Opthamology Flashcards

0
Q

What is entropion? What breeds is it common in?

A

Common in young dogs, retrievers, pointers, setters and larger breeds. Lid margins roll inwards causing hairs or lashes to irritate and potentially abrade the cornea. The pathophysiology is complex and involves the relationship between the eyelid and the counterpressure from the globe, tone of the orbicularis muscle and size of the palpebral fissure. The most common site is the lateral lower lid. Pain with lacrimation and blepharospasm are always present.

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1
Q

Describe the anatomy of the canine eyelids?

A

3 layers - outer layer of normal skin, middle layer of muscle, fibrous connective tissue and glands, inner layer of palpebral conjunctiva. The orbicularis oculi muscle encircles the lid margin and closes the eye. The tarsal (meibomian) glands run at right angles to the lid margin. Dog only has lashes on the upper lid, close to lid margin.

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2
Q

What is the treatment of entropion?

A

Surgery. Excisional correction not always required in younger patients where there is still considerable anticipated growth. Vertical mattress sutures or vertically oriented surgical staples left in place for a few weeks may be all that is required in the younger patient. For simple anatomical entropion the hots celsus technique is straightforward and effective.

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3
Q

What is atonic entropion/trichiasis?

A

Loss of tone in the skin of the upper eyelid, combined with an excessive amount of head skin, can result in the lateral upper lid drooping to the extent that hairs and cilia impinge on the cornea, causing discomfort and corneal damage. It is best treated with a stades procedure.

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4
Q

What occurs in a stades procedure?

A

The skin adjacent to the lid margin is excised and the area left to granulate. Owners should be warned that the post operative appearance is unsightly for a couple of weeks but the final cosmetic result is good.

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5
Q

What are breed related medial canthal abnormalities?

A

Entropion of the medial lower lid may compress the lower punctum and caniliculis. Caruncular trichiasis and deep medial canthal grooves caused by tight medial canthal ligaments exacerbate the effects of entropion. Common in brachycephalics and toy breeds such as min and toy poodle. The cornea is unaffected and the problem is usually cosmetic rather than painful.

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6
Q

What is ectropion?

A

The lower lid turns outward, creating a gap between lid and cornea and exposing the conjunctiva. Usually requires no attention. With conjunctivitis or keratitis from chronic exposure, the problem is dealt with by wedge excision bordering the lateral canthus.

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7
Q

What is Diamond eye?

A

the lids take a diamond shape with a lateral upper lid entropion and mid lover lid ectropion. Diamond eye is the result of a combination of inadequate support from lateral canthal ligament, excessive skin and a large palpebral fissure.

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8
Q

How can excess facial skin be a problem for eyelids?

A

Cocker spaniel, clumber spaniel etc have excess facial skin that droops downwards causing upper lid entropion or extreme ptosis and lower lid ectropion. In the chow chow and sharpei entropion may be associated with the deposition of subcutaneous fat in the skin folds in the middle age. A face lift procedure or a modified stades procedure may be required. Referral is highly recommended.

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9
Q

What is lagopthalmos?

A

Macropalpebral fissure with lagopthalmos occurs in brachycephalic breeds, predisposing affected animals to chronic keratitis and progressive pigmentary infiltration. Conformational lagopthalmost may be complicated by low tear production, medial canthal entropion or irritation from lacrimal caruncle or nasal fold hairs.

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10
Q

What is Distichiasis?

A

A common condition where abnormally positioned cilia emerge from the lid margin usually at or close to the tarsal gland openings. Most dogs show no clinical signs. Dogs with evidence of discomfort (lacrimation, increased blink rate) should be referred for treatment.

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11
Q

What is conjunctival cilia?

A

A single hair emerging though the palpebral conjunctival a few millimetres from the lid margin at right angles to the cornea. This is a painful condition. There is often a shallow vertically oriented ulcer opposite the emerging cilia. Treatment is by excision of a wedge of tissue containing the cilium.

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12
Q

What is trichiasis?

A

Perioocular hairs growing in a normal location may be directed abnormally towards the ocular surface, which may cause conjunctivitis and keratitis. Trichiasis results from entropion and can be associated with nasal folds, medial canthus and caruncle.

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13
Q

What is blepharitis?

A

Inflammation of the eyelids.

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14
Q

What is meiobomianitis ?

A

Infection of the meiobomian (tarsal glands). unilateral or bilateral thickening/hyperaemia of the lid margins with swolen and inflamed tarsal glands visible when everting the lid. Treat with hot compress, topical & systemic antibiotics

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15
Q

What are external hordeolum?

A

Single or multiple abscesses caused by suppurative infection of glands of Zeiss or Moll. Focal abscesses may be opened by scalpel incision.

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16
Q

What is a Chalazion?

A

Obstruction of tarsal gland secretions by a blocked duct can cause the gland to rupture, liberating its content within the eyelid substance, visible through the palpebral conjunctiva as a firm spherical yellow lipgranuloma. If occular surface irritation is present then treat by incising into the lesion with a blade, under general anaesthesia and curretting out the contents, followed by topical antibiotics for 7-10days.

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17
Q

Describe Eyelid Neoplasia In the dog?

A

Most lid tumours occur in old dogs and are benign in behaviour. Tarsal gland adenomas are most common, followed by melanomas. May abrade the cornea or bleed and should be removed if causing problems.

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18
Q

What is the third eyelid?

