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VET433A > Week 5 - Optho > Flashcards

Week 5 - Optho Flashcards

1
Q

There are 3 layers to the eye. What are they?

A
  1. Outer - Fibrous tunic
  2. Middle - Vascular (uvea) tunic
  3. Inner - Nervous tunic
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2
Q

What are some anatomical structures that are a part of the Outer - Fibrous Tunic?

A

-cornea
-sclera
-limbus

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3
Q

What is the function of the Outer - Fibrous tunic? (3)

A
  1. protection
  2. transmission
  3. refraction
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4
Q

What are some anatomical structures that are a part of the Middle - Vascular/Uvea Tunic?

A

-iris
-ciliary body
-choroid

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5
Q

What is the function of the Middle - Vascular tunic? (3)

A
  1. nutrition
  2. immunity
  3. accommodation (change lens shape)
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6
Q

What is an anatomical structure that is a part of the Inner - Nervous Tunic?

A

-retina

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7
Q

What is the function of the Inner - Nervous tunic? (1)

A
  1. generate a neural signal in response to light stimulation
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8
Q

What are the 3 parts of the conjunctiva?

A
  1. papebral
  2. fornix
  3. bulbar

Lecture 33 Slide 8

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9
Q

What are the 6 parts of the Adnexa of the Eye?

A
  1. Orbicularis oculi muscle
  2. Meibomian glands
  3. Palpebral conjunctiva
  4. Superior palpebral levator m.
  5. Müller’s muscle
  6. Lacrimal puncta and canaliculi
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10
Q

What’s the function of the Orbicularis oculi muscle? (3)

A
  1. closes eyelid - innervated by CNVII
  2. responsible for blepharospasm (squinting)
  3. surgical holding layer
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11
Q

What’s the function of the Meibomian glands? What are some pathologies related to the Meibomian glands? (4)

A
  1. produce lipid layer of the tear film
  2. neoplasia in dogs (ex. meibomian gland tumor)
  3. distichiasis (hair follicle from meibomian gland), ectopic cilia (hair from meibomian through palpebral conjuctiva)
  4. duct is surgical landmark
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12
Q

What is the function of the Palpebral conjunctiva?

A
  1. Goblet cells –> mucous portion of tear film
  2. source of tissue for surgery
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13
Q

What is the function of the Superior palpebral levator m.?

A
  1. opens eyelids
  2. innervated by CNIII – usually not many issues with CNIII
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14
Q

What is the function of the Müller’s muscle?

A

-maintain palpebral fissure opening

-smooth muscle
-sympathetic innervation – Horner’s Syndrome

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15
Q

What is the function of the Lacrimal puncta and canaliculi?

A

-Drainage of tears

-Lid abnormalities affect drainage

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16
Q

The adnexa of the eye is HIGHLY VASCULAR. What are the 3 pros to this?

A
  1. acutely reactive
  2. heals quickly
  3. resistant to infection
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17
Q

What are the 4 functions of the adnexa of the eye?

A
  1. general protection
  2. spread tear film and prevent evaporation
    -issues when there is lagophthalmos (can’t close eyelids fully) and ectropion (rolling of eyelids)
  3. produce portions of the tear film
    -lipid and mucous
  4. contains portions of tear drainage system
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18
Q

What are general signs of disease of the eye? (5)

A
  1. redness (blepharitis)
  2. swelling
  3. blepharospasm (squinting)
  4. corneal disease
  5. epiphora – tearing accumulation/wetness around the eye
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19
Q

What is entropion?

A

-rolling in of the eyelids

-congenital (usually inherited)
-spastic (related to pain – ex. pain from ulcer)
-cicatricial (cyclical disease/inflammation)

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20
Q

Signalment for Entropion

A

-midsized and large dogs
-usually younger (but any)

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21
Q

CS for Entropion

A

-signs usually on LATERAL ASPECT OF LOWER LID
-blepharospasm
-epiphora
-corneal ulceration, vessels, melanosis (coloring of cornea) – esp. ventrolaterally

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22
Q

How do you DIAGNOSE Entropion?

A

-signalment
-clinical signs

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23
Q

How do you TREAT entropion? not benign neglect

A

-depends on breed, severity, and age

  1. adolescent <1 yr - orbit not fully grown, could outgrow entropion
    -lubrication (ideal if without corneal dz)
    -tacking - staples/suture
  2. adult >1 yr
    -surgical repair (Holtz-Celsus – SMILE)
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24
Q

What is the SIGNALMENT for Chronic Epiphora Syndrome?

A

-breed disposition - chihuahuas, poodles, brachycephalic

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25
Q

What is the underlying problem with Chronic Epiphora Syndrome?

A

medial entropion of the lower eyelid -> leads to malposition of the nasal lacrimal punctum (puncture responsible for drainage of tears)

-this can also “crimp the canaliculus” – the drainage tract

-entropion = trichiasis (normal hair in eye) > irritation > increase tearing
-trichiasis > wicking tears on to face

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26
Q

CS of Chronic Epiphora Syndrome

A

-chronic tear staining from medial canthus
-secondary moist dermatitis (esp in brachy)

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27
Q

How do you DIAGNOSE chronic epiphora syndrome?

A

-signalment
-clinical signs

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28
Q

How do you TREAT chronic epiphora syndrome?

A

BENIGN NEGLECT is fine – bc unrolling the eyelid does NOT mean you will unkink/uncrimp the canniculi

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29
Q

What is ectropion?

A

Eyelid turns more outward and causes droopiness

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30
Q

Signalment of Ectropion

A

-majority of dogs is breed related/inherited
1. cocker spaniels
2. bloodhounds
3. giant breeds

-age related (loss of muscle tone)

obicularis oculi muscle gets weaker – leads to lower eyelid slipping outwards

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31
Q

CS of Ectropion

A
  1. loss of contact of lower eyelid with eye
  2. leads to secondary corneal problems
    -blepharospasm
    -epiphora
    -corneal vessels, melanosis, ulceration
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32
Q

What is the DIAGNOSIS of ectropion?

A

-signalment
-CS

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33
Q

How to you TREAT ectropion?

A

-often not necessary since the UPPER eyelid (not the LOWER) is mainly responsible for blinking/protecting the eye
-lubricating ointments
-antibiotic or steroid ointments
-wedge resection

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34
Q

Meibomian Gland Tumors are tumors of the EYELID in the dog. What are its CS?

A

-papilloma like projection from eyelid margin (friable)
-swelling affected gland
-upper lid more common
-variable in size
-blepharospasm if ulcer present
-metastasis VERY rare

USUALLY BENIGN
Age-related (usually only over 9yr)

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35
Q

What neoplasias can dogs get of the eyelid?

A

-meibomian glad tumors (adenoma/epithelioma)
-melanoma
-lymphoma

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36
Q

How do you DIAGNOSE Meibomian Gland Tumors?

A

-signalment (specifically age)
-CS
-confirm with biopsy

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37
Q

What is the most common Eyelid Neoplasia in a cat?

A

Squamous cell carcinoma

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38
Q

CS of Squamous cell carcinoma

A

-ulcerative lesion
-lower lid
-white or lightly pigmented
-metastasis late

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39
Q

What causes Squamous Cell Carcinoma?

A

-lack of eyelid pigmentation
-UV exposure

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40
Q

How do you DIAGNOSE Squamous Cell Carcinoma?

A

-clinical signs
-cytology (eyelid scraping)
-biopsy

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41
Q

How do you TREAT Squamous Cell Carcinoma?

A

-RADIATION super effective (Sr90) - kills superficial cells
-surgical excision
-cyrotherapy

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42
Q

What is distichiasis? Which breeds are pre-disposed?

A

-when meibomian glands produce a hair follicle/cilia emerges from meibomian gland duct

-breed related - american cocker spaniels, golden retrievers

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43
Q

CS of Distichiasis

A

-fine hairs emerging from eyelid margin

-difficult to see without magnification

-usually does not cause dz

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44
Q

What CAUSES Distchiasis?

A

-inherited
-developmental

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45
Q

How do you DIAGNOSE Distichiasis?

A

-signalment (breed)
-CS

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46
Q

How do you TREAT Distichiasis?

A

-manual epilation (to remove hair from root) initially to confirm diagnosis - but it will grow back
-cyrotherapy

treatment will always damage/destroy meibomian gland – so can lead to tear deficiency

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47
Q

What is ectopic cilia?

A

-cilia from meibomian gland BUT it protrudes through the palpebral conjunctiva

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48
Q

CS of Ectopic Cilia

A

-marked blepharospasm
-epiphora
-vertically linear superficial cornea
-raised papilla (12 o’clock transition in upper eyelid) - raised area around hair

-Corneal Ulcer @ a 12 o’clock POSITION - tell tale sign

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49
Q

What CAUSES ectopic cilia?

A

-inherited
-developmental

you’ll see it in young animals, not older

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50
Q

How do you DIAGNOSE ectopic cilia?

A

-signalment
-history
-CS
-finding the cilium

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51
Q

How to you TREAT Ectopic Cilia?

A

-excision
-cryoptherapy

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52
Q

Ectopic Cilia is the most offensive eye issue? T/F

A

True

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53
Q

What is TRICHIASIS?

A

-hair from normal site coming in contact with the ocular surface

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54
Q

Signalment for Ecoptic Cilia

A

-8-12 months (young animals, never old)

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55
Q

What breeds are predisposed for Trichiasis

A

more frequently in dogs
-brachycephalic
-yorkshire terriers
-poodles
-breeds with long facial hair

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56
Q

CS of Trichiasis

A

-periocular hair touching ocular surface
-medial canthus, nasal folds
-usually does not cause irritation
-often wicks tears onto face

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57
Q

What CAUSES Trichiasis?

A

-breed related (essentially smaller breed dogs with longer hair)
-conformational

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58
Q

How do you DIAGNOSE Trichiasis?

A

-signalment
-CS

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59
Q

How do you TREAT Trichiasis?

A

-usually not indicated
-cryotherapy
-lid surgery

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60
Q

What are some TRAUMATIC INJURIES to the eye?

A

-abrasions (first aid care)
-full thickness lacerations (require repair)

-lateral aspect of upper lid most frequent
-check patency of nasolacrimal system if medial

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61
Q

CS of Traumatic injuries fo the eye

A

-lacerations, obvious trauma
-important to examine underlying globe

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62
Q

2What CAUSES Traumatic injuries?

A

-fight wounds
-environmental objects

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63
Q

How do you DIAGNOSE Traumatic injuries?

A

-CS

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64
Q

How do you TREAT Traumatic eye injuries?

A

-minimal debridement
-2-layer closure for laceration
–obicularis oculi m - holding layer
–skin - careful realignment of margin
-identification, reconstruction of inferior nasolacrimal system
-systemic, topical antibiotics

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65
Q

What is Bacterial Blepharitis?

