in anterior chamber, white/cream/yellow, can be sterile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Define hyphaema.

A

Blood in the anterior chamber, diffuse, clots, its presence is inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What are the causes of hyphaema?

A
  • Vascular changes
  • Neoplasia
  • Systemic hypertension
  • Coagulation disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What are the clinical signs of chronic uveitis?

A
  • Hyperpigmentation of the iris
  • Cataract
  • Synechia – adhesions
  • Iris bombe
  • Glaucoma with/without Haab’s striae
  • Lens luxation – decimates membrane
  • Phthisis bulbi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Define phthisis bulbi.

A

Very low pressure, inside of the eye is dying/degenerate and the eye shrinks because the body stops producing aqueous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Distinguish conjunctival and episcleral hyperaemia.

A

Conjunctival – fine branching vessels, continue to limbus, supply surface

Episcleral – deep, straight vessels, stop before limbus to supply uveal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What is the normal intraocular pressure?

A

10-25mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Distinguish the intraocular pressures of uveitis and glaucoma.

A

Uveitis = low

Glaucoma = high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Distinguish uveitis and glaucoma in typical pupil size.

A

Uveitis = miosis

Glaucoma = mydriasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Distinguish uveitis and glaucoma in vision.

A

Uveitis = yes, reduced

Glaucoma = no, blind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What are 4 shared characteristics of uveitis and glaucoma?

A

Painful
Conjunctival hyperaemia
Corneal oedema
Episcleral congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are the signs of reflex uveitis?

A
  • Ciliary spasm
  • Miosis
  • Pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

How does reflex uveitis occur?

A
  • Antidromic stimulation of corneal nerves
  • Cytokines and neuropeptide release at ganglion
  • Direct action on smooth muscle in uveal tract
  • Activation inflammatory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

How does the lens develop in the early embryo?

A

Optic stalk > lens placode > lens vesicle > lens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Why is the lens hidden in a capsule?

A

Formed before the immune system so are recognised as foreign if exposed to the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is phacolytic lens induced uveitis?

A

Leaky lens, chronic, hypermature cataract – proteins in the lens are foreign so if these leap out during an advanced cataract for example, will leak out into the eye and cause inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is phaecoclastic lens induced uveitis caused by?

A

Sudden acute fracture, trauma or busting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

How can the primary cause of uveitis be removed in uveitis treatment?

A
  • Removal of lens material surgically/close corneal perf
  • Antibiotic/antiviral/anthelmintic treatment
  • Anti-hypertensives
  • Chemotherapy/radiotherapy/surgery/dental
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

How is uveitis treated after diagnosis?

A
  • Control inflammation with anti-inflammatory
  • Prevent complications with atropine (except glaucoma) – relief of painful ciliary muscle spasm, mydriasis reduced synechiae
  • Analgesia - NSAIDs, atropine, opioids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What is senior nuclear sclerosis?

A

Senior nuclear sclerosis slight opacity is normal – misty in the middle of the lens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is lens transparency?

A
  • Soluble crystallin proteins
  • No vessels, few organelles
  • Fibres regularly arranged
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What do cataracts look like on examination?

A
  • Looks white in direct illumination
  • See a shadow on retroillumination (distant direct)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

How are cataracts categorised?

A

Incipient <15% affected

Immature = light reflex

Mature = no reflex

Hypermature = shrinking, dissolving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What are the causes of cataracts?

A

Inherited - juvenille, early/late onset, senile

Secondary to - uveitis, lens luxation, PRA toxins, diabetes mellitus

Trauma - radiation, nutritional, electrocution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

How does a diabetic cataract form?

A
  1. Hyperglycaemia
  2. Glucose is a small molecule so diffuses in
  3. Increased glucose concentration overwhelms hexokinase pathway
  4. Metabolism shunted to aldose reductase pathway
  5. End product is sorbitol which is a large molecule so is trapped
  6. Increased sorbitol concentration causes osmotic draw
  7. Tumescent often used to describe swollen cataract
  8. Water clefts along suture lines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

How are cataracts treated?

A
  • Phacoemulsification and IOL surgery
  • Topical NSAIDs recommended if surgery not appropriate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Why is treating cataracts challenging?

A
  • No medical treatment can reverse lens fibre damage
  • Requires intensive medical support post operatively/lifelong
  • Risks of persistent inflammation/2’ glaucoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is lens luxation/subluxation?

A
  • Zonule loss
  • Aphakic crescent – space between pupil and lens edges
  • Iris or lens wobble – phaecodoesis/iridodonesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What are the causes of lens luxation?

A
  • Inherited zonule defects
  • Severe trauma
  • Uveitis – chronic, severe
  • Chronic glaucoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What are the consequences of lens luxation?

A

Acute glaucoma
Uveitis
Cataract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

How are lens luxations investigated?

A

DNA test inheritance

Referral ophthalmology examination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

How is lens luxation treated?

A

Surgical lentectomy

Medical couching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

When examining the canine and feline fundus, what is assessed?

A
  • Colour and reflectivity of tapetum if present
  • Blood vessels
  • Optic nerve head
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

What is progressive retinal atrophy?

A

Inherited
Early Degeneration of rod cells then cone cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What does progressive retinal atrophy cause?

A
  • Hyperreflectivity as retina thinner (cell loss)
  • Vascular attenuation
  • Nyctalopia (night blindness)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

How is progressive retinal atrophy investigated and diagnosed?

A
  • Examination by ophthalmologist
  • DNA testing
  • Electro Retinography (ERG) – trace reduced
  • Colourimetry PLR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

How does the blood ocular barrier protect the eye?

A

Immune privileged site but BOB prevents immune cells, no lymphatic drainage and immune reactions in the eye are catastrophic for delicate contents. Intraocular pressure maintained locally. Production = drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

How does the blood ocular barrier affect ocular pharmacology?

A

Drugs trying to get into the eye must have certain properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

What is the general rule of target sites in ocular pharmacology?

A

Surface and anterior segment = topicals

Posterior segment = systemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Name the barriers to topical penetration in the eye.

A
  • Tear dilution
  • Palpebral blinks
  • Lacrimal drainage
  • Permeability of the cornea, conjunctiva and sclera
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Why should topical ocular medications ideally be non-irritant?

A
  • Maximises patient acceptance and client compliance
  • Irritants > inflammation > increases tear osmolarity > increases drug protein-binding > reduces drug availability > less efficacy
  • Irritants > epiphora > dilution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What are the 2 main routes that topical medication penetrates in the eye?

A

Transcellular – across the corneal epithelial cell

Paracellular – between individual cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Describe the corneal structure top to bottom.

A

Corneal epithelium = largely lipophilic barrier, lipid soluble drugs cross more easily

Corneal stroma = hydrophilic, polar water soluble drugs more easily

Descemet’s membrane supporting

Endothelium = lipophilic barrier, although less significant than the epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

What do transcellular and paracellular routes rely on?

A

Transcellular route relies on lipophilic-hydrophilic balance of drug

Paracellular route relies on small molecular weight molecules passing between tight junctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What is the best pH for topical ocular medications?

A

pH 4.5 -9 quoted for comfort

Normal tear pH 7.4 is best

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

When are topical ocular steroids contraindicated?