A

A large fold of conjunctiva supported internally by a T shaped cartilage. The base of the cartilage is surrounded by the nictitans gland, which produces about 30-40% of the aqueous component of the PTF. It is important in the distribution of the tear film. Movement of the TEL of the cat can be both active and passive.

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19
Q

What is a prolapse of the nictitans gland?

A

Dorsal prolapse of the nictitans gland appears acutely as a smooth pink swelling at the medial canthus (cherry eye). Thought to result from a weakness in the connective tissue attachment between the gland and the periorbital tissue. Although the gland may be excised there is an unacceptably high post operative risk of dry eye. Surgical replacement should therefore be attempted.

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20
Q

What is scrolling of the third eyelid?

A

Also known as eversion or kinking of the cartilage. Usually giant breeds. The straight stem of the cartilage kinks forcing the membrane to fold outwards so that the leading edge no longer contacts the cornea. Treatment is by excising the kinked portion of the cartilage from the deep surface of the membrane.

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21
Q

What is plasma cell infiltration of the third eyelid?

A

A condition affecting the GSD and collie types, with bilateral depigmentation of the membrane, a pink/red fleshy infiltrate and a rough irregular surface. The infiltrate consists of plasma cells and lymphocytes and is often concurrent with chronic superficial keratitis. Treatment is with Topical corticosteroids. Topical cyclosporine may also be used.

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22
Q

What may cause third eyelid protrusion?

A

Retrobulbar space occupying lesions with exopthalmost e.g extraconal abscess or tumour. Retraction of the globe - active or passive with enopthalmos, reduction in globe size, reduction in orbital contents e.g dehydration, cachexia, masticatory muscle atrophy, alteration to nervous control e.g horners syndrome, tetanus.

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23
Q

What is the conjunctiva?

A

A thin mucous membrane which extends from the lid margins where it is continuous with the epidermis to the limbus where it meets the corneal epithelium. It lines the inner surface of the upper and lower lids, reflected forwards at the fornixes as the bulbar conjunctiva over the globe.

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24
Q

What is conjunctivitis?

A

The whole conjunctiva becomes diffusely reddened with a variable amount of discharge. In significant bacterial infections the discharge has a typically purulent yellow green appearance. The majority of bacterial conjunctivitis in the dog are secondary to causes such as an eyelid mass, eyelid irregularity or foreign body. Infection most commonly with staphylococcus. Fusidic acid has good activity against G+ve bacteria and need only be applied once or twice daily.

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25
Q

What is opthalmia neonatorum?

A

Infection within the conjunctival sac before the eyelids are opened (usually at 10-14 days) will cause swelling of the eyelids, sometimes with a small amount of pus escaping at the medial canthus. This must be treated promptly to avoid corneal ulceration and penetration. The lids should be opened along their line of fusion digitally or with blunt ended scissors. The surface should be irrigated with sterile saline and the infection treated with broad spec topical antibiotic ointment.

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26
Q

how does distemper affect the eyes?

A

A purulent occular discharge may accompany the other signs of the disease. Treatment is symptomatic, check tear production as the virus attacks the lacrimal gland, possibly leading to corneal damage. A chorioretinitis may also be present.

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27
Q

What is follicular conjunctivitis?

A

Hypertrophy of the lymphoid follicles scattered on the bulbar suface of the nictitans and the conjunctival fonixes occurs with chronic antigenic stimulation. Most cases respond to treatment with saline irrigation and symptomatic use of topical steroids.

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28
Q

How can allergy affect the eyes?

A

Conjunctiva and lids may be involved in local allergic reactions or generalised atopy. The finding of a single eosinophil on cytology is Diagnostic of allergic process.Immediate hypersensitivity reactions are occasionally encountered with rapid and dramatic chemosis.

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29
Q

Describe chronic conojunctivitis

A

A low to medium grade mucupurulent chronic conjunctivitis seen as a generalised problem in association with marginal tear production, seborrhea, pyoderma, otitis externa, ectropion etc. Treatment is symptomatic with a view to contol.

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30
Q

What is keratoconjunctivitis sicca (dry eye)?

A

A common condition in the dog resulting from a deficiency in the aqueous potion of the tear film produced by the lacrimal and nictitans glands. May be immune mediated, endocrine disease, Drug induced (sulphadiazine), viral adenitis.

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31
Q

How is the schirmer I tear test used to diagnose keratoconjunctivitis sicca?

A

Schime tear test strips are sterile, individually wrapped filter paper stips. The paper is placed in the conjunctival sac of the lower lid so that the notch is at the liid margin. >15mm is normal. The mean normal STT is around 21mm in the dog. values of 13-15mm should be interpreted on the basis of the occular surface appearance and level of discomfort.

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32
Q

How is dry eye managed with tear stimulation?

A

Topical 0.2% cyclosporine ointment either alone or in conjunction with tea replacement. Tacrolimus and pimecolimus also used.

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33
Q

What is a fluoescein drainage test?

A

Fluorescein instilled into both eyes - especially if unilateral problem as normal eye acts as a positive control. External nares observed for the passage of fluorescein. dye usually seen within 4 minutes.

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34
Q

What is nasolacrimal cannulation?

A

The upper punctum is cannulated with a lacrimal cannula and a syringe containing 5ml of saline attached. Saline should appear at the lower punctum when the upper punctum is flushed or at the nares when the lower punctum is occluded by gentle digital pressure. Do not use force when injecting as this can rupture the caniliculi.

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35
Q

What is dacryocystorhinogaphy ?

A

0.5-1.0ml positive contrast used to delineate the nasolacrimal system.

