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Small Animal Medicine II > Tear Film Diseases > Flashcards

Tear Film Diseases Flashcards

1
Q

How does the nasolacrimal system work?

A
  • lacrimal gland creates the aqueous portion of tears
  • lacrimal puncta wick away excessive tears into the canaliculi and into the NL duct —> nasal punctum
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2
Q

What are 4 functions of precorneal tear film?

A
  1. maintain smooth and lubricated optical surface
  2. protect from dessication and bacteria
  3. provide the eye with nutrients and growth factors
  4. waste removal
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3
Q

What are the 3 parts of precorneal tear film? Functions of each?

A
  1. LIPID - meibum prevents evaporation and tear overflow (expressed by blinking)
  2. AQUEOUS - flushing, lubrication, nutrition, antibacterial, protease inhibitors, smooths surface
  3. MUCIN - stabilizes, helps tears stick to corneal epithelium (hydrophobic), fills in corneal defects, bacteria resistance
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4
Q

What is keratoconjunctivitis sicca? What happens when left untreated?

A

quantitative dry eye disease due to deficiency of aqueous portion of tear film (most common cause of conjunctivitis in dogs!)

BLINDNESS —> corneal scarring, vascularization, pigmentation

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5
Q

How is KCS diagnosed?

A

Schirmer tear test I WITHOUT proparacaine to measure reflex (irritation) and basal tearing over a minute

  • quantified aqueous tear production
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6
Q

What is the normal value for Schirmer tear tests? What are abnormal values?

A

> 15 mm/min

  • 11-14 mm/min = early or subclinical KCS
  • 6-10 mm/min = moderate or mild KCS
  • <5 mm/min = severe KCS
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7
Q

What is thought to be the most common cause of KCS? How does it present? What treatment is recommended

A

immune-mediated - breakdown of blood/tear barrier allows immune destruction of lacrimal glands (usually not associated with other immune diseases)

usually bilateral lymphocytic-plasmacytic infiltrates in lacrimal glands

immunomodulatory therapy - topical Cyclosporine

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8
Q

What are 4 additional causes of KCS?

A
  1. infectious - distemper, herpes (cats)
  2. neurogenic - loss of parasympathetic innervation to lacrimal glands
  3. trauma - facial or trigeminal nerves
  4. removal of gland of the third eyelid or prolonged uncorrected prolapse
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9
Q

What specific drugs can cause KCS?

A
  • sulfa drugs
  • Etodolac (NSAID)
  • topical atropine (dries secretions)
  • sedation/anesthesia
  • radiation therapy

check STT prior to starting these meds!

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10
Q

What is unique about neurogenic KCS?

A

usually presents unilaterally with a dry nostril

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11
Q

What is the most common congenital cause of KCS?

A

congenital alacrima - lacrimal gland hypoplasia or aplasia —> Boston Terrier, Yorkie, Pug puppies with painful eyes upon opening

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12
Q

What 3 metabolic diseases can cause KCS?

A
  1. hypothyroidism
  2. DM* - decreased corneal sensitivity, neuropathy
  3. Cushing’s

decreased tear production

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13
Q

How does immune-mediated KCS compare to other etiologies? What are 3 common signs? What 2 signs are due to chronic irritation/poor nutrition?

A

tends to be more progressive rather than acute

  1. red eye
  2. intermittent mucoid/mucopurulent discharge = mucin overcompensates + prone to bacterial infection due to decreased aqueous compartment of tears
  3. blepharospasm

corneal vascularization + pigmentary keratitis

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14
Q

What are 5 less common signs of KCS?

A
  1. lackluster cornea
  2. corneal scarring
  3. ropy, mucoid discharge (white or yellow)
  4. blepharitis
  5. periocular alopecia
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15
Q

What is severe purulent discharge indicative of with cases of KCS? How is it diagnosed/treated?

A

secondary bacterial conjunctivitis or corneal ulcers

conjunctival/corneal cytology

broad-spectrum topical antibiotics + dry eye therapy

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16
Q

KCS, secondary bacterial infection:

A

corneal ulcer = chronicity

  • prone to infection and deepening
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17
Q

What are 3 aspects of KCS medical treatment?