A

Corneal ulceration as these need to the immune system to heal and won’t be able to do this with steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

How can the penetration of topical ocular medications be improved?

A
  • Combining drugs with organic salts
  • Addition of preservatives that disrupt the corneal epithelial barrier – improve penetration, epitheliotoxic which is okay if the rest of the eye is okay but can delay healing of epithelium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

How can oenetration of medications be improved with suspended particles?

A
  • Improve tear retention
  • Uniform and micronized to prevent irritation
  • But can feel gritty
  • Smaller particles = shorter retention time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Describe topical ocular ointments.

A
  • Retained for extended periods on ocular surface
  • Lipophilic character – retained in surface of tear film as low as 0.5% dose vol. clearance per minute significant amounts retained 4hrs after dosing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Give the order of application of ocular formulations by retention and so washout periods?

A

Solution = 5-10mins retention, every 1-6h

Suspension = hour retention, every 2-12h

Gel = few hours retention, every 2-6h

Ointment = several hours retention, 4-12h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What is the typical dose frequency of ocular topical medications?

A

Wait 10 mins between applications of different drops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Name the periocular and intraocular injection sites.

A

Intrastromal corneal
Subconjunctival
Intracameral
Intravitreal
Retrobulbar behind eye, LA for enucleation
Suprachoroidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What are the advantages of subconjunctival injections?

A
  • Solutions typically last 8-12hrs
  • Injections of suspensions last for extended periods
  • Can be useful where there is little compliance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

What are the disadvantages of subconjunctival injections?

A
  • Can’t withdraw drug once given
  • Can be useful where there is little compliance or on farm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

What are sustained release implants in ocular pharmacology?

A
  • Drug within a silicone vehicle, such as cyclosporine
  • Intravitreal, suprachoroidal or subconjunctivally
  • Effective for immune mediated conditions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What does the penetration of systemic ocular medications depend on?

A
  • Integrity of blood-aqueous barrier and blood-retinal barrier is reduced in uveitis
  • Lipid solubility
  • Low molecular weight molecules cross most easily
  • Degree of protein binding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Name the ocular therapeutic classes.

A

Antimicrobial
Anti-inflammatory
Anti glaucoma drugs
Mydriatics local anaesthetics
Tear replacement and stimulants
Anti collagenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Which bacteriostatic antimicrobials are used in ophthalmology?

A
  • Chloramphenicol - gram positive and negative
  • Fusidic acid - gram positive, pom-v
  • Tetracyclines - chlamydia, pom-v
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Which bacteriocidal antimicrobials are used in ophthalmology?

A
  • Aminoglycosides/gentamycin - 2/3rd line
  • Flouroquinolones - not 1st line
  • Penicillins - not 1st line
163
Q

How are antifungals used in ophthalmology?

A
  • Fungistatic rather than fungicidal
  • Protracted treatment time
  • Requires functional host immune system for success
164
Q

How are antivirals used in ophthalmology?

A
  • Virostatic
  • Frequent application
  • Functional immune system
165
Q

What are the indications of corticosteroids in ophthalmology?

A

Reduce inflammation

166
Q

What are the contraindications of corticosteroids in ophthalmology?

A

Infections
Corneal ulceration
Diabetes
Lipid or calcific keratopathy
Laminitis

167
Q

What are the indications of NSAIDs in ophthalmology?

A

Reduce inflammation
Analgesia
Anti-pyrexia

168
Q

What are the contraindications of NSAIDs in ophthalmology?

A

Gastric ulceration
Renal disease
Hypovolaemia
Topical use may worsen corneal ulceration

169
Q

Name 3 classes of anti-glaucoma drugs.

A
  • Prostaglandins – increase outflow of aqueous
  • Carbonic anhydrase inhibitors – decrease aqueous production
  • Beta blockers – decrease aqueous production
170
Q

Define cycloplegia.

A

Iris spasm

171
Q

What is the onset, duration and use of atropine?

A
  • Slower 40mins
  • 1-14 days
  • Therapeutic use
172
Q

What is the effect of atropine on cycloplegia?

A

Marked paralysis

173
Q

What are the contraindications of atropine?

A

Glaucoma and keratoconjunctivitis

174
Q

What is the onset, duration and use of tropicamide/cyclopentolate?

A
  • Rapid 10-20mins
  • 6-8 hours
  • Diagnostic use
175
Q

What is the effect of tropicamide/cyclopentolate of cycloplegia?

A

Moderate relaxation

176
Q

What are the contraindications for tropicamide/cyclopentolate?

A

Reduces tears in cats

177
Q

Name 4 local anaesthetics used in ophthalmology.

A

Proxymetacaine
Tetracaine
Lignocaine
Bupivacaine

178
Q

Name 4 tear replacements.

A

Aqueous substitutes
Mucinomimetics
Viscoelastics
Lipid based substitutes

179
Q

Name a tear stimulant.

A

Cyclosporine

180
Q

What drug class is used to treat keratomalacia?

A

Anticollagenases

181
Q

What happens in keratomalacia?

A

Corneal epithelial cells, bacteria or host WBCs can release collagenase enzymes, which “melt”/liquify collagen of cornea can digest its way through the front of the eye in under 24 hours and then there is risk of eyeball rupture

182
Q

How can keratomalacia be treated?

A
  • Serum and plasma created from blood contain anti-collagenases
  • EDTA drops – chelates zinc, cofactor in collagenases
  • Acetylcysteine
  • Tetracyclines – orally or topically
  • Frequent application
183
Q

What are the possible causes of red eyelids?

A
  • Periocular dermatitis
  • Blepharitis – meibomian glands disease and impaction, infected meibomian glands
  • Eyelid masses
  • Blunt trauma
  • Other injuries
  • Insect bite reactions
  • Cat bite abscesses
184
Q

How is a red eye examined?

A

Direct observation with additional source, close direct to examine the anterior segment and fundus

185
Q

What is minimum ophthalmic database?

A
  • Schirmer tear test
  • Fluorescein test
  • Neuro-ophthalmic tests
  • Tonometry
186
Q

What is a Schirmer tear test?

A
  • Quantitative test
  • Sterile graduated filter paper strips lateral lower fornix for 1 min
  • Normal reading in dogs 15-25 mm/min
  • Measures basal and reflex production
187
Q

What are the clinical signs of keratoconjunctivitis?

A
  • Dull reflection
  • Reduced Schirmer tear test
  • Corneal pigmentation
  • Ocular pain
  • Some discharge
188
Q

How is keratoconjunctivitis treated?

A
  • Ciclosporin ointment
  • Hyaluronate lubricant to reduce irritation in lids and smooth tear film while waiting for ciclosporin to work
  • Wouldn’t use dexamethasone drops long term as may reduce resistance to infection but is inflammatory so is appropriate
  • Steroid and antibiotics drops not long term
189
Q

What are some possible eyelid tumours?

A
  • Meibomian gland – epithelioma, adenoma, adenocarcinoma
  • Melanoma
  • Squamous papilloma
  • Mast cell tumour
  • Histiocytoma
190
Q

List the causes of 3rd eyelid protrusion.

A
  • Enophthalmos
  • Microphthalmos
  • Exophthalmos
  • Inflammation of TEL
  • Neoplasia of TEL
  • Horner’s Syndrome
  • Scrolled Cartilage of the 3rd eyelid
  • Prolapsed gland of the TEL
  • Genetically small eye
191
Q

What happens in 3rd eyelid prolapse?