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36
Q

What is congenital imperforate puncta?

A

Produces epiphora in young animals from about 8 weeks of age. The duct system is present but the punctum is occluded by a thin covering of conjunctiva. The diagnosis is made by direct visualisation confirmed by flushing, the saline will form a bleb at the site of occlusion. The covering membrane can simply be surgically excised.

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37
Q

What is dacryocysitis?

A

Inflamation of the lacrimal sac (usually plus inflammation of the duct and canaliculi.) Most often due to a foreign body such as a grass seed. Flushing the system from the upper punctum may allow foreign body to be gasped at the lower punctum.

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38
Q

Describe the 5 layers of the cornea

A

Anterior outer epithelium. - non keatinised, stratified squamous epithelium with a rapid turnover of cells. Basement membrane produced by deepest layer of epithelial cells. Connective tissue stroma - composed of collagen lamellae, separated by ground substance and fiboblasts. Descemets membrane - the basement membrane of the underlying endothelium. Endothelium - deepest layer, important forr maintaining corneal dehydration.

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39
Q

What do opacities in the cornea take the form of ?

A
Oedema
Cells - infiltrating the cornea or deposited on the endothelium
Blood vessels 
Pigment
Disorganised collagen 
Lipid
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40
Q

What is corneal dermoid?

A

A congenital mass of hairy skin on the cornea, usually at the lateral limbus. The hairs on the dermoid can irritate the corneal surface.

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41
Q

What is pigmentary kerratitis?

A

pigment may be carried in from the limbus along with new blood vessels in response to a variety of chronic corneal insults damaging the Occular surface.

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42
Q

What is chronic superficial kerratoconjunctivitis (pannus)

A

A chronic superficial vascular keatitis occuring mostly in GSD, geyhound, collie types. A rough fleshy looking infiltrate of inflammatory tissues, pigment and vessels advances across the cornea. The corneal epithelium is intact. Visual loss can occr. Immunosuppression with topical steroids.

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43
Q

Describe Age related corneal endothelial degeneration?

A

Bilateally but asymmetrical degenerative condition of the corneal endothelium occurring as a senile change in old dogs. The Loss of endothelial cells causes failure of the endothelial pump mechanism resulting in steamy blue appearance of stromal oedema.

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44
Q

What is corneal degeneation?

A

Occurs when deposition of lipid is seen in association with inflammation and vascularisation. Lipid may be produced in situ or circulating lipid may enter the cornea. Lesions consist of cholesterol, phospholipids, fatty acids and calcium.

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45
Q

What is corneal dystrophy?

A

Primary, bilateral and inherited disorder characterised by well demarcated central or paracentral white grey crystalline opacites, composed of cholesteol, phospholipids and fatty acids unde mafnigication show a fibreglass like quality.

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46
Q

What is lipid keratopathy?

A

uuni or bilateral occular manifestation of systemic disease characterised by peripheral or central crystalline opacities and a clear peri limbal zone. Corneal vascularisation may develop with chronicity.

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47
Q

What is corneal arrcus?

A

Bilateral peripheral lipid deposition which is uncommon, is un variably associated with plasma hyperlipoproteinaemia and the underlying cause should be determined.

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48
Q

What is corneal ulceration?

A

The Corneal epithelium provides a protective barrier which is resistant to bacterial colonisation and prevents water entering the cornea. Loss of full thickness of the epithelium exposes the underlying stroma. Most often as a result of mechanical trauma. Successful bacterial colonisation may occur and there may be further stromal loss and full thickness corneal perforation.

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49
Q

How does normal healing of corneal ulcers occur?

A

Healing of epithelial defects is usually rapid achieved by the migration of adjacent basal epithelial cells to cover the defect which then replicate to restore the full epithelial thickness. The stromal defects of deeper ulcers are initially filled by a fibrin clot. Activated keratocytes at the wound edges secrete collagen, aided by invading fibroblasts. This new collagen tends to be disorganised.

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50
Q

What are the clinical signs of corneal ulceration?

A

Discomfort - usually marked. Lack of pain indicates abnormal corneal sensation, conjunctival hyperaemia, variable amounts of localised corneal oedema and irregularity of the surface contour. Neovascularisation and cellular infiltration of the cornea is common with chronic ulcers.

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51
Q

What are the causes of corneal ulcers?

A

External trauma, hair/lash trauma, entropion and ectopic cilia, infection, bacterial colonisation secondary to trauma, rarely fungal, tear film abnomalities, exposure keratopathy.

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52
Q

What is exposure keratopathy?

A

The central corneal damage resulting from inadequate protection of the conea by the eyelids and third eyelid which may be compounded by inadequacy of the pre ocular tear film. Causes are varied and include 1) Prominent globe with poor lid closure - brachycephalics. 2) Facial nerve paralysis - not usually a problem fo breeds that can retract their globes sufficiency to spread the tear film but brachycephalics cannot do this. 3) Trigeminal nerve paralysis - absent corneal sensation results in a severe keratitis affecting the area of the cornea exposed between the lids.

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53
Q

What are superficial under run ulcers (SCCED)

A

Ulcer healing will be severely compromised if the edges of the epithelium fail to adhere to the underlying stroma. This creates a flap or Underrun edge at the ulcer margin which may be recognisable by pentorch examination

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54
Q

How are mid stromal ulcers managed?

A

Can be managed medically with broad spectrum topical antibiotics every 2-6 hours such as neomycinbacitracin/polymixin. Treat accompanying reflex uveitis with atropine as needed to dilate the pupil and anti collagenase 3-4 x daily.