A

-overgrowth of eye surface bacteria – ascends into eyelid via meibomian gland ducts

-staphylococcus and streptococcus spp.
-satphylococcus toxins exacerbate

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66
Q

CS of Bacterial blepharitis

A

-severe eyelid swelling
-blepharospasm
-excoriation
-alopecia
-mucopurulent discharge
-granuloma formation
-bilateral (dogs)
-recurrent (dogs)

puffy painful eyes

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67
Q

What CAUSES bacterial blepharitis?

A

-infection from ascending bacteria
-fight wounds

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68
Q

How do you DIAGNOSE Bacterial blepharitis (see Lecture 33-34, slide 65)

A

-CS
-biopsy
-culture and sensitivity

-squeeze eyelids – stuff from meibomian glands

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69
Q

How do you TREAT Bacterial Blepharitis?

A

-topical antibiotic/steroid
-oral antibiotics
-oral prednisone
-warm compresses

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70
Q

What is Chalazion?

A

-the obstruction of meibomian ducts > accumulation of meibum

-the gland can rupture

-lipgranulomatous inflammation

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71
Q

CS of Chalazion

A

-nodular swelling within lid
-no inflammation
-no pain
-yellow/white appearance through palpebral conjunctiva (lipid material)

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72
Q

What CAUSES Chalazion?

A

-obstruction of meibomian duct due to inflammation, infection, etc.
-age-related

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73
Q

How do you TREAT Chalazion?

A

-curettage of gland
-topical antibiotic/steroid

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74
Q

What is Agenesis of the eyelid? (cats)

A

-when the eyelid does not develop fully/correctly

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75
Q

CS of Agenesis of the eyelid (see Lecture 33-34 slide 72)

A

-absence of lateral 1/2 to 2/3 upper eyelid
-trichiasis
-always BILATERAL, not not symmetric
-may have exposure keratitis (inflammation of cornea)
-may have other developmental abnormalities

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76
Q

What CAUSES agenesis?

A

-heritable
-developmental

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77
Q

How do you TREAT Agenesis?

A

-topical ointments - keep cornea comfortable/smooth
-cyrotherapy - limit trichiasis which can be secondary issue
-surgical blepharospastic procedures – surgery techniques not great

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78
Q

What is neonatal ophthalmia?

A

-infection under the eyelids before they open (around 10-14 days after birth)

-usually from staph, strept, or feline herpes

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79
Q

CS of Neonatal ophthalmia

A

-inflamed, distended eyelids
-purulent discharge
-conjunctival hyperemia, chemises
-corneal ulceration

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80
Q

What are the 4 functions of the tear film?

A
  1. provides nutrients, oxygen, growth factors, electrolytes (aqueous) (bc cornea doesn’t have blood vessels)
  2. protect from desiccation and bacteria (lipid and mucous)
  3. lubricate surface, eyelid movement, remove debris
  4. provide smooth and transparent ocular surface
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81
Q

What are the 6 components of the Lacrimal Functional Unit?

A
  1. lacrimal gland
  2. gland of the 3rd eyelid
  3. conjunctiva
  4. meibomian glands
  5. cranial nerves (V + VII)
    -CNV - senses dryness, tars are produced and mediated by CNVII and CNV again
    -so dysfunction of these nerves and lead to decreased sensation and or decreased tear production
  6. nasolacrimal duct
    -take tears to nasal cavity and +/- back of mouth
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82
Q

Lipid layer of tear film is made by the _______ ______.

A

Meibomian glands

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83
Q

The aqueous layer of the tear films is by the _________ ____ and the _______.

A

Lacrimal gland and the 3rd eyelid

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84
Q

The mucous layer of the tear film is made from the ________

A

Goblet cells

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85
Q

What is the location of the lacrimal gland?

A

Dorsolateral orbit

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86
Q

What innervates the lacrimal gland/What CNs are involved in the lacrimal duct?

A

Sensory: CNV - Ophthalmic branch - SENSES DRYNESS - input goes to brain then…

Parasympathetic (how tears are made): CNVII (until pterygopalatine ganglion) then CNV via lacrimal nerve

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87
Q

What is the location of the gland of the 3rd eyelid?

A

-inferior and posterior aspect third eyelid

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88
Q

Where are the Goblet cells located?

A

throughout conjunctiva

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89
Q

Goblet cells make mucous. What is the function of the mucous component of the tear film?

A

-anchor tear film to surface of eye
-collect pathogens and debris on surface

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90
Q

Where are the Meibomian Glands located?

A

-within the upper and lower eyelids
-secretes meibum (lipid)

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91
Q

Meibomian glands secrete the lipid component of the tear film. What is the function of the lipid?

A

-prevents tear evaporation
-provides tear film quality

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92
Q

What does the Nasolacrimal Duct play a part in?

A

-tear drainage

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93
Q

Where do tears accumulate?

A

-inferior conjunctiva sac

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94
Q

What is the pathway of tears?

A
  1. accumulation of tears in the Inferior Conjunctiva Sac
  2. Lacrimal Puncta (during blinking)
  3. Canaliculi
  4. Lacrimal Sac (in lacrimal fossa)
  5. Nasolacrimal Duct
  6. Nasal or Accessory Punctum
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95
Q

What are the CS of Tear Disorders?

A

-blepharospasm
-ocular discharge (epiphora, mucoid, mucopurulent, thick/tenacious discharge)
-conjunctival hyperemia
-3rd eyelid hyperemia
-corneal dz (vascularization, fibrosis, pigmentation)

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96
Q

There are many Tear Film Diagnostics? What does the Schirmer Tear Test measure? (STT)

A

-measures aqueous component of tears
–basal tear production
–reflex tear production
–tear lake (tears that are already there)

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97
Q

What factors affect the Schrimer Tear Test?

A

-age
-diurnal effects
-medications (atropine, TMS/sulfonamides - decrease tear production)
-endocrinopathies
-surgical excision of the gland of 3rd eyelid – DON’T DO THIS

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98
Q

What is a normal Schirmer Tear Test for dogs? Cats?

A

Dog: >15mm/min
Cat: >9mm/min

Dog grey zone: 10-15mm/min
Dog low zone: <10mm/min

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99
Q

There are many tear film diagnostics. What does the TEAR FILM BREAKUP TIME (TFBUT) measure?

A

-measure qualitative factors of the tear
-assesses stability of tear

-use fluorescein droplet to the cornea
-“breaks” in the film = exposed corneal epithelium

-very SUBJECTIVE

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100
Q

You can implement Tear Film Imaging. What does Optical Coherence Tomography evaluate/measure?

A

-evaluate/measure the tear meniscus (pooling of tears on the lower eyelid)
-can measure height or area of meniscus

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101
Q

What is Keratoconjunctivitis sicca?

A

-dry eye

-quantitative tear deficiency
-reduced aqueous tear production

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102
Q

CS of KCS

A

-mucoid discharge
-blepharospasm
-conjuncitval hyperemia
-conjunctival chemosis
-corneal vascularization
-corneal melanosis
-lackluster cornea

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103
Q

What CAUSES KCS in dogs? (8)

A
  1. IMMUNE MEDIATED – most common
    -bilateral KCS
    -breed dispositions - West Highland White Terriers, English Bulldogs
  2. NEUROGENIC
    -CNV and CNVII
  3. ENDOCRINE DZ
    -diabetes mellitus
    -hyperadrenocorticism
    -hypothyroidism
  4. TRAUMA
  5. INFECTIOUS DZ
    -lacrimal adenitis
    -canine distemper
  6. TOXIC/DRUG INDUCED
    -systemic sulfa-derivatives (TMS)
    -ATROPINE
    -anesthesia, sedation
  7. CONGENITAL
  8. IATROGENIC
    -excision of the gland of the 3rd eyelid
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104
Q

How do we DIAGNOSE KCS?

A

-hx
-CS
-Schirmer Tear Test

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105
Q

How do we TREAT KCS?

A
  1. Immunomodulating Agents (different from anti-inflammatory drugs)
    -cyclosporine (Optimmune) - FDA approved, must use first
    -tacromilus
  2. Topical tear replacement
    -many commercially available
    -viscous solution and gels
    -preference for higher amounts of hyaluronate
  3. Antibiotic/Steroid
    -Neomycin/PolymyxinB/Dexamethasone
    -ONLY USE IF NO ULCER PRESENT
  4. Surgery
    -parotid duct transposition
    -salvage procedure
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106
Q

There are Qualitative Tear Deficiencies. There are Qualitative MUCIN Tear Deficiency and Qualitative LIPID Tear Deficiency.

Why would a MUCIN deficiency happen?

A

-decreased goblet cells
-caused my chronic conjunctival inflammation
-feline herpesvirus 1 (FHV-1)

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107
Q

There are Qualitative Tear Deficiencies. There are Qualitative MUCIN Tear Deficiency and Qualitative LIPID Tear Deficiency.

Why would a LIPID deficiency happen? Remember, meibomian glands produce lipid.

A

-chronic blepharitis and meibomitis
-chemical burns
-severe eyelid cicatrization

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108
Q

How do we DIAGNOSE a Qualitative Tear Deficiency?

A

-hx
-CS
-eyelid examination
-Schirmer Tear Test
-TFBUT - tear film breakup time
-Meibometry

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109
Q

How do we TREAT a qualitative MUCIN tear deficiency?

A
  1. treat underlying cause (infection causing cicatricial change to conjunctiva)
  2. medical therapy
    -immunomodulatory (cyclosporine, tacrolimus)
    -topical tear replacement - w/ hyaluronate
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110
Q

How do we TREAT a qualitative LIPID tear deficiency?

A
  1. treat underlying case - inflammation of eyelids with damage meibomian glands (systemic abx/steroid therapy
  2. medical therapy
    -topical ointment therapy - white petrolatum
  3. additional therapy
    -warm compress – increases meibomian secretions
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111
Q

CS of Nasolacrimal Duct Obstruction

A

-variable - complete or incomplete obx
-chronic epiphora
-mucopurulent discharge
-medial canthal swelling
-difficult to flush Nasolacrimal Duct

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112
Q

What CAUSES NLD Obstruction? (3)

A
  1. developmental
    -imperforate punctum or micropunctum (most common)
    -canalicular atresia (rare)
  2. Foreign Body obx
    -plant awns, sand
    -seasonal variance
  3. Inflammatory obx
    -inflammatory debris without FB
    -descending infection/inflammation
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113
Q

How do you DIAGNOSE NLD patency?

A
  1. Jones Test
    -fluorescein dye passage
    -look for passage of dye from eye surface to nares
  2. Nasolacrimal Flush
    -identify and relieve obx
    -saline or dilute betadine solution
    -22/20g canula
    -look for fluid emerging from ipsilateral nostril
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114
Q

How do you TREAT NLD Obx?