A

Red, homogeneous mass arising from the bulbar aspect of the third eyelid

Irritation > inflammation > ulceration with continued exposure

192
Q

When treating 3rd eyelid prolapse, why should you not remove the gland?

A

Secondary keratoconjunctivitis

193
Q

How is 3rd eyelid protrusion treated?

A

Medical – reduce inflammation with topical or systemic NSAID, control secondary infection with topical first line antibiotics

Manual re-positioning of the gland – recurrence is common

Corrective surgery usually required - modified morgan pocket

194
Q

What is the technique for a modified morgan pocket procedure on a protruding 3rd eyelid?

A
  • Bury the gland in conjunctival pocket
  • Microsurgical instruments
  • Magnification
  • Microsurgical absorbable braided suture 5-0 or 6-0
  • Knot on palpebral aspect of TEL
195
Q

What can conjunctivitis be secondary to?

A
  • Irritants/chemicals/drugs (environment)
  • Abnormal eyelid conformation (entropion etc)
  • Aberrant hairs (trichiasis/distichiasis/ectopic cilia)
  • Keratoconjunctivitis sicca (dry eye)
  • Inflammation extending from proximal tissues
  • Trauma/foreign body
  • Corneal or intraocular disease
  • Systemic conditions (systemic hypertension/coagulopathy)
196
Q

What are the causes of primary infectious conjunctivitis in dogs?

A

Viral - CDV, CHV-1, CAV-2

Parasitic - thelazia, Leishmania

197
Q

What are the causes of primary allergic conjunctivitis in dogs?

A

Concurrent skin disease
Contact/drug reaction
Environmental factors
Atopy
Demodex

198
Q

What is primary follicular conjunctivitis in dogs?

A

Non-specific to cause, sign of chronicity

199
Q

What is primary juvenile conjunctivitis in dogs?

A

Starts in dogs under 18months, often resolves by adulthood

200
Q

How is conjunctivitis treated empirically?

A
  • Topical anti-infectives - treat opportunistic flora until cause resolved
  • Topical anti-inflammatories - corticosteroids or NSAIDs, immune-mediated cause suspected
  • Lubrication, support innate defence of tear film
  • Lid hygiene and warm compresses to help meibomian gland discharges (unless pruritus)
201
Q

Describe superficial neovascularisation of the cornea.

A
  • Surface inciting cause
  • Focal to cause
  • Branching trees of bright red, vessels
  • Extend from bulbar conjunctiva
  • Do not cross the limbus
202
Q

Describe deep neovascularisation of the cornea.

A
  • Deep stromal/intraocular cause
  • Circumferential
  • Fine, short, straight vessels
  • Arise from the limbus
  • Don’t cross the limbus
203
Q

What are the clinical signs of pink proliferative cellular infiltrate?

A
  • Superficial vessels
  • With/without pigments
  • Pink tissue in acute phase
  • White crystalline spots
204
Q

What is chronic superficial keratitis?

A
  • Progressive bilateral condition, can cause blindness
  • Thought to be of immune mediated origin
205
Q

How is chronic superficial keratitis treated?

A

Can be controlled but not cured:

  • Topical steroids
  • Topical cyclosporine
  • Radiotherapy/superficial keratectomy
206
Q

What happens in uveitis?

A
  • Breakdown of blood aqueous barrier and blood retinal barrier
  • With/without swelling of iris
  • Aqueous flare – protein in aqueous
  • Hypopyon – WBC, pus
  • Hyphaema – RBC, clots
  • With/without corneal oedema with/without intraocular pressure
207
Q

What may cause blood in the eye?

A
  • Hyphaema – blood in the anterior chamber
  • Vitreal Haemorrhage
  • Retinal haemorrhage
  • Mass
208
Q

What are the clinical signs of acute glaucoma?

A
  • Conjunctival hyperaemia
  • Episcleral congestion
  • Ciliary flush
  • Corneal oedema – no vascular so takes a while to heal
  • Haabs Striae
  • Prominent 3EL
  • Blindness
  • Pain
  • Fixed pupil
209
Q

What is the histological structure of the cornea, limbus and sclera?

A

Cornea – transparent stratified squamous epithelium

Limbus – transition zone stem cells here

Sclera – fibrous tunic gives globe rigidity

210
Q

What is the corneal stroma made up of?

A

A collagen matrix maintained in a dehydrated state, so when oedematous it gets cloudy

211
Q

Describe the epithelium mechanical barrier of the cornea.

A
  • Lipophilic layer 6-8 cells thick
  • Constantly regrown from basal cells
  • Basal cells replaced by centripetal migration from limbal stem cells
212
Q

Describe the endothelium mechanical barrier of the cornea.

A
  • 1 cell thick, nutrition from aqueous
  • On Descemet’s basement membrane
  • Contain Na+/K+ ATPase physiologic pumps to constantly remove water
213
Q

What is the total thickness of the canine cornea?

A

0.55mm

214
Q

What ophthalmic techniques are used to examine the cornea?

A
  • Spot opacities with distant direct – localise using parallax
  • Colour change with close examination
  • Structural change with slit beam
  • Sampling for cytology/culture
  • Fluorescein testing for ulcers
  • Shirmer tear test if eye is not fragile
215
Q

What can the slit beam of an ophthalmoscope be used for?

A
  • Highlights contours and deviations in depth
  • Spotting particulates in aqueous as ‘flare’
216
Q

How does fluorescein staining work?

A
  • Fluoresces green when water bound so is a hydrophilic dye
  • Does not adhere to normal corneal epithelium
  • Binds to exposed corneal stroma
217
Q

What considerations are used for fluorescein testing?

A

Mildly irritant - apply LA?

Flush out with saline

218
Q

What is the purpose of fluorescein staining?

A

Highlight defects in cornea surface

219
Q

How does the corneal epithelium heal and repair?

A
  1. Basal epithelial cells release attachments to basement membrane
  2. Cells slide to full defect across basement membrane
  3. Proliferation phase epithelial cell mitosis, increase thickness
  4. Reattachment to basement membrane and adhesion complexes

About 2 weeks

220
Q

How does the corneal stroma heal and repair?

A
  1. Fibroblastic proliferation, new collagen components form
  2. New extracellular matrix produced
  3. Disorganised arrangement of fibres = corneal scarring

Months to years

221
Q

How does the corneal endothelium heal and repair?

A
  • Cells at margin of wound elongate
  • Cells get spread thinner and migrate
  • No mitosis possible
222
Q

What are the clinical signs of corneal ulcers?

A
  • Epiphora
  • Blepharospasm
  • Conjunctival hyperaemia
  • Colour change in cornea
  • Pain
  • With/without anisocoria
223
Q

Define anisocoria.

A

Asymmetry to pupil size, relative miosis on affected side, sign of reflex uveitis

224
Q

How are corneal ulcers assessed by depth?

A

Superficial = epithelial ulcer

Deeper ulcer = stromal ulcer

Descemetocoele = complete stromal loss

Perforation = rupture of entire cornea

225
Q

How are uncomplicated superficial epithelial ulcers treated?