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55
Q

How is a deep ulcer managed?

A

Cytology and culture should be performed. The edge of the ulcer is swabbed then gently scraped using the blunt end of a scalpel blade. Followed by surgery to support the conea. Treat empirically with a topical fluoroquinolone.

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56
Q

What is a melting ulcer?

A

Enzymatic breakdown of the cornea can accelerate, causing rapid dissolution of the stroma. The enzymes responsible originate from bacteria, PMNs, and from the cornea itself. The edges appear gelatinous. An anti collagenase should be given at frequent intevals. Serum woks well in dogs and cats.

57
Q

Describe corneal acid and alkali injury?

A

Lavage immediately. Acid injury less dangeous than alkali as proteins coagulate to limit penetration. Treat with copious lavage with sterile saline, analgesia and then as for corneal ulceration. Alkali - causes corneal melting, severe uveitis, irrigate over several hours and treat the uveitis.

58
Q

What is the iriS?

A

A diaphragm to control the amount of light entering the eye. The posterior epithelium is densely pigmented (the back of the iris is black) but the amount of pigment in the stroma vaies, determining the eye colour.

59
Q

What is pupil size controlled by?

A

The amount of parasympathetic tone in nerve III. Anxious animals have increased sympathetic tone causing dilatation of the pupil. This should be remembered when assessing the pupillary light esponses.

60
Q

What are the functions of the ciliary body/?

A
  1. Accomodation: produced by ciliary mm.
  2. Attachment of the zonule supporting the lens via ciliary processes.
  3. Active secretion of aqeous by inner zone non pigmented epithelium.
61
Q

What are persistent pupillary membrane remnants?

A

Strands of iris tissue running from mid iris (the iris collarette) to the cornea - where they cause a focal corneal opacity at the point of attachment or to the lens where they may cause a capsular/subcapsular cataract at the point of attachment, or across the pupil to the ris sometimes in a web like pattern.

62
Q

What are Uveal Cysts?

A

cysts may arise from the posterior surface of the iris or ciliary body, usually spontaneously, but sometimes following uveitis. They often break free and move around the anterior chamber. They may ruptue. The main concern is distinguishing them from intraocular melanoma.

63
Q

What are Naevi?

A

A Naevus is a patch of hyper-pigmentation which may increase in area but does not protrude beyond the contour of the iis. Observe only. Difficult to distinguish in the cat from early intaocular melanoma.

64
Q

What is anterior uveal melanoma?

A

The most common intraocular tumour in all species. Usually the appearance is of heavily pigmented solid mass within the iris or the ciliary body. Often unrecognised untill the development of secondary glaucoma. In dog & horse they are generally benign and grow slowly & enucleation is curative.

65
Q

What is a limbal melanoma?

A

Heavily pigmented tumours arising at the limbus. They are not uveal tumours but can resemble a tumour invading out through the sclera. They grow slowly gradually invading the cornea and sclera and do not metastasise.

66
Q

What is a ciliary body adenoma?

A

Presents as a well defined pink mass protruding into the pupill. The moe aggressive ones may invade the iris. Prognosis is generally favourable following enucleation.

67
Q

What are non pigmented limbal masses?

A

Other non pigmented masses are seen at the limbus and or invading the cornea. They are rare, proliferative inflammatory lesions of unknown cause, classified according to their appearance and extend as episcleritis, nodular episcleritis and nodular episclerokeratitis. Most respond to steroids.

68
Q

What is anterior uveitis?

A

Inflammation of the iris and ciliary body. Pain can be intense, as a result of ciliary and iris muscle spasm.

69
Q

What are the signs of acute anterior uveitis?

A

Pain, visual disturbance, red eye - hyperaemia/congestion, corneal oedema, breakdown of blood aqeuous barrier allowing protein and inflammatory cells into the aqueous (aqueous flare). Miosis, swelling of the iris.

70
Q

What are keratic precipitates?

A

Focal accumulations of inflammatory cells that settle with gravity and adhere to the corneal endothelium, often obscured by the third eyelid. Often a feature of anterior uveitis in the cat.

71
Q

What are the complications of anterior uveitis and signs of chronic uveitis?

A

1) Synechiae formation - iris may form adhesions to the cornea, to the lens capsule, glaucoma, iris colour change, vitreal opacities, cataract formation and lens luxation, phtisis bulbi.

72
Q

What is iris bombe?

A

If 360 degrees of the pupillary margin is adhered, aqueous is unable to flow from the posterior chamber to the anterior chamber, causing a pupil block glaucoma. This is known as iris bombe.

73
Q

What are the possible causes of anterior uveitis?

A

Corneal injury and ulceration, blunt and penetrating trauma, release of antigenic lens protein, intraocular neoplasia. Septicaemia, bacteraemia, toxaemia (e.g pyometria, bite wounds). 2) infectious diseases, lymphoma.

74
Q

What is the treatment therapy for anterior uveitis?

A

Control of intra ocular inflammation. 1) deal specifically with the cause. 2)Reduce intraocular inflammation and restore the blood aqueous barrier. 3) Achieve moderate mydriasis and pain relief. 4) Monitor IOP in order to detect any secondary glaucoma. Nsaids may be used to control inflammation. Topical corticosteroids should begin immediately if cornea is intact. Topical Nsaids if the cornea is ulcerated. Systemic steroids when inflammation is severe and involves posterior segment.