A

Developmental cause - surgical opening

FB obx cause - flushing, stenting

Inflammatory obx cause - flushing stenting

surgery
flushing
stenting

MEDICAL MANAGEMENT
-topical antibiotic
-oral NSAID
-4-6week tx
USE SOLUTION, not ointment – want to make sure things are getting through NLD

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115
Q

What are the 4 layers of the cornea? Which layers are hydrophobic (repel fluorescein stain) and which layers are hydrophilic/”stick” to it?

A
  1. Epithelium - hydrophobic
  2. Stroma -hydrophilic, stick to stain
  3. Descemet’s Membrane - hydrophobic
    -thickens with age
  4. Endothelium

Descemet’s Membrane and Endothelium indistinguishable – go together essentially

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116
Q

Cornea AND the lens play a part in refraction of light. T/F

A

True

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117
Q

Which is the thickest layer of the cornea? What does it contain?

A

STROMA

has:
-keratocytes (makes collagen fiber)
-collagen fibers

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118
Q

What are the functions of the cornea? (3)

A

-refraction
-protection of interior structure from injury/infection
-CLEAR medium for vision (aids in transmission visual input)

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119
Q

Why is the cornea transparent?

A
  1. avascular
  2. No pigment
  3. Non-keratinized epithelium
  4. Precise arrangement of collagen fibers
  5. Relatively dehydrated
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120
Q

CNV innervates the cornea, with most nerve endings in the epithelium/superficial cornea. Which dog breeds have decreased sensitivity to the cornea?

A

-Brachycephalic

-diabetic dogs

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121
Q

Explain the Axonal Reflex – why do you get REFLEX UVEITIS if you have a corneal ulcer?

A

-stimulation of corneal nerves –> reflex stimulation of CNV, which branches to the anterior uveal tract

-with an ulcer, you have constant stimulation of CNV, thus constant spasm of the ciliary muscles –> thus, resulting in REFLEX UVEITIS (inflammation)

REFLEX UVEITIS is painful – bc of ciliary muscle spasms

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122
Q

What are the 3 essential steps in epithelial healing in corneal ulcers? Remember – this would just be a superficial layer if it ONLY required epithelial healing.

A
  1. slide (sliding of epithelial cells from adjacent epithelium and limbus)
  2. divide (proliferation)
  3. adhere
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123
Q

What are the 4 essential steps in STROMAL healing?

A
  1. arrest collagenolysis
  2. fibroplasia
    -keratocyte activation
    -fibrovascular ingrowth
  3. remodeling
  4. epithelialization
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124
Q

How long does it take for simple corneal ulcers to heal?

A

7 days

can take up to 6 weeks for epithelial cells to adhere to basement membrane

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125
Q

Corneal Ulcers can either be ______ or ________.

A

Simple or complicated

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126
Q

What makes up a simple corneal ulcer? (4)

A
  1. Superficial (Lecture 37-38, slide 19)
  2. not infected
  3. heals in appropriate amount of time (7 days)
  4. No complicating factors

Complicating factors are:
-Entropion
-KCS (dry eye)
-Eyelid tumors
-Lagophthalmos
-Ectopic cilia
-Trigeminal neuropathy
-Systemic disease (ie. Cushings, diabetes mellitus)
-Distichiasis

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127
Q

What makes up a complicated corneal ulcer?

A

-deep (loss of stroma) (Lecture 37-38, slide 25)
-infected melting
-other complicating factors
-slow to heal

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128
Q

What is a Descemetocele?

A

Lecture 37-38, slide 26

-when the Descemet’s Membrane is exposed (epithelium and stroma loss)
-DM may bulge due to pressure from Aqueous Humor
-will see a fluorescein donut, bc dye will not stick to DM, but will stick to stroma

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129
Q

How does corneal perforation present?

A
  1. fibrin plug
  2. iris prolapse
  3. active leakage
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130
Q

Why does the cornea melt with complicated ulcers? (It becomes a deep ulcer)

A

A melting cornea means you have degradation of the stromal collagen.

An insult to the cornea increases enzymatic activity, specifically Matrix metalloproteinases (MMPs) and Serine protease (NE). Body should be able to bring the increased enzymatic activity back to normal levels. But sometimes it is not enough. -> degredation

looks like a gelatinous appearance

Bacteria, Fungi, and WBCs and contribute to the degradation.

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131
Q

You get mydriasis or miosis with uveitis?

A

MIOSIS – bc of ciliary body spasms/inflammation acting on the iris sphincter muscles

contraction of the iris sphincter schusses chases miosis

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132
Q

What DIAGNOSTICS can you run with a Corneal Ulcer?

A
  1. Rule out infection with CULTURE or CYTOLOGY
  2. STAIN the eye

-stain every eye that shows sign of pain

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133
Q

What’s the medical therapy of corneal ulcers? (The 5 As)

A
  1. Antiprotease - reduce tear protease activity
  2. Antibiotic - prevent/treat
  3. Atropine - treat reflex uveitis – PAIN
  4. Analgesia -
  5. Address Cause - treat etiology
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134
Q

What is the MEDICAL THERAPY for SIMPLE Ulcers?

A
  1. Broad-spectrum topical antibiotic TID - QID (until healed)
    • Prevent infection!
    • Broad-spectrum, non-epitheliotoxic
    • Neomycin, Polymyxin B, Bacitracin (NPB), Gramicidin (NPG)
  2. Treat reflex uveitis
    • Topical atropine 1% (once at office or SID)
    • Oral NSAID (~ 5 days) (+/-)
  3. Analgesia (+/-)
  4. Anti-protease (+/-)
  5. Prevent self-trauma
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135
Q

What is the MEDICAL THERAPY for COMPLICATED Ulcers?

A
  1. Anti-protease: (q1-6h)
    • Serum, plasma, EDTA, NAC, Tetracyclines
  2. Antimicrobials:
    • Based on culture/cytology – q2-4h
    • Antibiotic
    • Antifungals (LA)
  3. Treat reflex uveitis
    • Topical atropine 1% solution BID - QID
    • Oral NSAIDs
  4. Provide analgesia
  5. Consider surgical stabilization
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136
Q

What general topical antibiotics would we consider for the eye?

A

-Gram-positive: Cefazolin 33mg/ml; fluoroquinolones (oflox/ciprofloxacin), TAB
-Gram-negative: Tobramycin; gentamicin; fluoroquinolones, TAB

-all antibiotics DAMAGE epithelial cells

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137
Q

Do we use steroids when treating corneal ulcers?

A

NO NEVER DON’T YOU DARE

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138
Q

When do we consider SURGICAL STABILIZATION of a corneal ulcer? What does it entail?

A

-surgically stabilize when stromal loss is >50% of corneal thickness

-vascular support
-fibroblasts
-physical support
-conjunctival grafts
-biological grafts (amniotic membrane, urinary bladder, sub-intestinal mucosa, corneal graft)

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139
Q

Which breeds are predisposed to have Lagopthalmos?

A

-shitz zhu
-pugs

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140
Q

When in doubt, question the ______, not the ______.

A

Question the DIAGNOSIS, not the TREATMENT.

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141
Q

What are Canine Indolent Ulcers?

A

-aka Boxer ulcer, non healing ulcers, SCCEDS (spontaneous chronic corneal epithelial defect syndrome)

-chronic blepharospasm, epiphora, photophobia
-painful
-superficial corneal ulcer with epithelial lip
-flurosecin diffuses under epithelium

-ulcer waxes and wanes – or ulcer doesn’t heal
-CAN get infected but not common

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142
Q

PATHOGENESIS of Canine Indolent Ulcers

A

-Epithelium is growing, but just CANNOT stick to the basement membrane.
-no adhesion between epithelium and basement membrane and underlying hemidesmosomes

-hyaline membrane forms over ulcer with chronicity – which is why epi doesn’t stick to basement membrane

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143
Q

How do you TREAT Canine Indolent Ulcers?

A
  1. Cotton Tip Applicator debridement (CTA debridement)
  2. CTA debridement + grid keratotomy
  3. CTA debridement + diamond burr debridement

Purpose: remove non adhered epithelium (CTA) and disturb hyaline membrane (grid keratotomy)

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144
Q

What does a Grid Keratotomy entail? What’s its purpose?

A

-25g needle

-create lines with needle across ulcer bed
-should only involved 1mm of cornea

-purpose - disturb hyaline membrane, create area for epithelium to attach and dive into stromal area

-85-95% success rate

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145
Q

When is a Grid Keratotomy contraindicated?

A

-complicated ulcers (infection, melting, stromal loss, deep ulcers, descemetocele)
-cats
-horse

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146
Q

With the DIAMOND BURR DEBRIDEMENT, is it safer that a Grid?

A

Yes, diamond burr debridement is safer than a grid keratotomy.

it creates fine abrasions in anterior stroma

85% success rate
heals in about 12 days

MUST GO FROM EDGES to center, to know where to stop debriding/know margins

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147
Q

What do you want to implement post treatment for ulcers?

A
  1. hard e-collar
  2. broad spectrum antibiotic (triple antibiotic/ofloxacin)
  3. atropine
  4. analgesia
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148
Q

How does Feline Herpes Virus 1 cause ulcers?

A

-it is the most common cause of ulcers in cats
-a dendritic ulcer is a classic sign of FHV1 (but they don’t have to be dendritic)

-FHV1 causes ulcers bc the virus lies dormant in neurons – and its elicited by a stressful event –> the virus targets epithelium cells as they grow/multiply (thus the eye)

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149
Q

How do you TREAT FHV1?

A
  1. topical anti-viral therapy (cidofovir, idoxuridine, trifluridine)
  2. systemic anti-viral therapy (if respiratory signs present)
    -famciclovir
    -L-lysine
  3. minimize stress
150
Q

What are WHITE Corneal Dz?

A
  • Dystrophy
  • Degeneration
  • Fibrosis
  • Keratic precipitates
151
Q

What does Corneal Dystrophy - White Corneal Dz entail?

A

see Lecture 37-38 slide 79-80

opacities on cornea, crystalline opacities, mineral deposit under epithelium usually

•Bilateral (not always bilaterally symmetric, so one side shows up first)
•Purebreds (cavaliers, dachshunds
•Non-painful
•Non-progressive
•NO TREATMENT
•Does not interfere with vision
•Recommend against breeding?
•NO vessels present

152
Q

What does Corneal Degeneration - White Corneal Dz entail?

A

see pics Lecture 37-38, slide 81

•Uni or bilateral
•Usually asymmetric
•Lipid / Mineral deposits in cornea
•May be secondary to systemic alterations
–Hypothyroidism, hyperlipidemia
•Vascularization a frequent finding (vessels are present)
•Often associated with ulceration of overlying epithelium

153
Q

What is the TREATMENT for Corneal Degeneration?