A

Analgesia, antibiotic prophylaxis, lubrication, with/without a buster collar

Minimal scar formation, heal in 1 week

226
Q

What does a white corneal colour change indicate?

A
  • Corneal fibrosis – scarring
  • Inflammatory cell infiltrates initially
  • Remodel stroma and return to near normal structure
  • Scars contract but remain visible
  • No Fluorescein uptake
227
Q

What is inherited corneal dystrophy?

A
  • Lipid/mineral dystrophy
  • Little progression or impact on vision
  • Rarely ulcerate
  • No treatment in most cases
228
Q

Name and describe 2 common causes of white corneal change.

A

Lipid deposits - associated with hyperlipidaemia or endocrinopathies – recommend bloods

Mineral deposits – endocrine disease, geriatric patients

229
Q

What is SCCED?

A

Spontaneous chronic corneal epithelial defect - superficial ulcer not healed in 1-2 weeks, persist, no apparent inciting cause

230
Q

What is the pathogenesis of SCCED?

A
  • Poor epithelial adhesions to stroma
  • Abnormal basement membrane
  • Abnormal superficial stroma – has a superficially hyalinised acellular zone
  • Typically, a glancing abrasion knocks off poorly adhered epithelium
  • Often creates a flap of loose epithelium
231
Q

Describe the histopathology of SCCED.

A
  • Stromal abnormality develops prior to ulcer creation
  • Mild, glancing trauma causes epithelium loss
232
Q

What are the clinical signs of SCCED?

A
  • Superficial ulcer (epithelium loss only)
  • Loose epithelial edges
  • Halo of fluorescein
  • ‘Under-run’ edges
  • Minimal corneal oedema
  • Potential neovascularisation in time
  • Variable pain
  • Can recur in novel corneal sites
233
Q

How are SCCED treated medically?

A
  • Prophylactic topical antibiotherapy
  • Lubrication
  • Systemic NSAID analgesia
  • With/without topical atropine if reflex uveitis/miosis
  • With/without oral doxycycline but may promote epithelialisation
  • Elizabethan collar
234
Q

How is SCCED treated surgically?

A
  • Epithelial debridement
  • Remove loose, detached epithelium
  • Use dry, sterile cotton buds
  • Disrupts anterior stroma/removes hyalinised zone
235
Q

What is a special consideration of SCCED?

A

SCCEDs are the only ulcers you should debride. Diamond burr debridgement removes superficial abnormal cornea

236
Q

What are 2 possible second line treatments for SCCED?

A

Punctate keratotomy/anterior stromal puncture or grid keratotomy

Both techniques require local anaesthesia with/without sedation

237
Q

Which further tests can be used for deep ulcers?

A
  • Swab for culture and sensitivity and cytology
  • Fragile eye so care not to increase intraocular pressure
238
Q

What can keratomalacia progress to?

A

Progress to ruptured globe within 24hours without treatment

239
Q

How is keratomalacia treated medically?

A
  • Topical antibiotics – empirical until cytology/C&S. Justified use of Fluoroquinolone Ofloxacin
  • Systemic broad spectrum antibiotic (like doxycycline)
  • Antiproteolytic drops
  • Lubrication
  • Analgesia
  • Systemic NSAIDs, with/without atropine for uveitis
  • Cone, lid hygiene
240
Q

Name 3 surgical procedures that can be done to treat keratomalacia.

A

3rd eyelid flap/tarsorraphy/Gunderson flap

Reconstructive corneal surgery

Enucleation

241
Q

What clinical judgement can you use for ulcers at the edge and centre of the eye and recurring ulcers?

A

Ulcer at the edge – look for focal mechanical cause

Ulcer in centre – consider exposure

Ulcer keeps coming back – consider KCS or repeated insults

242
Q

What is the field of vision of a cat?

A

Field of view 200˚
Binocular vision – 140 degrees

243
Q

What are the some specific anatomical characteristics of a cat’s eye?

A
  • Large cornea
  • Deep anterior chamber
  • Posterior location of the lens
  • Vertical slit pupils to allow wider dilation at night
244
Q

What allows cats to have increased sensitivity to light?

A

Have lots of light sensitive rods

245
Q

Describe exohpthalmos in feline ophthalmology.

A
  • Brachycephalic breeds
  • Exposure keratitis likely
246
Q

What could be the cause of exophthalmos in feline ophthalmology?

A
  • Orbital space occupying lesion – cellulitis, foreign body, cat bite abscess
  • Orbital neoplasia
247
Q

How is proptosis/lids trapped behind the globe caused in cats?

A

Trauma to create pressure change to move to globe, so assess/treat ABC/check stable:

  • Head trauma
  • Exposure keratitis
  • Secondary uveitis
  • Extraocular muscle damage
  • Avulsed CN II
248
Q

When is tear production mature in feline ophthalmology?

A

Before 10-14 days old, tear production is not mature

249
Q

What is eyelid agenesis?

A

Most commonly part of upper lid missing – bilateral

250
Q

How does entropian form in cats?

A
  • Weight loss, fat loss from orbital
  • In rolling of eyelid
251
Q

How does entropian in cats present?

A
  • Present as conjunctivitis
  • Hair rub on eye
  • Corneal vascularisation
252
Q

What is the Hotz-Celsus technique and what is it used to correct?

A

Removing a crescent of skin and orbicularis muscle from the affected area of thin and then closing it. Corrective surgery for entropian

253
Q

When can cats get dry eye?

A
  • Lower tear production
  • Iatrogenic – atropine, opioids
  • Sequel of chronic blepharoconjunctivitis
  • Associated with FHV-1 as goblet cells are reduced
254
Q

Describe the normal conjunctival flora of cats.

A
  • Less numerous flora than dogs
  • Some gram negatives
  • Low/no fungal flora
  • No eosinophils or basophils
  • Epithelial cells (may contain melanin)
  • Lymphocytes
  • Mast cells
  • Neutrophils
255
Q

What are the clinical signs of conjunctivitis in cats?

A
  • Conjunctival hyperaemia
  • Chemosis
  • Epiphora
  • Blepharospasm
  • Unilateral or most commonly bilateral
  • Acute or can become chronic
  • Often recurrent
256
Q

What are the possible causes of feline conjunctivitis?

A
  • FHV-1
  • Chlamydophila felis
  • Mycoplasma felis
  • Feline calicivirus/bordetellosis, B. bronchiseptica
  • Eosinophilic kerato-conjunctivitis
257
Q

What can feline conjunctivitis be secondary to?

A
  • Eyelid conformation
  • Abnormal hairs
  • Keratitis
  • Uveitis
  • Glaucoma
  • Trauma
  • Foreign body
258
Q

How is chlamydia felis diagnosed?

A

Cytology – C. felis inclusion bodies in epithelial cell cytoplasm (day 3-14 after infection)

PCR – positive on day 3 until day 25

259
Q

How is chlamydia felis treated?

A
  • Sensitive to tetracyclines, erythromycin, rifampicin, fluoroquinolones
  • Doxycycline for 4 weeks
  • Mitigate risks of oesophagitis and stricture by giving with food
  • Vaccination with live chlamydial vaccine available
260
Q

How is mycoplasma diagnosed?

A

PCR, cytology (inclusions), culture

261
Q

How is mycoplasma treated in cats?

A

Sensitive to doxycycline, tetracycline, erythromycin

262
Q

What can develop later in the presentation of mycoplasma in cats?