75
Q

What are mydriatics/cycloplegics?

A

Atopine dilates the pupil, reducing the risk of extensive posterior synechiae formation. It relieves pain due to muscle spasm.

76
Q

What is Glaucoma?

A

Aqueous is produced by the ciliary body, passes through the pupil iinto the anterior chamber and drains at the iridocorneal angle. Glaucoma is an elevation in intraocular pressure incompatible with normal function. Outflow of aqueous is compromised by mechanical obstuction or functional failure of the irido corneal drainage angle. It may also occur if the passage of aqueous though the pupil is blocked.

77
Q

What are signs of acute glaucoma in the dog?

A

Pain, visual loss, episcleral congestion, corneal oedema, moderately dilated pupil, poorly responsive to light, ELEVATED IOP. confirmed by tonometry.

78
Q

What are the signs of chronic glaucoma?

A

Can occur from previous bouts of acute glaucoma or with an insidious rise in IOP until irreparable ocular damage. 1) megaloglobus, variable corneal vascularisation and pigmentation, lens luxation/subluxation, tears in descemets membrane, visible retinal degeration and optic disc cupping, variable degee of pain.

79
Q

What is primary glaucoma?

A

Generally seen in predisposed breeds, the developmental abnormality is bilateral although one eye tends to de compensate before the othe. this does not usually occur until early middle age although the abnormality may be present for years beforehand.

80
Q

What are the causes of secondary glaucoma?

A

Primary lens luxation, uveitis, intraocular neoplasia, Intraocular haemorrhage, retinal detachment, pigmentary glaucoma of the cairn terrier.

81
Q

What are prostaglandin analogues?

A

Potent topical ocular hypootensives. causes pronounced miosis and should be avoided in glaucoma secondary to uveitis and patients with anterior lens luxation. Used to treat primary glaucoma. Rapid reduction in IOP achieved by increasing outflow through the unconventional uveoscleral pathways.

82
Q

What are osmotic diuretis?

A

Used only in emergency situations, most often treatment of primary acute glaucoma, they contract the vitreous and will keep down the IOP for several hours.

83
Q

What are carbonic anhydrase inhibitors?

A

reduce aqueous production by up to 40% reducing the amount produced by active secetion.

84
Q

What are B blockers?

A

Small reduction in aqueous production by reducing blood flow though the ciliary processes eg timolol.

85
Q

Describe the anatomy of the lens?

A

The lens is transparent and avascular & receives its nutritional requirements via the aqueous. It is made up of lens fibres enclosed within an elastic capsule. The capsule prevents exposure of lens fibres to the foetal circulation so it remains antigenic throughout life. The lens fibres meet at suture lines to form an upright Y anteriorly an inverted Y posteriorly. The lens is suspended by zonular fibres from the ciliary body which attach at the lens equator.

86
Q

What is Nuclear Sclerosis?

A

A normal ageing change, gradually becoming apparent from about 6 yeas onwads. As more secondary lens fibres are laid down, condensation and compression of the nucleus occurs, imparting a blue grey appearance to the nucleus frequently mistaken for a cataract by the owner. It can be distinguished readily from a cataract as it does not appear as an opacity in distant direct opthalmoscopy.

87
Q

What is primary lens luxation?

A

Typically seen in terrier breeds. Abnormality of the zonule, leading to subluxation initially followed by luxation as the last zonule breaks down. Primary lens luxation is invariably bilateral. Signs include iridodenesis - a wobble like oscillation. The iris appears flat and the anterior chamber deeper. when the lens is free to move within the eye i.e the last of the zonule has broken down, it may move either anteriorly into the anterior chamber or posteriorly into the vitreous.

88
Q

Describe anterior lens luxation?

A

almost invariably causes acute glaucoma, the lens and the vitreous physically obstructing the flow of aqueous through the pupil. Degenerate prolapsed vitreous coming forward with the lens may also block the drainage angle. The usual presentation is therefore one of an acutely uncomfortable red eye. The lens is visible in front of the iris and the iris is pushed backwards by the lens.

89
Q

What are signs of posterior lens luxation?

A

Similar to those for subluxation although the aphakic crescent may disappear if the lens falls right back into the vitreous. 90% of lens will luxate forward into the anterior chambe at some point and may cause glaucoma.

90
Q

What is the treatment for a lens luxation?

A

An anterior lens Luxation needs to be surgically removed as a matter of urgency as the glaucoma cannot be controlled with medical treatment. Subluxated lenses may be managed medically with prostaglandin analogues to keep behind the constricted pupil and maintain a low IOP, or surrgically by elective lendectomy. Posteriorr lens luxation does not usually cause acute problems and the lens may be left in the vitreous with judicious use of a prostaglandin analogue.

91
Q

What is Secondary lens luxation?

A

May also occur secondary to the following; chronic glaucoma (enlargement of the globe stretches then ruptures the zonules), chronic anterior uveitis (uncommon in dogs - seen mostly in cats), severe ocular trauma, hypermatue, inflexible cataracts. The management is determined by thee cause - lendectomy may be appropriate if there remains the potential for a comfortable and visual eye e.g in some cases with uveitis or cataracts. Enucleation is often indicated in chonic glaucoma or trauma.

92
Q

What is a cataract?

A

A cataract is any opacification - focal, partial or total of the lens or its capsule. Disruption of fibre arangement, accumulation of insoluble proteins and oedema due to accumulation of osmotically active substances may all be involves in the pathogenesis. The presence of a cataract does not impair the pupillary light response. There are many ways to classify cataracts according to site, stage of maturity, age at onset, ateiology.

