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CVS2 Ophthalmology > 2 - examining the ocular surface > Flashcards

2 - examining the ocular surface Flashcards

1
Q

Define…
1. Epiphora.
2. Hyperaemia.
3. Chemosis.

A
  1. Excessive tear production and/or tear overflow.
  2. Increased blood flow to a tissue.
  3. Conjunctival oedema - more common in cats than in dogs.
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2
Q
  1. Episclera.
  2. Conjunctiva.
  3. Blepharospasm.
A
  1. Vessels and tissue exterior to sclera and under conjunctiva.
  2. Ocular mucus membrane lining eyelids to limbus.
  3. Spasm of the orbicularis oculi causing eyelid closure.
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3
Q

What does a normal ocular surface require?

A

A fully functional lacrimal surface unit.
Physical and chemical barrier to debris and infectious agents.

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4
Q

What comprises a functional lacrimal surface unit?

A

Normal eyelids for tear film distribution.
Normal tear film so normal stimulation of functional glands and ducts.
Corneal epithelium to adhere tear film to the eye to create optical surface for light refraction into the eye.
Functional tear drainage via patent punctae and ducts.
Conjunctival Associated Lymphoid Tissue (CALT).
- Recruit immune cells w/ chemical mediators.
- Activate the complement cascade and promote clearance.
- Identify and remove foreign substances by white blood cells.
- Activate the adaptive immune system through antigen presentation.

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5
Q

Composition of the pre-corneal tear film from deep to superficial.

A

Mucin layer.
Aqueous layer.
Lipid layer.

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6
Q
  1. What do the meibomian glands produce? - function of produce?
  2. What do the conjunctival goblet cells produce?
  3. What does the orbital and nictitans lacrimal glands produce?
A
  1. Lipid layer - prevent evaporation of aqueous phases beneath it.
  2. Mucus layer.
  3. Aqueous layer.
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7
Q

Proximal to distal nasolacrimal duct.

A

Upper and lower puncta.
Nasolacrimal canaliculi.
Lacrimal sac (dacryocyst).
Nasolacrimal duct.
Nasal puncta.

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8
Q
  1. Lipid layer functions.
  2. Aqueous layer functions.
  3. Mucus layer functions.
A
  1. Prevents evaporation, aids distribution.
  2. Supplies nutrition to avascular cornea (dissolved O2 etc), antibacterial properties, removal and remodelling - proteases and antiproteases.
  3. Lubrication, refractive properties, anchors aqueous layer to cornea by microvilli on corneal surface.
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8
Q

Ophthalmoscopy techniques to examine the corneal surface.

A

Direct observation with light source.
Close direct ophthalmoscopy - anterior (+5D to +20D).

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9
Q

Eyelid surface observations.

A

Look along whole eyelid margin.
Observe tear film:
- aqueous meniscus, mucus strings?, sharp reflection?
Meibomian gland opening.
Observe for aberrant hairs / cilia.
Third eyelid edge and position.

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10
Q

Exam of conjunctiva and third eyelid.

A

Close observation - evert lids.
Retropulse globe to show the 3rd eyelid.
Close direct ophthalmoscopy.
Important to check behind for FB.
LA - proxymetacaine 0.5%.
Eversion w/ atraumatic forceps or cotton buds.

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11
Q
  1. Normal flora of the conjunctiva.
  2. Normal cytology of the conjunctiva.
A
  1. Gram positive aerobes.
    Staphylococcus spp.
    Bacillus spp.
    Corynebacterium spp.
    Streptococcus spp.
  2. Non keratinised epithelial cells predominate.
    Bacteria occasionally seen.
    Leucocytes rare.
    Environmental debris - hair, dust, pollen.
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12
Q

Inflammation.

A

Oedema - Fluid influx to affected tissues so swelling.
Hyperaemia - Increased blood flow so redness.
Cellular infiltrate - e.g. WBC so purulent / yellow / green (+/- exudate).
Pain - Cell dysfunction stimulates the nerves so there is a locally protective mechanism e.g. blepharospasm.