A

•Identify any concurrent ocular or systemic diseases and treat it!
•check Lipid panel
•Change diet (change to low fat diet)
•If mineral - EDTA topically since it chelates calcium
•Fair to guarded prognosis

154
Q

What does Corneal Fibrosis - White Corneal Dz entail?

A

•Fibrosis: disorganized collagen (scar) - from previous ulcers
•Previous keratitis
•Usually associated with vascularization
•Non-painful
•Variable effect on vision depending on size of lesion
•NO TREATMENT, can’t remove the scar

155
Q

What does Keratic Precipitates - White Corneal Dz entail?

A

•Clumps of inflammatory cells/protein/fibrin adhered to the endothelium when you have Uveitis – NOT KERATIN!!!
–inside eye, affects cornea
•Can also look tan or brown if chronic (accumulate pigment with time)
•Pathognomonic for anterior uveitis
•NOT corneal disease – just means there’s inflammation or WAS inflammation in the eye

156
Q

What does BLUE corneal color mean?

A

EDEMA

157
Q

What 2 barriers prevent water/fluid from getting/building up into eye?

A

Epithelium - prevents tears from getting into eye
Endothelium - prevents aqueous from getting into eye
-also has pump, so active barrier that removes water from stroma

158
Q

Where can edema come from?

A

-Epithelium via cornea
-Endothelium via endothelial dz
-Vessels – if you have corneal vascularization, then they can leak into eye

159
Q

What causes DIFFUSE CORNEAL EDEMA?

A

more focuses on endothelial issues

•Glaucoma
•Anterior uveitis
•Endothelial dystrophy / degeneration
•Immune-mediated endotheliitis
–“Blue-eye” -CAV I

160
Q

What causes FOCAL corneal edema?

A

more focused on vessels and epithelium…

•Ulcerative keratitis
•Non-ulcerative keratitis (vessels)
•Keratic precipitates
•Anterior lens luxation

161
Q

Can Corneal Edema cause vision loss?

A

YES

162
Q

What are the Primary Endothelial Dz that can cause Corneal Edema?

A
  1. Corneal endothelial dystrophy (CED)
    •Breed-related (Boston terriers, German wirehaired pointers, Dachshunds)
    –GENETICS, inherited
    •Middle-aged dogs when presenting
    •Starts laterally, progressive towards generalized
    •TREATMENT: Corneal transplant
  2. Endothelial degeneration (senile, traumatic)
    •Geriatric dogs
    •Secondary to intraocular inflammation/surgery (phaco)
163
Q

How do we TREAT Corneal Edema?

A

•Treatment depends on cause
•Treatment of the primary disease
•Primary endothelial disease
–requires unique treatment – give new endothelium via transplant
–guarded prognosis

•Topical hyperosmotics - get fluid out
–5% saline (ointment better than solution) - TID to QID
–30 minutes apart from other medications
•Rho Kinase inhibitors (ROCK) - available in Japan
–endothelium regeneration?
–Netarsudil (Rhopressa®)
–Repasudil (Glanatec®)

164
Q

Other Treatments for Endothelial Dz

A

•corneal transplant (boo)

•Thermokeratoplasty
–Cautery of the superficial stroma - fibrosis, prevents water from getting into eye

•SKCAHF
–Superficial keratectomy and conjunctival advancement hood flap (remove layer of cornea, and conjunctiva graft – vessels from conjunctiva will absorb fluid, but cornea won’t be clear)
–Helps absorb some edema from cornea

165
Q

What is RED corneal dz?

A

-Blood vessels
-Granuloma
-Hemorrhage
-Neoplasia (can be any color)

166
Q

Blood vessels in the eye means _______

A

there was inflammation from an insult.

it’s non-specific

167
Q

What is Eosinophilic Keratitis? (LOOK at Lecture 39, slide 4-5)

A

• Predominantly feline immune-mediated disease
• May be related to FHV-1
• Seasonally recurrent

168
Q

CS of Eosinophilic Keratitis

A

Clinical signs
• Raised pink/white plaques on cornea or conjunctiva
• Associated vascularization
• Ocular pain - variable
• Usually unilateral; may be bilateral

169
Q

How do you DIAGNOSE Eosinophilic Keratitis?

A

Cytology (eosinophils, mast cells)

170
Q

How do you TREAT Eosinophilic Keratitis? (5)

A

• Broad spectrum topical atb if ulcerated

• Cyclosporine A - suppress local immune system
–Slower response, safer for long term
–May need treatment for 8-12 weeks
–BETTER IF RECURRENCE

• Topical steroids
–DO NOT use if cornea is ulcerated
–May exacerbate FHV-1, steroids wake up the virus
–Less common treatment choice

• Subcutaneous triamcinolone
–Single dose
–Beneficial if ulcer present

• Megestrol acetate 0.5% ophthalmic suspension
–CAN use with ulcer

171
Q

What is Pannus?

A

AKA chronic superficial keratitis

GRANULATION tissue on cornea that can affect vision

• Immune-mediated corneal disease
• German shepherds and sighthounds (italian greyhounds, whippets)
• Both sexes, middle-age (starts at ~4/5yo)
• Non-painful, progressive, exacerbated by exposure to UV light and high altitudes (thinks Colorado hiking dog)

172
Q

CS of Pannus

A

• Superficial vascularization (STARTS LATERALLY, progresses axially)
• Pigmentation follows vessels
• Fibrosis

173
Q

How do you TREAT Pannus? (3)

A

• Topical steroid - start with this, then taper
–Dexamethasone or prednisolone

• Topical immunemodulators
–Cyclosporine A 1-2%
–Tacrolimus 0.03%
–Great for long term management

• Subconjunctival CsA implant (Cyclosporine Implants)

• Treatment is lifelong!

174
Q

What is BROWN Corneal Dz?

A

it’s MELANOSIS

-pigment
-neoplasia (melanoma)
-sequestrum
-iris prolapse
-foreign body

175
Q

Pigment is a sign of ______

A

chronic corneal dz (non-ulcerative keratitis or as part of healing process in ulcerative keratitis)

176
Q

What is Pigmentary/Exposure Keratits?

A

inflammation of the cornea due to eye being exposed/not protected – chronic exposure of the eye

• usually non-ulcerative keratitis (NO ulcers)

• Brachycephalic breeds, also facial paralysis (since dogs can’t blink), exophthalmia

• Usually due to macroblepharon, breed related exophthalmia, lagophthalmia, decreased corneal sensation, decreased tear production
–Leads to tear film evaporation / poor protection

• Development of pigmention, vascularization, fibrosis

• May cover entire cornea
–blindless
–Hard to eliminate pigment once it occurs
–Prevent it!!

177
Q

CS of Pigmentary/Exposure Keratitis

A

• Corneal vessels, melanosis/pigmentation, fibrosis
• Usually medially, or where irritation is located
• May lead to ulcers

178
Q

What CAUSES Pigmentary/Exposure Keratitis?

A

• Conformation, breed related (brachys)
• Age related (young, but not pups)
• Eyelid conformation (macroblepharon, breed related exophthalmia, lagophthalmia, decreased corneal sensation, decreased tear production)

179
Q

How do you DIAGNOSE Pigmentary/Exposure Keratits?

A

-signalment
-history
-signs

180
Q

How would you MEDICALLY MANAGE Pigmentary/Exposure Keratitis?

A

• Correct the cause (KCS, eyelid coformation, etc)

• Lubricants
–protect cornea from tear evaporation

• Immunomodulatory medications
–Cyclosporine A
–Tacrolimus

• Treatment will be lifelong

181
Q

The uvea is part of which layer of the eye/which tunic?

A

The Vascular Layer (Middle layer)

182
Q

The uvea is split into the anterior and posterior uvea. What does the anterior uvea contain?

A

-Iris (Anterior border - no epithelium, stroma)
-iris muscles
-ciliary body
-ciliary body processes

183
Q

What are the parts of the Iris? (4)

A
  1. Anterior border - no epithelium
    -fibroblasts
    -mleanocytes
  2. stroma
    -blood vessels
    -collagen fibers
    -fibroblasts
    -melanocytes
  3. Posterior epithelium - PIGMENTED
    -densely melanotic
    -iris atrophy
    -posterior synechia of lens
  4. iris muscles (sphincter and dilator)
184
Q

Which iris muscle is in charge of pupil constriction?

A

Iris sphincter muscle
-when contracts -> miosis – makes pupil smaller
-stronger than dilator
-CNIII
-parasympathetic
-circular orientation (contraction closes in on pupil)

185
Q

Which iris muscle is in charge of pupil dilation?

A

Iris Dilator muscle
-when contracts -> mydriasis – makes pupil larger
-sympathetic
-radial orientation (contraction stretches open pupil)

186
Q

What does Synechia mean?

A

Iris is adhered to something else

-anterior synechia (iris attached to cornea)
-posterior synechia (iris attached to lens)
-iris to iris synechia

187
Q

What is the ciliary body?

A

It is a part of the anterior uvea.

Muscle in charge of accommodation of eye (to change focus)

It has a lot of muscles and is controlled by the parasympathetic system/CNIII

When there is inflammation, there will be a lot of pain bc of muscle spasms

Dilation means your ciliary body muscles are relaxed and you can’t focus

188
Q

What are ciliary body processes?

A

-where lens zones attach (anchors lens to ciliary body, holds lens in place)

2 layers of processes:
1. pigmented epithelium (PE) (inner portion)
2. non-pigmented epithelium (NPE)
-contains carbonic anhydrase -> produces aqueous humor
-problem with ciliary body, aq. humor is gone
-part of Blood Aqueous Barrier, epithelium portion

189
Q

We have two main blood eye barriers. What are they called?

A

BAB - Blood Aqueous Barrier (prevents things entering into aqueous from ciliary body)
BRB - Blood Retinal Barrier

barriers prevent protein and molecule movement into eye

190
Q

Blood Aqueous Barrier has an epithelial and endothelial portion. What are the differences?

A

Epithelial Portion: does NOT allow any crossing – tight junctions of non-pigmented epithelium of ciliary body

Endothelial Portion: a little more fenestrated
-iridal vessels - a little can pass, but non fenestrated
-ciliary body vessels - located in storm, fenestrated

191
Q

Blood Retinal Barrier has an epithelial and endothelial portion. What are the difference?

A

Epithelial Portion: tight junctions retinal pigmented epithelial cells

Endothelial portion:
-retinal capillary endothelium - non fenestrated
-choroidal capillaries - highly permeable

192
Q

What are the functions of the anterior uvea?