A
  1. lacrimostimulation - topical immunomodulation with cyclosporine A or Tacrolimus
  2. lacrimomimetics - artificial tears —> hyaluronic acid, methycellulose, petrolatum

give both daily, 2-3x a day

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18
Q

What 5 effects do cyclosporine A and Tacrolimus have when treating KCS? How are they able to do this?

A
  1. increase aqueous teat production
  2. decrease inflammation
  3. normalizes mucin production
  4. decreases pigmentation
  5. decreases vascularization

absorned into lacrimal glands

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19
Q

How is response to therapy typically dependent on the severity of KCS?

A

STT > 2 mm/min = 80% respond to medical therapy, usually within 4-6 weeks

STT < 2 mm/min = 50% respond to medical therapy, can take up to 6 months for response

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20
Q

KCS, medical treatment:

A
  • pigment dispersion
  • decreased vascularization
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21
Q

What surgical therapy is available to treat KCS? When is it recommended?

A

parotid duct transposition - substitutes saliva for normal tears (technically challenging!)

cases of severe and non-responsive KCS (typically congenital)

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22
Q

What 3 complications are associated with parotid duct transposition?

A
  1. mineral deposits on cornea
  2. overproduction
  3. blepharitis - saliva doesn’t have the same immunoregulatory effects
23
Q

What is qualitative tear film dysfunction? Most common etiology?

A

poor tear quality due to mucin or lipid deficiency

previous severe conjunctivitis or blepharitis

24
Q

What are 4 signs of qualitative tear film dysfunction?

A
  1. blepharospasm
  2. corneal vascularization
  3. pigmentation
  4. (milder) mucoid discharge
25
Q

What is the diagnostic of choice for qualitative tear film dysfunction? Why?

A

tear film break up time —> will have a normal STT because tears are still produced, just with a different composition that makes them evaporate quicker or slide off the eye

26
Q

How is qualitative tear film dysfunction treated?

A
  • artificial tears
  • cyclosporine A or tacrolimus
27
Q

How is a tear film breakup time (TFBT) performed?

A
  • place fluorescein on the eye and blink it, keep it open without rinsing
  • wait to see breaks in the fluorescein to appear, seemingly darker and drier spots indicative of tear evaporation (use UV (cobalt) blue light for observation!)
  • NORMAL = 8-9 s
28
Q

TFBT:

A

dark spots = tear film breakup

  • normal = 8-9 s
29
Q

What are the 3 most common signs of feline dry eye disease? How does this compare to canine?

A
  1. dull, lackluster cornea
  2. (non)ulcerative keratitis
  3. conjunctivitis

more corneal presentation, uncommon to have mucoid/purulent discharge

30
Q

What is thought to be the 3 most common causes of feline dry eye disease? What do they cause?

A
  1. previous/current FHV-1 infection
  2. neurogenic
  3. concurrent ocular disease - eyelid agenesis, symblepharon, corneal sequestrum

decreases corneal sensitivity

31
Q

What are 3 diagnostics used for feline dry eye disease?

A
  1. STT - normal = > 9mm/30s / > 15 mm/min
  2. TFBT - normal = 8-9s
  3. corneal touch threshold (+ cotton swab wisp)
32
Q

What is epiphora? What is the most common cause? Some others?

A

excessive lacrimation

painful diseases causes reflex production of tears - corneal ulcers, distichia, ectopic cilia, entropion

  • breed-related
  • imperforate puncta = decreased drainage
  • dacryocystitis
33
Q

What are the 2 overall causes of epiphora? What are the most common clinical signs?

A
  1. increased tear production
  2. decreased tear drainage
    - differentiated with good optho exams (disease causes pain vs. discharge), Jones test, and flushing of NL duct

tear staining, wetness on face

34
Q

What are 5 indications for performing NL duct flushes or Jones test?

A
  1. epiphora
  2. mucopurulent punctal, ocnjunctival, or nasal discharge
  3. swelling of ventral medial canthal region or fistulas
  4. suspected punctal/duct FB
  5. eyelid trauma
35
Q

What is Jones test? Why are false negatives common?

A

fluorescein dye passage test - time pass of dye from eye to nares, commonly 5 mins —> not seen or takes longer with complete vs. partial obstructions

time needed for passage based on duct/nostril size, may need an additional flush if unsure

(positive = epiphora NOT caused by blockage, rather caused by increased production of tears)

36
Q

Where are the puncta located? How is a NL duct performed?