93
Q

Descibe the different stages of maturity of a cataract?

A

Incipient - the earliest stage with small opacities or vacuoles affecting <15% of the lens. No obvious effect on vision. Not all are pogessive. Immature - more extensive opacities, but a fundic reflex is still present. Vision variably affected depending on extent and position of opacities. Mature - total opacity with no fundic reflex causing blindness. Hyper mature - the lens may contract giving an irregular winkled surface and a deep anterior chamber. It may leak potein, leading to a low grade uveitis. Morgagnian - resorption and clearing of cataractous cortex may occurr in some cataracts. The cortex liquifies and may take on a metallic glistening appearance before resorption but uveitis is a risk at this stage. Intumescent - very rapidly developing cataract eg in diabetes, which may swell sufficiently to cause a shallow anterior chamber and even obstruct drainage or leak lens protein.

94
Q

What age do cataracts onset?

A

Most congenital cataracts are not hereditary but caused by some disturbance in utero. They may be associated with other ocular defects e.g micropthalmos. They tend to be nuclear cataracts and be non progressive and as more secondary lens fibres are laid down around the nucleus they become relatively smaller and vision may improve. Topical atropine can be used weekly to improve peripheral vision around a nuclear cataract.

95
Q

What is posterior polar subcapsular cataract?

A

Develops in the first few months or years of life. Seen at the confluence of the suture lines. In golden and Labrador retrievers. This is only rarely progressive and in the great majority of affected dogs causes no obvious visual impaiment.

96
Q

Describe Diabetic cataracts?

A

Usually bilateral and rapidly progressive, sometimes leading to blindness within days. Typically the cataract is total and diffuse with clearer zones along the suture lines. The accumulation of osmotically active sobitol within the lens causes waterlogging.

97
Q

Describe cataracts that may occur secondary to Occular disease?

A

Most importantly gPRA (especially in miniature and toy poodles, english cocker spaniels and labradors.) These arise as secondary to the retinal degeneration and generally progress to maturity. Cataracts may also arise secondary to glaucoma (changes in aqueous composition and damage to anterior lens epithelium), retinal dysplasia and RPED. Uveitis causes secondary cataract formation in cats and horses, but this is rare in the dog.

98
Q

What are senile/spontaneous/idiopathic cataracts?

A

Common in the dog, N-acetyl carnosine may reduce the rate of progression and reduce the extent of opacity if given to these dogs with early lens changes, but has no effect on lens clarity in mature cataract.

99
Q

How are cataracts managed?

A

Surgery - elective. Hypermature cataracts associated with a worse outcome and surgery should not be unduly delayed.

100
Q

What is the vitreous?

A

The vitreous is a soft gel comprising 90% water with some collagen and hyaluronic acid. It fills the posterior part of the eye, conforming to the shape of the surrounding structures. It is quite firmly attached to the posterior lens capsule and plays an important role in retaining the retina in position.

101
Q

What is persistent embryonic vasculature?

A

The hyaloid artery and the hyperplastic posterior vascular tunic of the lens may persist in definately appearing as a fibro vascular plaque immediately behind the lens along with a posterior capsular cataract. Treatment is not usually attempted. It is inherited in the SBT and doberman. As an incidental finding of no clinical significance the hyaloid artery can remain as a worm like projection from the optic disc or the back of the lens intro the vitreous. Sometimes the vessel may be seen in its entirety from the disc to the back of the lens.

102
Q

What is vitreal syneresis?

A

Liquefaction of the vitreous occurs as an irreversible degenerative change secondary to glaucoma, lens luxation, uveitis or senility. It predisposes the eye to retinal detachment as liquified vitreous can percolate beneath any holes in the neurosensory retina.

103
Q

What is asteroid hyalosis?

A

Numerous minute opaque spheres of a calcium/lipid complex suspended throughout the vitreous are not uncommonly seen in older dogs. They may be unilateral. Eye is sometimes otherwise normal but they can be associated with other Intraocular disease or systemic hypertension.

104
Q

What are vitreal opacities?

A

Vitreal floaters are sometimes seen as an incidental finding or they may be condensed exudate from previous posterior segment inflammation. Exudate or haemorrhage attached to the retina can cause traction, detaching the retina as it contracts. In active posterior segment inflammation they may be vitreal haze due to the presence of inflammatory cells in the vitreous. This can interfere with the view of the fundus as it appears out of focus.

105
Q

What are clinical signs of orbital disease?

A

Exopthalmost, difficulty in digital retropulsion of the globe, third eyelid protrusion, paiin on opening the mouth, deviation of the globe, conjunctival hyperaemia, chemosis, congestion, lagoptholmos and exposure keratpathy, enopthalmos due to destruction/loss of orbital contents, orbital swelling. Unilateral problems are most common, bilateral involvement would suggest myositis.

106
Q

What are the differential diagnosis for orbital disease?

A

Retrobulbar tumour, retrobulbar cellulitis/abscess, masticatory or extraocular myositis, adenitis of the zygomatic salivary gland, retrobulbar foreign body, retrobulbar haemorrhage, space occupying lesions of the nictitans gland or zygomatic salivary gland.

107
Q

What is a retrobulbar abscess/cellulitis?