A

FHV-1

263
Q

What is corneal ulceration/ulcerative keratitis primary and secondary to in cats?

A

Primary FHV-1

Secondary to:
- Corneal dryness, such as in GA
- Exophthalmos/lagophthalmos
- Trauma – foreign body, entropion

264
Q

What is sequestrum in feline ophthalmology?

A
  • Usually after chronic corneal irritation
  • Initially brown cornea
  • Becomes black corneal plaque with vascularisation, granulation, pain
  • Pain > entropion > worse irritation cycle
  • Necrotic corneal cells
265
Q

How is sequestrum in cats treated?

A

Surgical removal – keratectomy

266
Q

What is the epidemiology of feline herpes virus-1?

A
  • Virus attacks conjunctival and corneal epithelium
  • Causes conjunctivitis and corneal ulceration
  • Direct contact or aerosolisation of virus
  • Most develop latency and carrier status (80%)
267
Q

What are the primary ocular signs in kittens with feline herpes virus-1?

A
  • Conjunctivitis
  • Ophthalmia neonatorum – open lids with/without tenotomy
  • Symblepharon – adhesions develop, can be permanent. Treat kittens early with topical anaesthesia, cotton-tipped swabs or fine forceps
  • Supportive care for URT infection
268
Q

What are dendritic ulcer pathognomic for?

A

Ulcers that are dendritic or branch like, pathognomic for FHV-1, there is active virus coursing through the nerves in the cornea, creating ulceration

269
Q

What is stromal keratitis in cats?

A
  • Immune mediated inflammatory reaction to virus
  • Can occur after active infection
  • Corneal vessels, oedema
  • Non-ulcerative
270
Q

How is stromal keratitis treated in cats?

A

Topical corticosteroids – treat condition, risk recrudescence

271
Q

How is herpetic keratoconjunctivitis in cats diagnosed?

A
  • PCR assay
  • Virus isolation and fluorescent antibody
  • But many false negatives – infected cat negative PCR, also negative cats can shed FHV-1
  • History of recrudescence and latency
272
Q

When are cats with herpetic keratoconjunctivitis treated?

A
  • Cats/kittens with moderate to severe signs
  • Severe conjunctivitis, corneal ulceration and acute symblepharon
273
Q

How are cats with herpetic keratoconjunctivitis treated with antivirals?

A
  • Virostatic – only reduce replication
  • Oral Antiviral
  • Topical antivirals
274
Q

What are the other treatments available for herpetic keratoconjunctivitis cats?

A
  • Debride corneal ulcers after local to remove dead epithelium and viral particles
  • No grid keratotomy as this leads to sequestrum in cats
  • Topical or oral NSAIDs
  • With/without topical or systemic antibiotic therapy prevent secondary infection
  • Mucinomimetic tear supplements
  • Nursing, fluid and nutritional support, minimise environmental stressors
275
Q

How is eosinophilic keratitis in cats characterised?

A
  • White to pink spots or proliferative plaque
  • May have vascular response, ocular discharge
276
Q

How is eosinophilic keratitis diagnosed in cats?

A

Cytology shows eosinophils

277
Q

How is eosinophilic keratitis treated in cats?

A

Topical steroids 4-6 days initially, taper over a 6-8 weeks or can recur with/without cyclosporin

Care as steroids may reactivate FHV-1

278
Q

What can cause iris pigmentation?

A
  • Benign ocular melanosis seen in cats over 10 year old
  • Melanoma
  • Lymphoma
  • Feline post traumatic ocular sarcoma
  • Limbal melanoma
279
Q

How can we differentiate benign melanosis and malignant melanoma

A

Signs of malignancy:

  • Dark black pigmentation vs benign brown
  • Mass elevated from iris surface
  • Change in iris structure ad texture
  • Dyscoria – abnormal pupil size
  • Free pigmented cells in anterior chamber
  • Increase intraocular pressure = invasion drainage angle
280
Q

What is FDIM?

A

Feline diffuse iris melanoma

  • Progressive pigmentation
  • Metastasis can develop up to 1-3 Y after enucleation
281
Q

What are some complications of FDIM?

A

Dyscoria
Glaucoma

282
Q

How can FDIM be treated?

A
  • Laser therapy of small or new lesions
  • Enucleation and histopathology
  • Ongoing monitoring
283
Q

What are the causes of anterior uveitis in cats?

A
  • Lymphoplasmocytic
  • FIP/FCoV/FIV
  • FeLV-associated lymphosarcoma
  • Trauma
  • Lens induced
284
Q

What are the clinical signs of anterior uveitis in cats?

A
  • Acute uveitis – hypotony, aqueous flare or fibrin, miosis
  • Corneal oedema
  • Hypopyon
  • Hyphaemia
  • Iridial hyperaemia
  • Iris colour change
  • Chronic uveitis – synechia, cataract, lens subluxation/luxation, secondary glaucoma
285
Q

What are the causes of posterior uveitis in cats?

A
  • Many infectious conditions
  • Neoplasia
  • Systemic hypertension
286
Q

How does hypertensive retinopathy develop in cats?

A
  1. Initial retinal arterioles constriction due to high pressure in these vessels
  2. Ischemic necrosis of the vessel walls when this occurs over a long time
  3. Increased vascular permeability due to pressure
  4. Serous retinal exudate, haemorrhages and oedema
  5. Choroidal vessels involved
  6. Subretinal fluid and retinal detachment
287
Q

Distinguish bullous and total retinal detachment in cats.

A

Bullous retinal detachment – early stages, sheets of detached retina

Total retinal detachment possible – see thin veil of retina at pupil

288
Q

What are the ocular sigs associated with retinal detachment in cats?

A

Hyperreflectivity
Retinal haemorrhage
Mydriasis
Reduced PLR
Asymmetry
Limited vision

289
Q

How should equine eyelashes be positioned?

A

Should be virtually horizontal

290
Q

What are you looking for on close visual examination of the equine eye?

A
  • Blepharospasm
  • Epiphora
  • Swelling
  • Signs of pain – tension above the eye, orbital tightening, potentially more head shy
291
Q

Describe the auriculopalpebral nerve block in a horse.

A
  • Motor function blocked
  • Upper eyelid only
  • Branch of CNVII/facial nerve
  • Usually necessary for examination
292
Q

Describe the supra-orbital nerve block in a horse.

A
  • Sensory function blocked
  • Upper lid
  • Branch of CNV/trigeminal nerve
  • Need dependent on pain
293
Q

Which topical local anaesthetic is used for equine ophthalmic examination?

A

Proxymetacaine or tetracaine

294
Q

Outline how to administer a auriculopalpebral nerve block in a horse.

A
  1. Palpate nerve )
  2. Pinch skin over site
  3. Insert needle subcutaneously
  4. Swift needle motion best
  5. Attach syringe
  6. Subcutaneous bleb
295
Q

Where does the supra-orbital nerve block desensitise in the horse?

A

Majority of upper lid, inject over the foramen/nerve, not in it

296
Q

How can horses that are difficult to medicate be managed?

A
  • Induce lacrimation by diluting/wash out meds
  • Use training and bribery can be useful, as not sufficient positive reinforcement may not support giving medication daily
  • Change husbandry/use during treatment
297
Q

What are 2 disadvantages of sub-palpebral lavage in horses?