A
  1. regulates light entry (pupil size)
  2. Blood aqueous barrier
  3. accommodation (focus/refraction)
  4. producing aqueous humor
193
Q

General CS of anterior uvea dz

A

• Change in appearance iris
• Change in pupil shape
• Change in aqueous
• Secondary effects on cornea
• Secondary effects on lens
• Secondary effects on globe

194
Q

Signalment of Uveal Cysts? (lecture 40-41, slide 24-25) - congenital uveal dz

A

-congenital, but not present at birth (embryology-related) – not present at birth bc cyst isn’t “full/filled up” yet
-middle-aged

195
Q

CS of Uvea Cysts

A

• Round structures
• Darkly pigmented vs transparent
• 3 locations:
–Attached posterior surface iris/ciliary body
–Attached to

lary margin
–Free floating in anterior chamber

196
Q

What CAUSES uveal cysts?

A
  1. idiopathic
  2. secondary to inflammation
197
Q

How do you DIAGNOSE Uveal Cysts?

A

• differentiate from neoplasia (could be a single mass attached to anterior face of iris)
-Location
-Shape
- +/- Transillumination
• Ultrasound

if free floating not a melanoma
melanomas attached to iris usually have a broad base

198
Q

How do you TREAT uveal cysts?

A

-usually not necessary
-can have inflammation if cysts rupture
-monitor IOP - if cysts are in anterior chamber, it can affect the drainage of aqueous humor by blocking ICA -> thus increasing IOP
-can do surgery to remove cysts

199
Q

What is a Persistent Pupillary Membrane? (PPM) - congenital uveal dz

A

-a condition of the eye involving remnants of a fetal membrane that persist as strands of tissue crossing the pupil (attachment of iris to iris across pupil)

-normal development structure
-normally regresses late gestation/early postnatal

200
Q

CS of PPMs?

A

• Originate at collarette of iris (middle portion of iris - NOT the pupil margin and NOT the periphery)
–if you see bits of the iris coming from the pupil margin or the periphery – then most likely synechia

• Iris to iris (normal in horses)
• Iris to anterior lens capsule (opacity)
• Iris to posterior cornea (opacity)

201
Q

What CAUSES PPMs?

A

• Heritable in certain breeds (Basenjis)
• Developmental defect

202
Q

How do you DIAGNOSE PPMs?

A

CS

203
Q

What is the TREATMENT for PPMs?

A

• Usually not indicated
• Iris to lens > cataract surgery

204
Q

What is Iris Atrophy? (acquired uvea abnormality)

A

-normal aging change
-can be very prominent in dogs

-bc muscles get weak and thin – if atrophy of muscle AND stroma, you’ll see holes

-can affect PLRs (ex. atrophy affects sphincter muscle)

205
Q

CS of Iris Atrophy (Lecture 40-41, slide 34)

A

• Scalloping at pupil margin (affects sphincter muscles since that’s where sphincter m. is located)
• Moth eaten appearance to iris stroma
• Slow, incomplete PLRs
• Anisocoria
• Dyscoria (change of shape of pupil)

206
Q

What is the CAUSE of Iris Atrophy?

A

-age-related
-chronic anterior uveitis

207
Q

How do you DIAGNOSE Iris Atrophy?

A

Signalment (old age)
CS

208
Q

How do you TREAT Iris Atrophy?

A

not indicated, can’t put iris back in eye, no iris transplant

209
Q

Uveal Neoplasia - What are primary uveal neoplasia?

A

-Melanoma/melanocytoma - most common
-Ciliary body adenoma

more common in dogs and cats

210
Q

Uveal Neoplasia - What are secondary uveal neoplasia?

A

Lymphomas (can also affect corneas too)

more common in cats

211
Q

CS of Uveal Neoplasias

A

• Melanoma
–Arise from anterior surface iris, raised/elevated
–Cats have multiple dark spots multiply, coalesce

• Ciliary body adenoma/carcinoma
–Fleshy mass through pupil

• Lymphoma
–Nodules, multiple or singular

212
Q

Melanocytomas (being behavior) are more common in ______. Melanomas (malignant) are more common in ____.

A

Melanocytomas - dogs
Melanomas - cats

213
Q

What can cats have that trick you into thinking it’s NOT a melanoma? lecture 40-41, slide 42

A

Feline diffuse iris melanoma – quiet tumor that can spread - MALIGNANT

214
Q

What is Iris Melanosis? Can easily get mixed up with Iris MELANOMA

A

-benign
-pigment deposition on anterior surface of iris
-flat
-amber coloration
-no changes of pupil
-no changes in PLR
-no therapy needed

215
Q

What is Iris Melanoma? Can easily get mixed up with Iris MELANOSIS

A

• Tumor
• Raised, irregular surface – can also be flat in beginning
• Dark brown / black, but can start as amber
• Leads to dyscoria, but not always
• Change in pupil shape
• May affect PLR
• Malignant (metastasis) always – slowly metastatic
• Enucleation recommended

216
Q

What’s the definitive diagnostic for iris melanoma vs iris melanosis?

A

histopathology

217
Q

What is a ciliary body adenoma? lecture 40-21, slide 45

A

-fleshy mass through pupil

-benign
-usually not inflammatory
-locally expansive
-lead to glaucoma bc it pushed iris forward and kink ICA – reduces drainage

-sometimes need to dilate to see

-TX - can have surgery, but clients can just remove the eye

218
Q

What is Lymphoma in the eye? lecture 40-41, slide 46

A

-most common secondary neoplasia of the uvea
-nodules - multiple or singular
-severe uveitis - thickened iris

219
Q

How do you DIAGNOSE anterior uveal neoplasia?

A

CS
ocular ultrasound
histopathology (biopsy)

220
Q

How do you TREAT anterior uveal neoplasia?

A

usually enucleation - prior to glaucoma

-laser ablation - doesn’t remove tumor, kills blood vessels to tumor
-sector iridectomy - cut a piece of iris

221
Q

What is uveitis?

A

-inflammation of the uveal tract

-most common uveal disease
-all species
-recurrence common
-many causes
-most common ophthalmic manifestation of systemic dz

222
Q

What are the 3 types of uveitis?

A
  1. Anterior uveitis: iris + ciliary body inflamed
  2. Posterior uveitis: choroid inflamed (usually retina inflamed too)
    –Chorioretinitis: inflammation of choroid + retina (rare that retina is not involved)
  3. Panuveitis: iris + ciliary body + choroid
223
Q

What are NONSPECIFIC CS for acute/active anterior uveitis?

A

• Blepharospasm (sign of pain)
• Epiphora
• Enophthalmos - retrobulbar – pulling eye in
• Conjunctival hyperemia
• Episcleral injection
• Decreased IOP (initially)
• Corneal edema
• Corneal vascularization

224
Q

What are specific CS for acute/active anterior uveitis?

A

• Aqueous flare = uveitis!!!! proteins and molecules in aq. humor bc BAB is broken
• Miosis - PLR may not be evaluable
• Change in iris color
–Blue eyes turn yellow / green
• Hypopyon - accumulation of WBCs in aq humor
• Hyphema - RBCs in eye, blood in aq humor
• Keratic precipitates - inflammation
• Inflammatory cells in corneal endothelium
• Swollen, inflamed iris
• Rubiosis iridis – iris is more red

225
Q

What is Rubeosis Iridis?

A

red iris = uveitis!

226
Q

What are CHRONIC CS of anterior uveitis?

A

• Corneal scarring
• Anterior / Posterior synechia* (iris attached to lens)
• Iridal scarring*
• Iris bombé - posterior synechiae on pupil margin, so aq. humor can’t pass through pupil, so it bulges the iris forward (360 degrees synechia, aq humor cano’t flow thru)
• Cataracts
–(Uveitis is the main cause of cataracts in cats and horses)
• Secondary glaucoma
• Hyperpigmentation of iris

227
Q

What are CHRONIC CS of anterior uveitis?

A

• Corneal scarring
• Anterior / Posterior synechia* (iris attached to lens)
• Iridal scarring*
• Iris bombé - posterior synechiae on pupil margin, so aq. humor can’t pass through pupil, so it bulges the iris forward (360 degrees synechia, aq humor cano’t flow thru)
• Cataracts
–(Uveitis is the main cause of cataracts in cats and horses)
• Secondary glaucoma
• Hyperpigmentation of iris

228
Q

PATHOGENESIS of Anterior Uveitis?

A

•Damage to anterior uvea

•Release inflammatory mediators (Prostaglandins / IL)
–Increase vascular permeability
–Breakdown BAB
–Leakage protein, fibrin, cells into aqueous - lead to Aq Flare!

229
Q

What are the CAUSES of uveitis?

A

• Idiopathic (#1 cause)

• Primary ocular disease
–Corneal ulcer - Reflex uveitis
–Lens-induced uveitis -Cataract/Lens capsule rupture

• Trauma

• Ocular manifestations of systemic disease
-Infectious (bacterial, fungal, viral, etc)
-Metabolic (systemic hypertension)
-Immune-mediated (VKH)
-Neoplasia

230
Q

What is Lens-Induced Uveitis?

A

• Immune-privileged structure
• Formed BEFORE immune system
• Involved by lens capsule
• Lens fibers are non-self to immune system

lens was created before immune system, immune system is not familiar with cortex of lens
-so when cataract happens, cortex proteins leak and immune system reacts > leads to uveitis

-can also have rupture of lens capsule — invasion of lens proteins into anterior chamber > worse uveitis

231
Q

Consequences of Uveitis?

A
  1. cataract
  2. posterior synechia
  3. glaucoma
  4. retinal detachment
232
Q

How does uveitis cause glaucoma?

A

Mechanism 1: Obx of ICA
-if blocked, drainage of aq humor is obx, so increase in IOP
-inflammatory debris
-proteins
-WBCs
-RBCs
-neoplasia

Mechanism 2: PIFVM - Pre-Iridal Fibrovascular Membrane
-a fibrovascular membrane forms over iris
-thickens the ICA > prevents aq humor from being drained
-increase in IOP

Mechanism 3: Iris Bombe + anterior synechiae (peripheral)
-obliterate ICA, increase IOP
-aq humor can’t get out via ICA, and aq humor can’t get thru bc of anterior synechia

ex. say there is a dog eye with flare – you take an IOP and find it is 17 (a normal reading) – the dog has secondary glaucoma bc you got a normal pressure on an eye that’s super inflamed –> the pressure should be lower!

233
Q

How do you DIAGNOSE anterior uveitis?

A

-hx (vaccination, travel - bc think of bacterial of fungal organisms that differ in different areas)
-opthalmic exam

-physical exam
-minimum database - CBC, chem, UA
–imaging (thoracic rads, abd US)
–blood pressure (hyphema)
–infectious dz panel

234
Q

What are the 3 goals fo treating uveitis?