A

2-5 cm from medial canthus + 1-2 mm bulbar to eyelid margin

flush saline though cannula to determine if NL is patent or to dislodge FB —> no excessive force, point downward and watch for exit from nostril

37
Q

What is the point of NL flushes?

A

indicated for suspected obstruction (epiphora, mucopurulent discharge)

  • physiologic - entropion, imperforate micropunta, dacryocystitis, neoplasia, stenosis
38
Q

What is breed-related conformational epiphora due to? What breeds are most common? How do they present?

A

tight eyelid conformation + hair grows long and drains down the fur = can’t drain very well

small breeds (Maltese, Poodle) - no underlying ocular disease. normal NL system that flushes normally

39
Q

What is imperforate puncta? When is this most common? How is it diagnosed?

A

puncta does not develop properly, causing epiphora

younger dogs - Goldens, Bulldogs

go to flush and observe outpouching of conjunctiva overlying the imperforate puncta ventrally

40
Q

What treatment is recommended for imperforate puncta?

A

cut conjunctival where the tissue outpouching is observed —> most common on ventral puncta

+ treat with anti-inflammatories to discourage stricture while healing

41
Q

What is dacryocystitis? What is the most common etiology?

A

inflammation of the NL duct/sac

focus of infection or FB

  • common in outdoor dogs (FB) and rabbits (tooth roots cause occlusion)
42
Q

What are 5 signs of dacryocystitis?

A
  1. epiphora
  2. thick, mucopurulent discharge from medial canthus
  3. conjunctivitis (medial!)
  4. painful dermatitis at medial canthus
  5. abscessation of sac with fistula formation
43
Q

How is dacryocystitis diagnosed?

A
  • purulent material from puncta
  • inability to flush
  • dislodgement of a FB on flush
  • culture
  • dacryocystorhinography, CT with contrast, MRI, cannulation
44
Q

How is dacryocystitis treated?

A
  • topical or oral steroids/antibiotics
  • flushing daily for the first few days
  • catheterization
  • advanced surgery if needed
45
Q

What is cicatricial NL duct obstruction? How is it treated?

A

scarring of the NL duct slows drainage of tears

flush under anesthesia and cannulate, leaving it in place until full healing takes place (3.5 Fr catheter or suture)

46
Q

What is the most common disease of the third eyelid? What is the most common signalment?

A

prolapsed gland of the nictitating membrane

young Bulldogs, Mastiffs, Pugs, or Chihuahuas - floppy third eyelids

47
Q

What underlying cause is thought to be responsible for prolapsed gland of the nictitating membrane? How does it appear?

A

laxity of the connective tissue of the third eyelid

mass-like protrusion behind 3rd eyelid

48
Q

How is prolapsed gland of the nictitating membrane treated? What is the most common procedure?

A

surgical replacement (no removal!!) - can bring tear production to 35-40%

Morgan pocket technique - 2 conjunctival incisions on the posterior (bulbar) surface of the third eyelid around the gland, tuck it back in the pocket, and use 5-0 or 6-0 vicryl with knots on anterior surface

49
Q

What signalment is most common affected by scrolled (everted) nictitating membrane cartilage? How does it affect patients?

A

young Great Danes, Mastiffs, or Bassets

typically cosmetic only, but can predispose to corneal ulcers

50
Q

How is scrolled (everted) nictitating membrane cartilage corrected?

A

surgical removal of the bent/rolled over piece of cartilage

51
Q

What 3 third eyelid tumors are most common? Which is a little more rare in dogs?

A
  1. adenocarcinoma
  2. hemangioma, HSA
  3. conjunctival lymphoma
    (overall uncommon, typically affects gland or tissues)

SCC —> more common in cats and horses

52
Q

Why are third eyelid tumors harder to diagnose?

A

can look like a prolapse, should biopsy for older patients

53
Q

How is third eyelid neoplasia most commonly treated?

A
  • edge of third eyelid = removal of third eyelid + histopathology —> often curative, removes gland, good margins
  • expansion into orbit —> enucleation/extenteration
54
Q

What is dacryops? What signalment is most commonly affected? How is it treated?

A

ectopic NL gland tissue reported as a cyst periorbitally, commonly within maxilla, near the medial canthus, or conjunctiva

young Bassett Houds or labradors

surgical removal or injection of sclerosing agent

Small Animal Medicine II (57 decks)

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