A
  • Must be stabled
  • Prone to breakage from trauma/self-removal
298
Q

What does subpalpebral lavage in horses involve?

A
  • Local in the skin – mepivacaine
  • Lower eyelid
299
Q

Why are eyelid injuries in horses difficult to manage?

A
  • Facial skin in horses is tight and limited
  • Upper eyelid contributes to 75% of eyelid movement
  • Very well vascularised
300
Q

What consideration should be used for equine eyelid injuries?

A

So minimal debridement and clean gently without pulling

301
Q

What does eyelid repair in horses depend on?

A
  • How extensive the deficit of eyelid tissue is
  • If the medial canthus is affected
  • If the tear ducts are involved
302
Q

How are eyelid injuries repaired in horses?

A
  • Figure of 8 suture so sides can be apposed but suture is away from the eyelid margin
  • Ensure suture material does not penetrate the conjunctiva as this will lead to corneal trauma
303
Q

What are the causes of conjunctivitis in horses?

A
  • Foreign body
  • Head trauma
  • Irritants
  • Flies
304
Q

How is conjunctivitis managed in horses?

A

Ventilation, bedding, diet, husbandry

305
Q

What are the causes of corneal ulceration in horses?

A
  • Traumatic is most common
  • Infectious cause EHV-2 uncommonly
  • Secondary infection with bacteria/fungus
  • Keratomalacia – is it melting?
  • Perforation by foreign body
  • Eosinophilic keratitis
306
Q

How are uncomplicated ulcers in horses treated?

A
  • Removal inciting cause
  • Antibiotic cover
  • Analgesia – phenylbutazone
  • Atropine if reflex uveitis
  • With/without stable, fly mask or bubble mask
307
Q

What is the characteristic of an infected ulcer in horses?

A

Creamy white infiltrate

308
Q

What is done with infected ulcers in horses?

A
  • Do cytology immediately
  • Bacterial culture and sensitivity
  • Fungal culture and sensitivity
309
Q

What does 50% stromal depth of an equine ulcer indicate?

A

Need tectonic surgical support

310
Q

What intensive medical therapy must be used for keratomalacia in horses?

A
  • Serum, plasma, EDTA drops
  • Surgery?
311
Q

What is eosinophilic keratitis in horses?

A
  • Immune mediated inflammatory condition
  • Cause not fully understood
312
Q

How is eosinophilic keratitis diagnosed in horses?

A

Cytology is diagnostic – eosinophils stain dark pink in horses

313
Q

How is eosinophilic keratitis treated in horses?

A
  • Topical steroids
  • Surgery – keratectomy
314
Q

What are 3 non-ulcerative forms of keratitis in horses?

A
  • Stromal abscess
  • Immune mediated keratitis
  • Spotty keratitis, common - Equine herpesvirus-2
315
Q

What is the pathogenesis for uveitis in horses, as with other species?

A
  • Traumatic
  • Septicaemia/septic focus
  • Reflex uveitis from anterior pain/ulcer
  • Other systemic disease
  • Neoplasia
316
Q

What is equine recurrent uveitis?

A

An autoimmune disease

317
Q

What are the anterior signs of uveitis in horses?

A
  • Miosis
  • Fibrin in anterior chamber
  • Aqueous flare
  • Keratic precipitates
  • Hypopyon
  • Yellow vitreal change
  • Synechia = iris adhesions, can create dyscoric pupil
  • Depigmentation pupil margin
  • Irregular pupillary margin
  • Loss of granula iridica
  • Cataracts – black bits on a cataract is little bits of iris
318
Q

What are some posterior signs of uveitis/ERU in horses?

A
  • Butterfly lesions – previous inflammation scarring
  • Active chorioretinitis
  • Bullet hole lesions
  • Focal retinal detachments
  • Yellow cellular infiltrate – vitreous
  • Vitreal degeneration
  • RPE loss – can see choroidal hyperaemia
  • Optic dis is axonal material accumulation
  • Optic nerve head atrophy (demyelination)
319
Q

What are bullet hold lesions in equine recurrent uveitis?

A

Scars from previous inflammation

  • Chorioretinal scars
  • In non-tapetal fundus
  • Inactive lesions
  • Signify past damage
320
Q

What is the appearance of the normal equine fundus?

A

Should have a paurangiotic fungus, oval pink optic disk, multiple short vessels and look ‘up and over’ iris

321
Q

How is equine recurrent uveitis classified?

A

Classic – acute flares and quiescent periods cycle

Insidious – persistent low grade, less pain and slow decay (appaloosas)

Posterior – posterior changes predominate, more leptospira related (warmbloods, draft, European)

End stage – severe/blinding changes: phthisis bulbi, cataract, luxated lens, detached retina

322
Q

What are the aims of treating equine recurrent uveitis?

A
  • Reduce inflammation
  • Relieve discomfort and pain
  • Prevent vision loss
323
Q

How is equine recurrent uveitis treated?

A
  • Atropine to prevent iris spasm
  • NSAIDs – topical and systemic (PBZ)
  • Steroids – largely topical
  • Wean/taper slowly
  • Husbandry changes
324
Q

Name 2 surgical procedures that can be done at referral to treat equine recurrent uveitis.

A

Cyclosporine implant
Pars plana vitrectomy

325
Q

What are the species specific characteristics about equine glaucoma?

A
  • More uveoscleral outflow than other species – this is quite visible in horses, is the drainage angle
  • Usually secondary
  • ERU most common primary cause
326
Q

How can equine glaucoma be treated?

A
  • CAi and B-blockers
  • Avoid PG analogues as they are pro inflammatory
  • Treat any underlying inflammation
  • Enucleation
327
Q

How can equine glaucoma be treated at referral?

A

Transscleral cycophotocoagulation TCP with small handheld laser to destroy some of the ciliary body, diode laser

328
Q

What causes luxation or rupture of equine lens?

A

Primary to blunt or penetrating trauma

329
Q

What are the 2 most common causes of cataracts in horses?

A

Uveitis is the most common
Trauma 2nd most common

330
Q

What is new forest eye in cattle?

A

Infectious bovine keratoconjunctivitis

331
Q

What is the epidemiology of infectious bovine keratoconjunctivits?

A
  • Moraxella bovis is a gram negative bacillus
  • Flies transmit
  • Summer outbreaks because UV light increases the pathogenicity of Moraxella bovis
  • Young cattle are increased risk of infection and severity of disease
  • Morbidity can be as high as 80%
332
Q

What is the aetiology of infectious bovine keratoconjunctivitis?

A
  • Ulcerative keratitis centrally
  • Marked cellular infiltrate and vascularisation
  • Progress to descemetocoele/perforation with iris prolapse
  • Rarely, corneal rupture leads to blindness
333
Q

What are the clinical signs of infectious bovine keratoconjunctivitis?

A

Blepharospasm
Lacrimation
Dull
Inappetent

334
Q

How is infectious bovine keratoconjunctivitis treated?

A
  • Topical antibiotics – kloxacillin
  • Long acting systemic antibiotics – amoxicillin, oxytetracycline
  • Subconjunctival antibiotic?
  • NSAIDs
  • Controlling flies – stocking density, housing, ventilation, repellents, parasitic wasp larvae to repel flies
335
Q

What is the prognosis of infectious bovine keratoconjunctivitis?