A

Orbital infection may be caused by penetration of the skin conjunctiva or oropharynx with or without a foreign body. Stick/bone chewers most prone. The clinical signs are typically of acute onset with pain on opening the mouth, exopthalmos, periorbital swelling and often marked conjunctival hyperaemia. Broad spec antibiotics and NSAIDS will generally result in rapid improvement. COntineue 3-4 weeks.

108
Q

Describe Retrobulbar neoplasia?

A

primary, secondary or Tumours arising from adjacent structures. Signs usually develop gradually with progressive exopthalost and deviation of the globe. Some focal masses can be removed along with the eye. Excisions paring the globe - rare to retain functional globe.

109
Q

What is masticatory myositis?

A

A rare idiopathic inflammatory condition of the masseter, temporal and pterygoid muscles characterised by infiltration with lymphocytes and eosinophils. In acute masticatory myositis there is bilateral exopthalmost, third eyelid protrusion and pain on opening the mouth. Treat with systemic steroids. Atrophy of the muscles leads to enopthalmost, third eyelid protrusion and mechanical restriction to opening of the mouth.

110
Q

What is extraocular polymyositis?

A

Typically affects young golden retrievers, causing a bilateral non painful Exopthalmos with reduced ocular movement. Swollen extraocular muscles seen on ultrasound. Treatment with systemic corticosteroids or azathioprine is required to avoid post inflammatory contracture.

111
Q

What is enopthalmos?

A

Sinking of the eye into the orbit which will cause a secondary third eyelid protrusion. Characteristic in doberans, rough collies, GT danes and FC retrievers which have small eyes and long noses. Mucus may accumulate at the medial canthus. Ocular pain will cause contraction of the retractor bulbi muscle and globe retraction. Atrophy of orbital tissue - severe dehydration and chronic masticatory myositis allow the globe to sink further into the orbit. Horners syndrome - functional denervation of the sympathetic supply to the eye and orbit.

112
Q

Describe the retinal arteries and veins?

A

The retinal vessels enter and leave the retina around the optic disc and travel alongside the axons of the ganglion cells. The venules are larger than the arterioles in the dog and may be seen to anastomose over the surface of the disc. These superficial vessels supply the inner layers of the retina. The outer layers are supplied by the choriocapillaris, a capillary network just beneath the RPE.

113
Q

What is the tapetal fundus?

A

It occupies a roughly triangular area dorsal to the disc in dogs. The extent is variable, extending to or below the disc in some dogs. The taeptum is found within the choiroid, acting as a mirror to reflect light back to the photoreceptors in dim light. In order for light to reach the tapetum, the cells of the RPE are non pigmented. The Tapetum is not fully developed at birth taking about 12 weeks to acquire its adult colour.

114
Q

What is the non tapetal fundus?

A

Where the fundus lacks a tapetum, it makes sense that the light be absorbed as soon as it passes beyond the photoreceptor layer. The RPE is therefore densely pigmented in this area.

115
Q

What is pigment dilution?

A

Occurs to varying degrees, often related to coat colour and the colour of the iris. In some individuals the pigment dilution of RPE allows the choroidal blood vessels to be seen. Choroidal vessels are arranged roughly parallel to one another in an organised network.

116
Q

What is tapetal hyperreflectivity?

A

If the retina is atrophic it becomes thinner. This presents less of a barrier to light reaching and returning from the tapetum. The tapetum will therefore appear brighter.

117
Q

What is acquired pigment in the tapetal fundus?

A

melanocyte activity with pigment deposition may follow a range of insults including inflammation. Lipfuscin accumulation occurs specifically in retinal pigment epithelial dystrophy and is paler than melanin.

118
Q

What is vascular attenuation in the fundus?

A

This occurs secondary to retinal degeneration, the vessels gradually disappearing over time. In early cases this is easiest to see in the peripheral fundus and in the finer arterioles around the disc. The larger venules last longest.

119
Q

What is haemorrhage in the fundus?

A

Subretinal haemorrhage appears as small dark spots. Superficial retinal haemorrhage is streaky and radial as it follows the nerve fibre layer and appears associated with the retinal vessels. Pre retinal haemorrhage settles under gravity assuming a keel shape.

120
Q

What is retinal detachment?

A

The neuroretina is firmly attached at the optic disc and the ora ciliaris (around the equator where the neuroretina terminates and becomes the ciliary epithelium). Elsewhere the attachents to the RPE are weaker and may separate. This varies in extent from small focal detachments to 360 bulbous detachment.

121
Q

What is collie eye anomaly?

A

A congenital abnormality in which defects of the choroid, optic disc, reitna and sclera may arise through impaired mesodermal differentiation. It is inherited as a recessive autosomal trait. The essential lesion is an area of choroidal hypoplasia lateral to the optic disc, around the junction of tapetal and non tapetal regions. The pigment in the RPE and choroid is depleted, exposing the whiteness of the sclera between the choroidal vessels. About 30% of dogs will also have an optic disc coloboma.

122
Q

What is retinal dysplasia?

A

A collective term used to describe a number of conditions arising from defective retinal differentiation during ocular development. Total retinal dysplasia - pups are born blind with total retinal detachment, sometimes seen in association with micropthalmia and cataracts. Multifocal retinal dysplasia - a pleomorphic clinical appearance varying from a few retinal folds to larger areas of hyperreflectivity and pigment in the area above the disc.

123
Q

What is generalised progressive retinal atrophy?