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13
Q

Types of exudation from the eye.

A

Serous (epiphora) - to flush.
Mucoid - to bind debris.
Purulent - WBC influx.
Sanguineous - haemorrhage.

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14
Q

Follicular hyperplasia.

A

Due to a chronic issue.
Overgrowth of the CALT in response to a chronic irritation.
Look for this in inner aspect of TEL and upper fornix.

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15
Q

Ocular surface response to insult.

A

Epiphora - flush out debris and pathogens, dilute toxins and a sign of pain.
Lacrimal ducts drain tears.
Mucoid discharge - increase in mucus to bind up particles.
Purulent discharge due to increased cellular content.
Blepharospasm - increased flow of tears and response to pain.
Conjunctival hyperaemia.

16
Q

Clinical signs of nasolacrimal obstruction.

A

Dry nostril on affected side.
Ocular or nasal discharge.
Conjunctival hyperaemia.
swelling of ventral aspect of medial canthus.
Epiphora w/ STT >25mm/min.
Appearance of FB usually ventral aspect of medial punctum.
Appearance of fistula at the ventral aspect of the medial canthus.

17
Q

Test of patency of the nasolacrimal system.

A

‘Jones’ test.
- Apply fluorescein in both eyes.
- Observed after several minutes at the level of the nostrils.
- Normal response w/in 5 mins.
- Check mouths/pharynx of brachycephalic breeds

18
Q

Other testing of the patency of the nasolacrimal system.

A

Exam of lacrimal punctum.
Nasolacrimal flushing.
Imaging - tooth roots, looks for trauma.
Cytology.
Culture and sensitivity.
Dacryocystorhinography - contract x ray study.

19
Q

What if the tear film goes wrong?

A

Keratoconjunctivitis sicca.
- Corneal inflammation.
- Conjunctivitis.
- Dry eye.

20
Q

KCS common clinical signs.

A

Adherent mucus strings.
Poor corneal clarity.
Poor corneal shine / poor Purkinje reflex.
Corneal pigmentation.
Corneal vascularisation.
Low STT reading.
Conjunctival hyperaemia.
Ocular pain / blepharospasm.
Decreased vision.
Corneal

21
Q

Quantitative KCS.
- predispositions.

A

Deficiency of aqueous tear.
Insidious onset.
Reversable if caught early.
Immune-mediated adenitis of lacrimal glands.
- Westies, Yorkies, Mini schnauzers.
- English bulldogs, pugs, Pekingese, Boston terrier, Lhasa Apso.
- American cocker, English springer, CKCS.
- Bloodhound, Samoyed.

22
Q

Other (less common) causes of KCS.

A

Iatrogenic - anaesthetics, atropine, drug toxicity (trimethoprim, sulphonamide).
Neurogenic - Facial nerve, trigeminal nerve, autonomic system (lack of innervation to glands due to lesion).
3EL excision, other trauma to lids and 3EL.
‘Congenital’ Lacrimal gland hypoplasia or aplasia (rare) - yorkie.

23
Q

Diagnostic tests for quantitative KCS.

A

STT and concurrent clinical signs.

24
Q

STT readings…
1. normal.
2. early/suspicion of KCS.
3. moderate KCS.
4. severe KCS.

A
  1. 15-25.
  2. 10-14.
  3. 6-10.
  4. 0-5.
25
Q

Qualitative KCS.
Diagnostics.
Treatment.

A

Tear film instability - inflammation of Meibomian glands (Meibomitis, Blepharoconjunctivitis), abnormal quantity or quality of goblet cells.

Close exam - lid margins, palpebral conjunctiva, corneal epithelial erosions?
Tear-film break up time low. (fluorescein).
Conjunctival biopsy and analysis of goblet cells.

Treat the cause.
Tear missing components with tear supplements (carbomer, hyaluronate, lipid).

26
Q

KCS - identify and treat cause.

A

For aqueous deficiency, immunomodulating agent: cyclosporine A ointment (0.2% Optimmune) BID. Tacrolimus (off license) BID.
STT still low, increase frequency to 3 times a day.
Surgical: Improve lid conformation for effective blink, remove masses.
Treat Meibomian gland disease/blepharitis: Warm compresses, lid hygiene, broad spec ABX, topical or systemic anti-inflammatory tx.
Aqueous neurogenic KCS: treat cause, pilocarpine orally.
Mucus deficiency: treat conjunctivitis if poss. tear replacement.

27
Q

Normal cornea.

A

Non-keratinised epithelium.
No vessels.
No pigments.
Stromal collagen fibres regimentally parallel.
Layered collagen - almost crystalline arrangement.

28
Q
  1. How does the corneal stroma maintain a relatively dehydrated state?
  2. Consequence if this fails?
A
  1. Epithelium is lipophilic layer that is 6-8 cells thick.
    - Cells constantly regrown from basal cells.
    - Basal cells replaced by centripetal migration from limbal stem cells.
    Endothelium 1 cell thick and gets nutrition from the aqueous tear.
    - On Descemet’s basement membrane.
    - Contain Na+/K+ ATPase physiologic pumps to constantly remove water.
  2. Corneal oedema.
29
Q

Ocular clinical signs of corneal lesions.

A

Epiphora.
Blepharospasm.
Conjunctival hyperaemia.
Colour change in cornea.
Anisocoria:
- Asymmetry to pupil size.
- Relative miosis on affected side.
- Sign of reflex uveitis.

30
Q

Types of corneal opacities.

A

Blue/grey - oedema, epithelial or endothelial loss.
Red - vascularisation, haemorrhage.
White - fibrosis, infiltrate (cellular), lipid or calcium.
Black/brown - pigmentation, sequestrum.

31
Q

How does corneal oedema occur.

A

Dehydrated state compromised.
Defect of epithelial layer:
- Ulceration, diffuse, focal, hazy.
Defect of endothelial layer:
- Mottled, diffuse blue.
- Often more generalised.
- Intraocular cause — uveitis, glaucoma, lens luxation.
- primary endothelial degeneration (geriatrics) / inherited dystrophy.

32
Q

Superficially ‘red’ cornea.

A

Surface inciting cause.
Focal to cause.
Branching trees of bright red, vessels.
Extend from bulbar conjunctiva.
Do cross limbus.

33
Q

Deep ‘red’ cornea.

A

Deep stromal/intraocular cause.
Circumferential.
Fine, short, straight vessels.
Arise from limbus.
Don’t cross limbus.

34
Q

Vascular patterns causes…
1. Superficial corneal vessels.
2. Deep corneal vessels.
3. Episcleral congestion.
4. Ciliary flush/brush border.
5. Conjunctival hyperaemia.

A
  1. Surface corneal / ocular disease.
  2. Deep corneal disease.
  3. Intraocular disease very likely.
  4. Severe eye disease.
  5. Non-specific - occurs w/ most eye disease.
35
Q

White cornea.

A

Fibrosis/scar, metabolic infiltrates (lipids show crystalline, minerals show fluffy), inflammatory cell infiltrates.

36
Q

Black/brown - pigmentary keratitis.

A

Chronic irritation.
Insufficient protection of the cornea. Part of Brachycephalic Ocular Syndrome.
Can cause blindness.
Correct cause of irritation e.g. excessive nasal fold, medial entropion.
Lubricate eyes on daily basis.
Topical immunomodulating agent (cyclosporin. Tacrolimus).

37
Q

Pink - proliferative cellular infiltrate clinical signs.

A

Superficial vessels.
+/- pigmentation.
Pink tissue in acute phase.
White crystalline spots.

CVS2 Ophthalmology (7 decks)

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