A

3-4 weeks, may leave a scar

336
Q

What is silage eye in large animals?

A

Listeriosis

337
Q

What is the aetiology of silage eye?

A
  • Listeria monocytogenes
  • Soil in the silage at bailing and bale fails to reach acidic pH to deactivate the bacteria
  • Excoriations in the mouth/broken teeth
  • Tracks up trigeminal nerve or directly into eye
338
Q

What are the clinical signs of silage eye?

A

Uveitis (clouding of the eye)
Keratitis

339
Q

How is silage eye treated?

A

Antibiotics – spectrum?

Systemic, best is early in course of disease, pencillins or tetracyclines reported effective 2-4 weeks

340
Q

What are 2 other differential diagnoses for uveitis in large animals?

A

Malignant catarrhal fever
Infectious bovine rhinotracheitis

341
Q

What is pink eye in sheep?

A

Infectious ovine keratoconjunctivitis

Mycoplasma conjunctivae and chlamydia psattaci ovis

342
Q

What are the risk factors of pink eye in sheep?

A
  • Higher stocking density
  • UV light possibly exacerbating factor, resulting in more severe clinical signs
  • Carrier animals
  • Relapse possible in treated and recovering animals
343
Q

What are the clinical signs of pink eye in sheep?

A
  • Blepharospasm
  • Lacrimation
  • Conjunctival hyperaemia with/without epiphora
  • Ocular discharge of mucopurulent nature
  • Corneal vascularisation and oedema
  • Corneal microabscesses and cellular infiltrate with/without corneal ulceration
344
Q

How is pink eye in sheep treated?

A
  • Tetracyclines effective clinically terms but ineffective in clearing, resulting in carrier status and will be expensive
  • Isolation
  • Flock-wide treatment with long-acting tetracycline may be considered in severe outbreaks
345
Q

What is the most common primary neoplasm of the eyelids, conjunctiva and cornea in cattle and sheep?

A

Squamous cell carcinoma

More in cattle than sheep, older animals

346
Q

How is squamous cell carcinoma treated in large animals?

A

Enucleation

Metastasis common to parotid lymph node

347
Q

What are the causes of cataracts in large animals?

A
  • Congenital – bovine viral diarrhoea can cause congenital cataracts
  • Primary congenital, hereditary and progressive cataracts have been reported in Holstein-Friesian, Hereford, Ayrshire and Jersey cattle
  • Secondary to uveitis or trauma
348
Q

What are 5 possible causes of blindness in large animals?

A
  • Meningoencephalitis/encephalitis
  • Pregnancy toxaemia in sheep/ketosis in cattle
  • Lead poisoning is rare
  • Salt poisoning – extremely rare
  • Hydatid disease/coenurus cerebralis in sheep – rare
349
Q

Describe the anatomy of rabbit ophthalmology.

A
  • Single nasolacrimal punctum and duct path runs close to maxillary cheek teeth and incisor. So dental disease can result in ocular symptoms.
  • Lower blink rate and will mostly hold eye open so surface disease is less common
350
Q

What is dacryocystitis in rabbits?

A
  • Inflammation/infection of lacrimal sac
  • Infection or inflammation here can cause an obstruction of nasolacrimal duct
351
Q

How can dental disease cause dacryocystitis?

A
  • Nutritional hyperparathyroidism from selective feeding causing maxillary osseous change and obstructive nasolacrimal duct
  • Genetics – brachycephaly
  • Dental overgrowth
352
Q

How can dacryocystitis be treated in rabbits?

A
  • Topical antibiotics
  • Systemic antibiotics
  • Oral NSAIDs – meloxicam
  • Nasolacrimal flushing can significantly help, as this can allow clearance, normal tears to flow and eyedrops to penetrate this area – caseous to mucopurulent discharge
  • Gentle cleaning of discharge
  • Occlusive ointment
353
Q

How can dacryocystitis be treated in rabbits long term?

A
  • Dental radiography
  • Dental treatment
  • Lifelong medications?
354
Q

What does encephalitazoon cuniculi cause in rabbits?

A
  • Vertical transmission in utero
  • Cataract causes lens capsule rupture causing phacoclastic uveitis with/without glaucoma
  • Can be other uveitis signs – lesions and pus in the eyes
355
Q

How is encephalitazoon culiculi treated?

A
  • Phacoemulsification – remove cataract and lens but not often chosen
  • Anti-inflammatory treatment
  • Fenbendazole to treat the E.cuniculi
356
Q

What are 2 less common differential diagnoses for uveitis in rabbits?

A

Systemic pasteurellosis
Staphylococcal uveitis

357
Q

What is myxamatosis and what ocular signs does it cause in rabbits?

A
  • Myxaoma virus
  • Arthropod vector
  • Purulent conjunctivitis and blepharitis
  • Myxoma formation on eyelids and other mucosal junctions – require a lot of nursing
358
Q

How does exophthalmos develop in rabbits?

A
  • Retrobulbar abscessation
  • Mediastinal mass/thymoma – jugular pressure, reduced drainage, increased orbital venous sinus pressure, pulsatile exophthalmos (usually bilateral)
359
Q

Describe rodent ocular anatomy.

A
  • Orbital venous sinus or plexus behind the eye
  • Harderian gland in orbit – which sometimes release pigmented discharge
  • Retinal vasculature varies species dependent
360
Q

What is chromodacryorrhoea in rodents?

A
  • ‘Bleeding eyes’ – overproduced porphyrin (pigmented compounds in the tears) and lipid in tears
  • Response to irritation, respiratory disease or general stress – nutritional, transport, handling
361
Q

How is chromodacryorrhoea in rodents treated?

A

Address management issues
Respiratory disease

362
Q

What are 2 possible causes of ulcerative keratitis in rodents?

A
  • Trauma
  • Foreign body
363
Q

What are possible causes of cataracts in rodents?

A
  • Diabetic cataracts – rates and cavies/guinea pigs
  • Secondary to retinal degenerations
364
Q

How are cataracts in rodents treated?

A

Most cope okay in captivity as long as there is no inflammation in the eye

365
Q

What is heterotopic bone formation in guinea pigs?

A

Scalloped ring calcification in anterior uvea (iris into ciliary body), doesn’t seem to invade drainage and cause glaucoma, insidious onset but no insidious outcomes, so often not treated unless concurrent problems

366
Q

What causes heterotopic bone formation in guinea pigs?

A

Cause unknown

Postulated, ciliary body concentrates plasma ascorbate into aqueous humour > promote bone formation in presence of rich vascularisation

367
Q

What are some examples of ophthalmic emergencies?

A
  • Acute blindness – glaucoma, anterior lens luxation, retinal detachment
  • Blindness with insidious onset – hypertensive retinopathy, cataract, severe KCS, secondary glaucoma, severe uveitis
  • Deep or melting corneal ulcers
  • Rupture can mean infection can get into the eye which is then hard to treat and this can be catastrophic to the eye
368
Q

How does handling change for when there is an ophthalmic examination?

A
  • Increased venous pressure = increased IOP
  • Ensure no pressure on neck, use fore-finger and thumb under the jaw to lift the head
  • Smooth pre-surgical preparation (catheter)
  • Smooth recovery post-op
369
Q
A
370
Q

Why is globe proptosis an ophthalmic emergency?