A

Inherited cause of blindness in pedigree dogs. A group of genetic distinc diseases affecting different breeds at all ages. The primary lesion affects the photoreceptors in all cases. either photoreceptor dysplasias or photoreceptor degenerations. Typical history is night blindness, granularity or colour of the peripheral tapetal fundus which is often striate or radial in appearance and early retinal vascular attenuation. Tapetal hyperreflectivity and vascular attenuation is more extensive and pronounced.

124
Q

What is retinal pigment epithelial dystrophy?

A

Rare, reduced ability to utilise vitamin E, seen in cocker spaniels, The Fundoscopic changes consist of pale brown spots within the tapetal fundus, which represent focal accumulations of lipofuscin. Visual loss is slowly progressive. Dietary supplementation with Vit E can prevent pregression.

125
Q

What is sudden acquired retinal degeneration?

A

A condition affecting mature adult dogs mean onset 8-10 years. Dachshunds appear predisposed, but any breed can be affted. Retinal insult of some sort leads to apoptosis of the photoreceptors leading to the visual loss, a normal fundic examination and non recordable electroretinogram. Melanopsin, a photopigment found in some retinal ganglion cells, unaffected by damage at the photoreceptor level, is why PLR persists when blue light is used in SARD patients.

126
Q

What is active chorioretinitis?

A

Inflammatory cells accumulating around blood vessels appear as distinct grey/white opacities. Thickening of the oedematous retina causes a focal hypo reflectivity and haemorrhage and retinal detachment may be present.

127
Q

What is post inflammatory changes? (inactive chorioretinitis)

A

With time the affected areas of retina atrophy leaving focal often sharply demarcated, areas of tapetal hyperreflectivity. Within the centre of these patches there are frequently dense deposits of pigment. In the non tapetal fundus, the areas of damage appear as depigmented irregular patches.

128
Q

What is retinal haemorrhage?

A

There are many causes of retinal haemorrhage including, hypertension, coagulopathies, retinal detachment, trauma, septicaemia, hyperviscosity syndrome.

129
Q

What are the possible causes of retinal detachment?

A

hypertension, chorioretinitis, trauma, CEA, retina dysplasia, loss of vitreous support, vitreal traction bands, idiopathic/immune mediated. Most detachments are bullous in nature, the retina remains attached at the ora ciliaris and fluid accumulates between the neuroretina and the RPE.

130
Q

What is idiopathic bullous detachment?

A

Frequently bilateral, and is traditionally treated with prednisolone at immunosuppresive doses initially, tapering gradually over weeks and eventually discontinued. Even very extensive detachments may reattach with return of vision but recurrence is a possibility.

131
Q

How may ivermectin toxicity affect the eyes?

A

Excessive dose or use in a susceptible animal may give rise to the occular signs of mydriasis, blindness, reduced or absent PLR, retinal folds or retinal oedema.

132
Q

What is optic nerve hypoplasia?

A

A rare congenital hypoplasia of the optic nerve which may be bilateral or unilateral. The disc appears not only small but greyish in appearance due to lack of myelinated fibres. Blindness if severe.

133
Q

What is a coloboma?

A

Any congenital non progressive discontinuity in the occular tissues. The optic disc is affected most often and most of these are CEA related The effect on vision relates to the size of the coloboma.

134
Q

What is optic atrophy?

A

The result of advanced retinal degeneration in which other Fundoscopic abnormalities will be obvious. These include tapetal hyperreflectivity, retinal vascular attenuation and patchy depigmentation of the non tapetal fundus. The disc appears dark or pale flat and small.

135
Q

What is papillooedema?

A

Oedematous swelling of the optic disc most often occurs as a result of pressure on the nerve within the orbit. e.g by a retrobulbar tumour. The disc protrudes forward so it is out of focus relative to the fundus, focussing on the disc surface using the direct opthalmoscope requires a more positive setting. Papillooedema by itself has no effect on vision or the pupillary light responses.

136
Q

What is optic neuritis?

A

Inflammation of the optic nerve, caused by infectious agents, toxins, granulomatous meningoencephalitis and trauma.. Many are idiopathic. May appear similar to papillooedema, although the disc margins are less distinct and the disc may look pinker than normal. Small haemorhages near the disc, retinal oedema and vitreal haze may accompany the signs. Most cases present bilaterally and are suddenly blind.

137
Q

What is micropthalmos?

A

A congenitally small eye, often associated with other congenital abnormalities e.g persistent pupillary membranes, corneal opacities, nuclear cataracts, nystagmus, retinal dysplasia.

138
Q

Describe a prolapse of the globe

A

Beyond the plane of the eyelids - usually following known trauma or this can be quite minor in brachycephalic breeds with naturally prominent globes. Cornea should be kept moist. Replacement of the globe should be performed under general anaesthesia. Spasm of the eyelids behind the globe may make reduction difficult, a lateral canthotomy and traction on the lids with stay sutures will overcome this. The globe is replaced using a scalpel handle or similar to protect the cornea as stay sutures are tightened. The prognosis for a functional eye is very guarded.

139
Q

What is buphthalmos?

A

Also known as hydropthalmos and megaglobus, this refers to the globe enlargement that results from chronic glaucoma. It should not be confused with exopthalmos - the globe is not particularly prominent when viewed from above, there is no third eyelid protrusion and there will be Intraocular signs of glaucoma in buphthalmos. These eyes are usually blind, unsightly , painful and prone to exposure problems.

140
Q

What suture material should be used in the eye?

A

4/0 - 6/0 polyglactin -vicryl persists about 4 weeks or vicryl rapide persists about 10 days. Ideal for lid surgery as handles well and they do not need to be removed.