A
  1. prevent complications of uveitis (glaucoma, cataracts, synechia)
  2. eliminate intraocular inflammation
  3. stabilize and roster blood aqueous barrier
235
Q

What if the eye is blind and unresponsive to therapy (in terms of uveitis)?

A

-surgical removal (long term comfort for patient)
-cane take samples for culture/cytology

236
Q

How do you TREAT Uveitis?

A

• Topical anti-inflammatories
–Corticosteroids -Prednisolone acetate, Dexamethasone
–NSAIDs - Diclofenac, Flurbiprofen, ketorolac…

• Systemic anti-inflammatories
–Corticosteroids - Prednisone / prednisolone
–NSAIDs - Carprofen / Meloxicam / Robenacoxib

-topicals are preferred bc it acts faster
-steroids stronger than non-steroidal
-CANT use systemic steroid or NSAIDs together – will mess up kidney (every other combo is fine)

ATROPINE (no tweaky, no leaky, no synechie)
• Parasympatholytic, relax ciliary muscles, stop spasms
• Stabilize blood-aqueous barrier, makes vessels less leaky
–Blocks acetylcholine (which dilates blood vessels)
• Cycloplegic
–Stops ciliary spasms (pain)
• Mydriatic
–Prevents synechia
• CAREFUL!!! Check IOP FIRST!

237
Q

What is Lipemic Aqueous / Lipid-laden aqueous? (uveitis)

A

• Lipid in aqueous humor
• Milky-white appearance
• Fast onset
• Hyperlipidemia
–Triglycerides
–Cholesterol
• Acute, temporary blindness
• May lead to glaucoma - so tx decrease IOP
• Treat as regular uveitis + cause

238
Q

What is Uveodermatologic syndrome (VKH)? (uveitis)

A

• Vogt-Koyanagi-Harada Syndrome (VKH-like)

• Nordic breeds (Akita, Huskie, Samoyed, Malamute)

• Immune-mediated
–Auto-destruction of melanocytes (mucocutaneous junction and eyes)

• Eye-skin condition
–Eye (precede dermatological disease)
—Uvea (uveitis, retinal detachment, glaucoma) - blindness

–Skin - Vitiligo
—Mucocutaneous junctions (eyelids, lips), nasal planum
—Generalized (uncommon)

-lips and nose, start to get pink and get ulcerated

239
Q

How do you DIAGNOSE VKH?

A

• Most common: Signalment, Clinical signs
• Physical exam / CBC / Chem – normal
• Histopath
–Skin lesions: T-cell mediated
–Ocular lesions: B-cell mediated

240
Q

How do you TREAT VKH?

A

immunosuppressive dog for life

no cure

241
Q

What is pigmentary uveitis?

A

-AKA Golden Retriever Uveitis /Pigmentary and Cystic Glaucoma

-cause is unknown

242
Q

What breeds get pigmentary uveitis?

A

Golden Retrievers, Great Danes, American Bulldogs

243
Q

What are the CS of pigmentary uveitis? lecture 40-41, slide 87

A

• Pigment dispersion on anterior lens
capsule (radial orientation)
• Thin-walled uveal cysts
• Classic signs of uveitis
–Flare
–Fibrin in AC
–Cataracts (chronic)
–Posterior synechia (chronic)
• Glaucoma (chronic) – blindness
–Within 1 year (62%)

244
Q

How do you TREAT pigmentary uveitis?

A

-Regular uveitis therapy
–Topical anti-inflammatories
–+/- systemic anti-inflammatories

-monitor and control IOP

245
Q

What are the 2 main function of the lens?

A
  1. refraction - bends light to focus on retina
  2. accommodation - Changes shape or position of lends to focus light on the retina allowing visualization of near or far objects
246
Q

Why is the lens transparent?

A

Mechanisms of transparency
- Non-pigmented
- Avascular
- Precise organization of fibers

247
Q

Describe accommodation

A

Zonules hold the lens and the ciliary body - hold lens in place

ACTIVE: If the ciliary body muscles contract, zonules get loose. This results in making the lens smaller – MORE ROUND. Bends light and brings focus to front for near things. (example, reading)

PASSIVE: Relax ciliary body muscles, zonules are tense/tighten, and FLATTENS the lens. Brings focus for far away things. (example, watching TV)

248
Q

What is Nuclear Sclerosis?

A

-it is normal with aging (>6yo)

-more and more fibers of the lens continue to grow for life, start at equator of lens and moves to center.

-when there is too many fibers/it’s too dense, then it can be hard to focus the lends/change the shape of the lens

-affects depth perception, not vision

-still visual, have tapetal reflection

-grey opacity/appearance

-does NOT interfere with fundic exam

-must differentiate from cataracts

249
Q

What is the cause of Nuclear Sclerosis?

A

aging, normal

250
Q

What is the TREATMENT for Nuclear Sclerosis?

A

none indicated

251
Q

What are cataracts?

A

-Any opacity on or within the lens of the eye, associated with abnormal lens fibers

-Impairs image formation/light passes – Image does not

-must differentiate from nuclear sclerosis which is accumulation of normal lens fibers

252
Q

Do cataracts effect PLR?

A

NO, bc light can still pass through

253
Q

What are the 4 classifications of cataracts?

A
  1. incipient
  2. immature/incomplete
  3. mature/complete
  4. hypermature/resorbing
254
Q

What is an incipient cataract?

A
  • < 15% of lens
  • Little clinical significance
  • Earliest changes
  • Focal
  • Monitor for progression
255
Q

What is an immature/incomplete cataract?

A
  • 15% – 99% of lens
  • Variable extent
  • Fundic reflex present, usually peripherally
  • Usually some vision, starting to decline
256
Q

What is a mature cataract?

A
  • 100% of lens
  • Vision loss
  • Lens totally opaque
  • No fundic reflex
257
Q

What is a hypermature/resorbing cataract?

A
  • lens become more permeable and resorbs cataracts
  • Resorption of lens fibers
  • Sparkling plaques
  • Wrinkling Anterior lens capsule
  • Deep AC
  • May have fundic reflex
258
Q

What CAUSES (etiology) of Cataracts?

A
  1. hereditary - most common in dogs
  2. metabolic
    -diabetes mellitus - second most commong
  3. Trauma
  4. Anterior Uveitis
    -bc you’re changing contents of aq. humor
    -most common in horses and cats
  5. senile degeneration
  6. toxic
  7. nutritional
    -hypercalcemic with puppy milk replacer
  8. congenital - often bilateral, most common in young
259
Q

How does diabetes lead to cataracts?

A

In a normal lens with NORMAL blood glucose, you will have normal lens glucose. Hexokinase metabolizes glucose.

When you have elevated blood glucose, you will have elevated lens glucose. Hexokinase needs help – gets saturated. Receives help via ALDOSE REDUCTASE — produces sorbitol.

SORBITOL - osmotic, draws water inside lens > disrupts lens, fiber arrangement - swollen

there is slow metabolism of sorbitol

260
Q

Clinical implications of cataracts

A

-Minimal to severe
-Scatter light, distorting image, decreasing acuity
-Dull colors
-Complete blindness
-Induce or exacerbate uveitis
-vision loss
-lens-induced uveitis (2 types)
–pain
–damage to intraocular structures
–secondary glaucoma

261
Q

There are two types of Lens-Induced Uveitis. The first one is Phacolytic Lens-Induced Uveitis.

A

-Intact lens capsule, but semi-permeable
-Slow release of abnormal lens proteins to aqueous
–Low grade uveitis

262
Q

There are two types of Lens-Induced Uveitis. The other one is Phacoclastic Lens-Induced Uveitis.

A

-rupture of lens capsule
–trauma/diabetics
–abrupt release of lens fibers
–SEVERE uveitis

-aggressive tx

-must act fast

263
Q

How do you TREAT cataracts?

A

-Currently no effective medical therapy
–Treat LIU (lens induced uveitis) and monitor IOP

-Surgery
–Phacoemulsification - DACVO

264
Q

Which patient would you select for cataract treatment? All patients can’t go to surgery!

A
  • Systemically healthy, regulated diabetics, normal triglycerides
  • Immature to mature stage - not incipient
    – Better success rates
    – Do not wait to refer
  • Agreeable temperament
  • Owner compliance
  • Controlled lens induced uveitis
  • Pre-operative testing
    – Ocular ultrasound - make sure there is no retinal degeneration/detachment
    – Electroretinography
265
Q

What is an ERG?

A

an electroretinal gram

-see how eye is capturing light with those electrodes

-see lecture 42, slide 29 for normal and abnormal

266
Q

What is the POST-OP care for Cataract surgery?

A
  1. control intraocular inflammation
    -topical steroids (pre acetate, dexamethasone)
    -systemic steroids OR non-steroids
    - mydriatics for IOP
  2. control possible infections
    -topical/systemic antibiotics
  3. monitor IOP (post op hypertension 24 hrs)
  4. frequent rechecks AND medications for life
267
Q

What are some post-op cataract surgery COMPLICATIONS?

A
  1. flare – will ALWAYS SEE 100% of the time
  2. Infection
  3. Suture dehiscence
  4. Corneal decompensation
  5. Uveitis
  6. Hyphema - iatrogenic
  7. Posterior capsular opacity
  8. Vitreous prolapse
  9. Retinal detachment
  10. Post-operative hypertension - dueng surto gel that is put in the eye to maintain the shape of the eye duri
  11. Secondary Glaucomagery
268
Q

What are the goals of cataract surgery?

A
  1. to get rid of the cataract
  2. to regain vision
269
Q

What if your patient cannot under go cataract surgery?

A

• All cataracts larger than incipient in size need to be treated with a topical anti-inflammatory for life

• Monitor IOP for life

270
Q

What happens with a lens luxation?

A
  • Zonules can break, causing the lens to become displaced (the space between ciliary body and lens)
  • Partial (subluxation)
    -Complete (luxation)
271
Q

There is anterior lens luxation and posterior lens luxation – which causes glaucoma faster?

A

ANTERIOR lens luxation (75% of glaucoma cases)

25% of glaucoma cases is posterior luxation

272
Q

What are the CS of a SUBluxation of the lens?

A

-Changes in AC depth
-Aphakic crescent **
-Phacodonesis/ Iridodonesis
-Vitreous in AC
-At risk for full luxation
-At risk for glaucoma

272
Q

What are the CS of a SUBluxation of the lens?

A

-Changes in anterior chamber depth - use slit lamp
-Aphakic crescent ** (aphakic = no lens)
-Phacodonesis/ Iridodonesis - lens or iris moves/shakes
-Vitreous in anterio chamber
-At risk for full luxation
-At risk for glaucoma

273
Q

What are the CS of a ANTERIOR lens luxation?

A

-Lens in AC
-Pain, blepharospasm
-Indistinct pupillary borders (esp with cataracts)
-Possible corneal edema (contact)
-Possible anterior uveitis
-Possible glaucoma

274
Q

What are the CS of a POSTERIOR lens luxation? see lecture 42, slide 39

A

-Lens in posterior segment
–apparent aphakia - little small white blob

-Deep AC - bc nothing is pushing on lens anymore/holding it place
-Vitreous in AC
-Usually comfortable
-Possible glaucoma (less likely)

275
Q

What CAUSES luxation of the lens?

A

1.Primary
- Zonular dysplasia (inherited)
- Terriers

  1. Secondary
    - Uveitis
    - Glaucoma (buphthalmos) - breaks zonules!
    - Senility
  2. Implications
    - Uveitis
    - Glaucoma
276
Q

How do you TREAT a lens luxation?

A

-Treatment depends upon many factors
-Location of lens
-Potential for vision
-Presence of glaucoma
-Acute vs. chronic
-Pain
-Other ocular abnormalities

277
Q

What can you do for an ANTERIOR LENS luxation?

A

• Removal of lens (ICLE)
• Trans-corneal lens reduction - “Couching”
–push lens to posterior segment, THEN use miotic drugs
• Enucleation (???)
• If none is possible, medical therapy to maintain IOP low
–Dorzolamide
–DON’T USE MIOTICS!!
–May not work….

-if it happens acutely = emergency!

-

278
Q

What is glaucoma?

A

disease characterized by elevated intraocular
pressure (IOP) resulting in damage to the optic nerve and subsequent vision loss

279
Q

IOP is a balance between what two things?

A
  1. aqueous humor production (via ciliary body)
  2. aqueous humor drainage
    -ICA (conventional)
    -uveoscleral pathway (nonconventional)
280
Q

What is a normal IOP?

A

10-20mmHg

281
Q

What causes an increased IOP (think mechanically, why does it happen?

A

-ALWAYS due to obstruction of aq humor

-NEVER due to overproduction of aq humor

282
Q

With ACUTE glaucoma, you have a chance to SAVE VISION. It is considered an emergency. What should you do at all costs?

A

Lower IOP fast!

283
Q

With CHRONIC glaucoma – you have a poorer chance to save vision. What is your main goal with CHRONIC glaucoma?

A

Patient comfort

284
Q

How do you differentiate between acute and chronic?

A

Hx and CS

285
Q

What are the ACUTE signs for glaucoma?

A

• Blind
• Episcleral injection
• Diffuse corneal edema
• Mydriasis
• Pale optic disc
• Pain (blepharospasm)
• +/- Epiphora

286
Q

What are the CHRONIC signs for glaucoma?

A

• Blind, episcleral injection, corneal edema, mydriasis
• Buphthalmos (big globe)
• Corneal (Haab’s) striae - corneal stripes (torn DMs)
• Lens (sub)luxation
• “Cupped” optic disc - atrophy of optic nerve
• Tapetal hyperreflectivity
• Retinal vascular attenuation

287
Q

Feline Glaucoma – cats don’t present such overt signs with glaucoma. What CS do they have?

A

• Relatively little ocular hyperemia and corneal edema
• Mydriasis and progressive buphthalmia often the only overt signs

288
Q

What is primary glaucoma?

A

INHERITED

  • The other eye will develop glaucoma in 6-12 months
  • Do all that you can to delay the onset!
289
Q

What is secondary glaucoma?

A

Glaucoma caused by a different ocular dz

-no age or breed disposition
-all species affected, most common form in horses and cats

290
Q

What breed’s can get primary glaucoma?

A

• Beagles
• Basset hounds
• Cocker spaniels
• Nordic breeds (e.g. Samoyed, Siberian Husky)

291
Q

What can CAUSE primary glaucoma?

A

• Inherited disease
–Pectinate ligament dysplasia (PLD), goniodysgenesis as a risk factor

• Iridocorneal angle increasingly
compromised first few years of life

• Drainage angle closes

• IOP spike

292
Q

How do you DIAGNOSE primary glaucoma?

A

• Tonometry
–IOP > 25 mmHg

• Signs of glaucoma

• No secondary causes identified

• Signalment
–Predisposed breed (4-7yo)

293
Q

What are the top 3 underlying diseases/causes for SECONDARY glaucoma?

A

• Anterior uveitis
–#1 cause of secondary glaucoma in all species
• Lens luxation/subluxation
• Intraocular neoplasia

294
Q

What are the GOALs of glaucoma TREATMENT?

A
  1. aimed at decreasing aq humor production
  2. and increasing aq humor outflow
295
Q

How would you TREAT the 3 underlying diseases/causes for SECONDARY glaucoma?

A

Address the underlying cause

• Uveitis –> Ocular and systemic work up to determine cause of inflammation
–Incorporate topical and systemic anti-inflammatories along with anti-glaucoma therapy

• Anterior-lens luxation –> Emergency surgery to remove the lens

• Intraocular neoplasia –> Enucleation

296
Q

How would you generally TREAT PRIMARY glaucoma?

A

• ACUTE: EMERGENCY to lower IOP immediately, maintain on anti-glaucoma drugs, prophylactic therapy for contralateral eye
• CHRONIC: start anti-glaucoma medications or consider enucleation

297
Q

What are the 5 Medical Therapies used for Glaucoma?

A
  1. Prostaglandin Analogues
  2. Carbonic Anhydrase Inhibitors
  3. Beta Blockers
  4. Parasympathomimetics
  5. Mannitol
298
Q

Name a Prostaglandin Analogue. By what mechanism does it work? In which case would you use it for glaucoma?

A

-Latanoprost 0.005%
-INCREASES aq humor OUTFLOW
–also utilizes uveoscleral pathway of outflow
-used for primary glaucoma, canines

-can cause intense miosis
-contraindicated with uveitis and anterior lens luxation
-ineffective in cats and dogs

299
Q

Name a Carbonic Anhydrase Inhibitor. By what mechanism does it work? In which case would you use it for glaucoma?

A

-dorzolamide 2%
-DECREASES aq humor PRODUCTION
–inhibits carbonic anhydrase in ciliary body
-Great for primary AND secondary glaucoma, all species

300
Q

Name a beta blocker. By what mechanism does it work? In which case would you use it for glaucoma?

A

-timolol 0.5%
-DECREASES aq humor PRODUCTION
–not really figured out - block B-receptors in ciliary body processes
-don’t use Beta-blockers alone (not potent enough) or with cardio dz (decreases heart rate)
-Work synergistically with CAIs (e.g. dorzolamide)

301
Q

Name a Parasympathomimetic. By what mechanism does it work? Why would you use it for glaucoma?

A

• INCREASES aqueous humor OUTFLOW
–conventional pathway (iridocorneal angle)
• Causes miosis
• PROPHYLACTIC MEDICATION FOR CONTRALATERAL EYE IN 1◦ GLAUCOMA
• Control eyes: 8 months to development of glaucoma
• Treated eyes: 31 months to development of glaucoma

302
Q

When would mannitol be used for glaucoma?

A
303
Q

What is apart of the fundus?

A

-vitreous

-choroid

-retina
–photoreceptors
–retinal ganglion cells
–vessels
–tapetal area
–non-tapetum

-optic dic

304
Q

What retinal vascular pattern do most mammals have? see lecture 44, slide 8-11

A

-Holangiotic
• retinal vessels extend to periphery in all quadrants
• most mammals

305
Q

When does the fundus mature?

A

3-4 mo old

306
Q

What are special about subalbinotic eyes? (Subalbino)

A

-usually blue or lighter pigments eyes

-all of RPE is non-pigmented

307
Q

How do dog and cat funduses differ?

A

DOG
-optic disk is white - due to myelin
-optic disk is more triangular/can be circular – due to myelin
-BVs of optic nerve cross over edge into center of disc

CAT
-optic disk is grey
-optic disk is more circular
-little to no myelin
-BVs of optic disk dont cross, they stop

308
Q

What are the functions of the Fundus? (Neurosensory Retina, Retinal Pigment Epithelium, Tapetum, Choroid, Sclera, Optic Nerve)

A

Neurosensory Retina: Convert light in neural potentials, part of blood retinal barrier

RPE: Recycle photopigments, remove photoreceptor waste products, pass nutrients

Tapetum: reflect light

Choroid: Vascular tunic, nutrition for photoreceptors, removes waste, blood vessels to do things (BRB, consist of choriocapillaries)

Sclera: Fibrous tunic, support and protection

Optic Nerve: impulse to brain

309
Q

What happens to fundic image when there is cellular infiltrate of the retina?

A

image gets fuzzy/blurry due to increase in thickness

310
Q

What happens to fundic image when there is degeneration of the retina?

A

degernation - atrophy

-losing layers of retina
-easier to see tapetum = more shiny

311
Q

What happens to fundic image when there is blood in retina?

A

see blood, retina gets thicker

312
Q

General signs of Fundic Dz

A

• Tapetal hyperreflectivity
• Retinal vascular attenuation – BVs thinned out/no branching
• Retinal separation / detachment - fuzzy and balooning
• Hemorrhage - tapetum should not have any red
• Cellular infiltrates - granulomas
• Non-tapetal hyper/depigmentation
• Blurred, swollen optic disc
• Pale optic disc with loss of myelination

313
Q

What does PRA stand for?

A

Progressive Retinal Atropy

314
Q

What is the end result of PRA?

A

-retinal degneration
-blindness

315
Q

What breeds are predisposed for PRA?

A

think cocker spaniels, poodles, labs (over 30 breeds)

316
Q

What CAUSES PRA?

A

-inherited
-mostly autosomal recessive

-onset of PRA depends on breed, type of gene

-progressive

317
Q

CS for PRA

A

• Vision loss
–Usually night blindness first (nyctalopia - rods affected first)
–Then day blindness also
• Diminished PLR’s - slow or incomplete
• Attenuation of vessels
• Tapetal hyperreflectivity
• Pale optic disc, bc vessels attenuated
• Depigmentation – non tapetum
• +/- Cataract formation (secondary)
–bc dying retinal cells release toxic substances to the lens > thus cataract forms

-important to do ERG before cataract surgery, bc PRA could be cause of cataract and realize dog isn’t visual

318
Q

What vision are rods and cones responsible for? (Bright or dark)

A

Rods - dark/dim light
Cones - bright light

319
Q

How do you DIAGNOSE PRA?

A

• Signalment
• History
• Clinical signs
• Electroretinogram (ERG)

320
Q

How do you TREAT PRA?

A

you don’t – no treatment

COULD GIVE VITAMINS, may delay or stop regression

321
Q

What does SARDS stand for?

A

Sudden Acquired Retinal Degeneration Syndrome

322
Q

CS for SARDS

A

• Sudden onset of complete blindness (ex. went to bed visual, woke up blind)
• Middle-aged dogs 7-8yo
• Spayed female overrepresented, Dachsunds
• May have systemic clinical signs similar to Cushing’s disease but no true association
• Retina INITIALLY NORMAL in appearance (fundic exam)
–Classic PRA signs start after 4-8 weeks
• FLAT ERG

-no menace
-Dazzle present, PLR usually normal

323
Q

If an ERG is not flat/normal, then where else would the blindness be stemming from?

A

Optic Nerve
Brain

324
Q

What causes SARDS?

A

unknown cause

325
Q

How do you DIAGNOSE SARDS?

A

• History
• Signs
• Electroretinogram ERG - FLAT
• Rule out ON and brain disease - do that with ERG

326
Q

How do you TREAT SARDS?

A

no tx

327
Q

What is chorioretinitis?

A

posterior uveitis

• both retina and choroid involved

• Sign of systemic disease
-bacterial
-fungal
-viral

-differentiate between active and non active bc active could mean something systemic is going on

328
Q

Fundic presentation of active chrorioretinitis

A

• Cellular infiltrates – granulomas
–Hyporreflective areas
–Indistinct borders
• Retinal separation / detachment
• Hemorrhage

329
Q

Fundic presentation of chronic chorioretinitis

A

• Retinal thinning
• Hyperreflective areas
• Hyperpigmented
• Well-distinct borders

330
Q

Causes of Chorioretinitis

A

• Infectious
-Fungal
-Viral (FeLV, FIV, FIP, CD)
-Bacterial
-Rickettsial (Ehrlichia, RMSF)
-Protozoal (Toxoplasmosis)
• Systemic hypertension – leads to bleeding in the eye
• Autoimmune disease
• Neoplasia (lymphoma)
• Coagulopathies

331
Q

How do you DIAGNOSE chorioretinits?

A

• Sign of systemic disease (w/ active case)
-find cause
• CBC
• Chemistry panel
• Fungal titers
• Special tests (FeLV, etc.)
• CSF taps
• Imaging techniques

332
Q

How do you TREAT chorioretinitis?

A

-systemic tx (drops don’t hit back of eye, etc)
-depends on cause

333
Q

What is RETINAL HEMORRHAGE, what causes it?

A

• Hypertension - if you see blood, check blood pressure
• Thrombocytopenia
• Coagulopathy
• Hyperviscosity
• Senile
• Trauma - Rare
• DIC (rare)

334
Q

What does Enrofloxacin do in cats?

A

toxicity!

• Loss of photoreceptors = blindness
• Unrelated to age, sex, or other medical conditions
• Onset of blindness - varies (a few days to months)
• Usually occurs with high dosages, but documented
with as low (rec dose is 5.0mg/kg PO)

335
Q

CS of Enrofloxacin Toxicity

A

• Acute blindness (sudden, not that it happens acutely after starting meds)
• Mydriasis
• Tapetal hyperreflectivity (rapid)
• Retinal vascular attenuation (rapid)
• Flat line ERG

336
Q

How do you TREAT Enrofloxacin Tox?

A

-cessation of drug
-some have retained vision if receiving drug for only short time

337
Q

What does Ivermectin do in dogs?

A

toxicity at high doses!

• Sudden onset of blindness after ingestion of ivermectin
• Often history of recent worming of horses
• Make complete recovery in 7-14 days
• Initial ERG extinguished or diminished but also
recovers

338
Q

CS of Ivermectin tox

A

• Blindness
• Mydriasis
• Negative to incomplete PLRs
• Linear retinal edema, folds along
tapetal / nontapetal border
• +/- systemic signs
–Hypersalivation
–Ataxia
–Tremors
–Coma/death

339
Q

Should central blindness affect PLRs?

A

no

340
Q

How do you DIAGNOSE Ivermectin tox?

A

• History of acute blindness and ivermectin exposure
• Clinical signs
• Serum ivermectin levels
-normal dose produces ~50ng/g
-affected dogs often have levels over 1,000ng/g

341
Q

How do you TREAT Ivermectin tox?

A

-not necessary
-Intralipid (20% lipid emulsion) IV (helps bind ivermectin esp with systemic signs)

342
Q

What is Optic Neuritis? see lecture 44 slide 48

A

• Inflammation of the ON
• Unilateral or bilateral
• Associated with systemic disease

343
Q

What comprises the rim of the orbit?

A
  1. Frontal bone
  2. Lacrimal bone
  3. Zygomatic bone
  4. Orbital ligament
344
Q

The medial wall and roof of the orbit is bony. Which bones?

A
  1. Orbital portion of frontal bone
  2. Orbital wing of the sphenoid complex
  3. Lacrimal bone
345
Q

The later wall and floor of the orbit is soft tissue (bc open orbit). Which tissues/muscles?

A
  1. Masseter muscle
  2. Pterygoid muscle
  3. Temporal muscle
  4. Zygomatic salivary gland
346
Q

What are the contents of the orbit?

A

• Optic nerve
• Extraocular muscles
• Fascial cone
• Veins, arteries, fat

347
Q

What are the extraocular muscles of the orbit?

A

6 total

• Four recti: Dorsal, ventral, medial & lateral
• Two obliques: Dorsal & ventral
• Retractor bulbi
• Functions
–Globe motility
–Protection

348
Q

What CNs innervate the extraocular muscles of the orbit?

A

3, 4, 6

• CN III: Dorsal, ventral & medial recti, Ventral oblique
-does most of the work
• CN IV: Dorsal oblique
• CN VI: Lateral rectus & Retractor bulbi

349
Q

What is evisceration? Enucleation? Exenteration? see lecture 45, slide 15

A

• Evisceration
• Removal of globe contents leaving the corneoscleral shell intact

• Enucleation
• Removal of the globe, eyelid margins, 3rd eyelid and conjunctiva

• Exenteration
• Removal of the globe, eyelid margins, 3rd eyelid, conjunctiva, and all orbital contents

350
Q

What are the 2 main indication for globe removal?

A
  1. pain
  2. irreversible vision loss
351
Q

What are general signs of orbital dz in regards to globe placement? lecture 45, slide 18

A

• Exophthalmos – Rostral displacement of the globe from the orbit

• Enophthalmos – Caudal displacement of the globe into the orbit

• Strabismus – Involuntary, fixed deviation of the visual axis in one or both eyes

352
Q

CS with Exophthalmos

A

• Wider palpebral fissure
• Third eyelid protrusion common
• Indicates space occupying lesion in orbit
• Verify by looking from above
• Need to distinguish from proptosis & buphthalmos

proptosis - eyelids are entrapped behind globe
buphthalmos - big globe

353
Q

CS and causes of Enophthalmos lecture 45, slide 21

A

• Narrow palpebral fissure
• Third eyelid protrusion common

• Causes:
–Horner’s syndrome (with concurrent miosis and ptosis)
–Loss of retrobulbar fat – senile, chronic inflammation, starvation
–Acquired globe shrinkage – phthisis bulbi (globe shrinks from chronic inflammation or uveitis)
–Developmentally small globe - microphthalmia

354
Q

CS and causes of Strabismus

A

• Convergent strabismus (esotropia) - globes rotated inward/medially deviated
• Divergent strabismus (exotropia) - laterally deviated

• Causes:
–Space occupying orbital lesion
–Extraocular muscle rupture
–Neurologic lesions of CN III, IV and/or VI
–Hydrocephalus

355
Q

General signs of orbital dz

A

• Third eyelid protrusion
–Results from any shifting of the globe in the orbit
–Non-specific sign
• Periocular swelling
• Pain (ex. pain when you open mouth, ramus of mandible can rotate into orbit of small animal)

356
Q

CS of Orbital Neoplasia

A

• Slowly progressive exophthalmos
• Relatively painless
• No heat or swelling
• Strabismus
-deviations, non symmetry
• Usually unilateral
• Third eyelid protrusion
• Decreased retropulsion
• Systemically well
• Usually older patients (~10 years)

-signs can be SUBTLE

357
Q

How do you DIAGNOSE Orbital Neoplasia?

A

• Clinical signs
• Skull radiographs - limitations - summation
•Orbital ultrasound
• Advanced imaging (CT, MRI)

358
Q

How do you TREAT Orbital Neoplasia?

A

• Orbitotomy - if mass just within orbit
• Exenteration
• Radiation

359
Q

What is Retrobulbar cellulitis/abscess? What causes it?

A

-inflammatory process behind globe

common bacterial infections

CAUSES
• Penetrating wounds - ex. foxtail
• Foreign bodies
• Spread from adjacent structures
-Sinuses
-Dental disease
-Hematogenous spread from distant site

360
Q

CS of retrobulbar dz

A

• Acute onset exophthalmos (fine then not)
• Painful to open mouth, palpate around globe - pain
• Decreased appetite
• Usually unilateral
• Periocular inflammation/swelling
• 3rd eyelid protrusion
• Deceased retropulsion with pain
• Often systemically ill, febrile
• Leukocytosis
• Swelling behind last molar, upper arcade

361
Q

How do you DIAGNOSE Retrobulbar cellulitis/abscess?

A

• Clinical signs
• Rule out orbital neoplasm
• Ocular ultrasound
• Advanced imaging

362
Q

How do we TREAT Retrobulbar cellulitis/abscess?

A

• Broad-spectrum antibiotics (eg. amoxicillin-clavulanate)
–IV
–Oral
• Systemic anti-inflammatory (NSAID/steroid)
• IV Fluids - patients can be dehydrated bc in pain not eating
• Topical lubrication
• Treat ulcer if present
• E-collar
• Exenteration if globe is blind & painful, esp if foreign material is still present

363
Q

What is Proptosis?

A

-forward displacement and entrapment of globe outside orbit by lids

364
Q

What CAUSES Proptosis?

A

blunt trauma or bite wound

365
Q

Which breed is predisposed to Proptosis?

A

brachycephalics

366
Q

Proptosis can cause damage to which eye structures?

A

• Extraocular muscles (EOM)
• Optic nerve
• Internal ophthalmic artery

367
Q

How do you assess and assign prognosis for vision for Proptosis?

A

SEE LECTURE 45, Slide 38

EXAM!!

368
Q

How do you TREAT proptosis?

A

-replace globe
-enucleate if severe

369
Q

What is Extraocular Myositis?

A

inflammation of the extraocular muscles

• Relatively rare
• Autoimmune disease
• Common in young Golden Retrievers

370
Q

CS of extraocular myositis

A

• Rapid onset, bilateral exophthalmos
• Painless
•Usually no periocular heat or swelling

371
Q

How do you DIAGNOSE extraocular myositis?

A

• Signalment & History
• Clinical signs
• Response to treatment
• US/CT/MRI
• Muscle biopsy

VET433A (8 decks)

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