A
  • Eyelids entrapped behind equator of globe
  • Huge trauma for non-brachycephalics – check systematic injuries
371
Q

How is globe proptosis triaged over the phone?

A

Advise on the phone to keep the eye moist and come quickly

372
Q

How is globe proptosis treated as an emergency?

A
  • Induce anaesthesia once stable
  • Lift lids over globe to replace
  • Copious flush conjunctival sac of debris
  • Roll out lids and place temporary tarsorraphy
  • Leave medial canthus open for topical treatment
  • Steroids for uveitis/optic neuritis
373
Q

Can the eye be saved in globe proptosis?

A

Earlier replacement better prognosis – strabismus often persists, check vision with indirect PLR. Even if the eye is saved there’s no guaranteeing that it is visual

374
Q

When is enucleation needed in globe proptosis?

A
  • Ruptured globe
  • 3+ extraocular muscles torn
  • Complete hyphaema
  • Owner unable/unwilling – potential long term post op treatment
375
Q

How often should drops with preservative in be given and why?

A

Make sure to not give drops with preservative in them more than every 4 hours, as many can be toxic to the eye

376
Q

How is vision assessed?

A

PLR reflex
Dazzle reflex
Menace response
Visual placing
Visual tracking

377
Q

What are the differential diagnoses for blindness?

A
  • Ocular opacity
  • Retinal dysfunction – glaucoma, chorioretinitis, retinal detachment
  • Optic nerve dysfunction
  • Optic tract lesion
  • Optic radiations lesion
  • Visual cortex lesion
378
Q

What are some neuro problems causing ophthalmic issues?

A
  • Optic neuritis
  • Papilloedema
  • Central blindness
  • Other cranial nerve problems?
379
Q

How is a condition determined to be neuro or ophthalmic?

A
  • Full neurological exam
  • Advanced imaging – MRI/CT?
380
Q

How is opacity of the ocular media assessed?

A
  • Distant direct ophthalmoscopy
  • Ocular ultrasound
381
Q

How is the fundus examined?

A
  • Close direct – high detail/small field of view
  • Distant indirect – low detail, large field
  • Dilate the pupil for best view
  • Only if IOP normal
382
Q

What is the appearance of active retinal inflammation?

A
  • ‘Active’ chorioretinitis
  • Hypo-reflective tapetal lesions
  • White/cream lesions of cellular infiltrate
  • Darker areas – oedema/effusion
  • Lesions show infiltrates, not causal agent
383
Q

What is the appearance of chronic retinal inflammation?

A
  • ‘Inactive’ chorioretinitis
  • Hyper-reflective tapetal lesions (thinned retina)
  • Pigmentation in tapetum
  • Depigmentation in non-tapetal lesion
384
Q

What is retinal haemorrhage due to hypertensive retinopathy?

A
  • Target organ damage
  • Vascular tortuosity
  • Vessel beading/boxcars
  • Haemorrhages
  • Multifocal bullous detachments
  • Total detachment
  • Can also be secondary to bleeding disorders
385
Q

What are the signs of retinal detachment?

A
  • Serous exudate
  • Explosive haemorrhage
  • Subretinal cellular infiltrate
  • Granuloma
  • Solid tissue/tumour
  • Tears/holes
386
Q

Describe blindness due to inherited progressive retinal atrophy.

A
  • Typically pedigree dogs 3+ years
  • Hyper-reflectivity
  • Vascular attenuation
  • Nyctalopia (night blind) first
387
Q

Describe blindness due to sudden acquired retinal degeneration.

A
  • Typically older, overweight
  • Acute blindness
  • Dilated pupils, reduced PLR
  • Normal ophthalmology exam
388
Q

Distinguish primary and secondary canine glaucoma.

A

1 = goniodysgenesis = pectinate ligament dysplasia, diagnose with gonioscopy

2 = differentials, invetsigate and histo. Commonly secondary to neoplasia, severe/chronic uveitis, lens luxation

Both = outflow obstruction, ocular hypertension

389
Q

Describe the characteristics of acute glaucoma.

A
  • Pain and blindness
  • Episcleral congestion (hyperaemia)
  • Conjunctival congestion
  • Pancorneal oedema (not cats)
  • Mydriasis – eye is forced open due to pressure on vessels and mydriasis develops
390
Q

Describe the characteristics of chronic glaucoma.

A
  • Globe enlargement (buphthalmos)
  • Secondary lens luxation
  • Cataract
  • Phthisis bulbi (degenerate globe)
391
Q

How is glaucoma diagnosed?

A

Use a tonometer to measure IOP. Normal IOP 10-25mmHg

392
Q

How do carbonic anhydrase inhibitors medically treat glaucoma?

A
  • Reduce aqueous production
  • Blocks bicarb entry to aqueous
393
Q

How do beta-blockers medically treat glaucoma?

A
  • Reduce aqueous production
  • Block β-receptors in ciliary epithelium
394
Q

How do prostaglandin analogues medically treat glaucoma?

A
  • Increase aqueous outflow through uveoscleral pathway
  • Contraindicated in uveitis (prostaglandins are pro-inflammatory)
  • Miosis
  • Potent, work to drop pressure significantly and quickly
395
Q

Which surgical methods are used to increase outflow and to decrease output to treat glaucoma?

A

Increase outflow – gonioimplant, paracentesis

Decrease output – transcleral cyclophotocoagulation (TSCP), endoscopic cyclophotocoagulation (ECP)

396
Q

How can glaucoma in blind eyes be surgically treated?

A
  • Enucleation – transpalpebral, transconjunctival
  • Referral options – evisceration and intrascleral prosthesis (not cats), chemical or cryo-cycloablation to destroy ciliary body
397
Q

What are the indications for enucleation?

A
  • Irreversible loss of vision
  • Ongoing pain and discomfort
  • Chronic glaucoma
398
Q

Distinguish transpalpebral and transconjunctival enucleation.

A
  • Transpalpebral indicated for en bloc removal of infection, neoplastic cells on globe surface, more common
  • Transconjunctival approach simpler/less haemorrhage
399
Q

How is a transpalpebral enucleation done?

A
  • Suture lids
  • Dissection
  • Avoid traction, especially in cats
  • Remove eye
  • Haemostasis
  • Closure in 3 layers
400
Q

How is transconjunctival enucleation done?

A
  • Lateral canthotomy
  • Dissection
  • Avoid Traction
  • Remove eye
  • Haemostasis
  • Closure in 3 layers – important to removal all of the conjunctiva and 3rd eyelid before closure
401
Q

How is the eye surgically prepped?

A
  • Povidone Iodine solution
  • Never Povidone scrub or tincture
  • 1 part povidone iodine:50 parts sterile saline for globe
  • 1 part povidone iodine:10 parts sterile saline for eyelids
  • 2 minute contact time required – then flush out with saline
402
Q

How is ectropian treated surgically?

A

Modified wedge excision with/without lateral canthus stabilisation

  • Take house shaped wedge
  • Close with ‘figure-8’ suture
403
Q

How is entropian treated surgically?

A
  • Simple cases – Hotz-Celsus technique
  • Complex cases – refer

CVSOH 4 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions