Small Animal Primary Care Test 1

Primary components of the adnexa

Orbit, extraocular muscles, eyelids, conjunctiva, third eyelid, lacrimal system.

Function of the orbit

A bony fossa which separates and protects the eyes, and contains foramina for vasculature and nerves.

Function of the conjunctiva.

Immune protection, tear composition, healing of corneal ulcers.

Function of the third eyelid (“nictitans”).

Protects cornea, produces aqueous portion of tears, immune function.

What components of the eye are tears produced by?

Aqueous: lacrimal gland, third eyelid gland.

Lipid: Meibomian (eyelid) gland.

Mucin: goblet cells.

Function of tear film.

Creates smooth eye surface, protects and lubricates, removes waste, provides nutrition to conjunctiva and cornea.

Chemosis

Conjunctival edema.

Conjunctival hyperemia.

Erythema, congestion of conjunctival blood vessels.

Blepharospasm

Spasm of orbicularis oculi, resulting in excessive blinking.

Keratitis

Corneal inflammation, may or may not be ulcerative.

Episcleritis

Inflammation of connective tissue exterior to the sclera.

Corneal edema

Fluid build up within the cornea, causing a cloudy blue appearance.

Signs of orbital disease

Exopthalmia (protrusion / bulging of eye), elevated nictitans, strabismus, reduced retropulsion.

Main considerations for exopthalmia

Inflammatory (usually acute, younger patients, may show pain on oral exam) vs. neoplastic (chronic, older patients, usually normal oral exam). Differentiate with advanced imaging.

Retrobulbar cellulitis / abscess

Usually due to penetrating injury behind maxillary molar (stick, bone) or an injected tooth root. Medically treated, may require surgery to remove foreign body.

Orbital neoplasia

Mostly malignant, aggressive with poor prognosis (fibrosarcoma, osteosarcoma). Common in older patients, chronic and without pain on oral exam.

Extraocular myositis

Causes “shook appearance”, an immune-mediated disease, responsive to corticosteroids or immunosuppressive aggents.

Eyelid neoplasia

In dogs majority (90%) are benign, meibomian gland adenomas. Cats, majority are squamous cell carcinoma. Must diagnose with biopsy, can treat conservatively or surgically.

Entropion

Inversion of the eyelids. May be congenital, spastic, or cicatricial (scarring). Mainly resolve in time if congenital, or if underlying cause is treated (spastic resolves with topical anesthetic). Some may require surgery which should not be conducted until facial maturity.

Ectropion

Exversion of the eyelids. Low clinical significance, usually congenital (rarely can be cicatrical).

Distichiasis

Hair growing out of meibomian gland orifice, usually no clinical significance (rarely epiphora, irritation). Treatment is generally benign neglect, or more rarely cryotherapy or surgery.

Ectopic cilia

Erupt from palpebral conjunctiva, usually around top of dorsal lid in young dogs. May cause non-healing corneal ulcers. Treated by resectioning of ectopic cilium + follicle.

Trichiasis

Normal hair contacting cornea / globe, can be primary (as in Shih Tzus) or secondary due to entropion or prominent nasal folds. Treated by grooming, correction of underlying issue.

Primary causes of conjunctivitis in cats

Feline herpesvirus-1 and Chlamydophila felis - consider infectious causes.

Feline herpesvirus-1

Causes URI signs, significant conjunctival hyperemia, dendritic ulcers (pathognomonic). Usually self-limiting, should reduce stress and may use anti-virals.

Chlamydophila felis

Causes significant chemosis and mild hyperemia without keratitis. Treated with erythromycin and tetracycline.

Follicular conjunctivitis

In young dogs secondary to antigenic stimulation. Displays as red eyes with discharge, conjunctival hyperemia with prominent follicles. Usually self-limiting, dexmethasone.

Allergic conjunctivitis

In dogs with allergies. Displays as red eyes with discharge and pruritis, conjunctival hyperemia, chemosis. If chronic, may cause lymphoid follicles. Treat atopy, flush with saline, and provide topical antihistamines or steroids.

Prolapsed third eyelid gland (cherry eye)

Some breed predisposition, due to weak ligaments holding the gland in place. Treatment is surgical replacement, do not remove the gland as it causes KCS.

Differentials for cherry eye

Scrolled / everted cartilage (especially large breeds), neoplasmia, trauma.

Dacrocystitis

Lacrimal sac and nasolacrimal duct inflammation, causing thick ocular discharge and mild conjunctivitis. Usually presents as recurring unilateral conjunctivitis with a negative Jones test. Treated with topical steroids / Abs, or nasolacrimal catheterisation.

Keratoconjunctivitis sicca (KCS)

Deficiency in tear production, many causes but commonly immune-mediated. Causes conjunctival hyperemia, mucopurulent discharge, keratitis, and a dull, dry corneal surface.

Quantitative tear film deficiency

Aqueous tear deficiency, shows abnormal Schirmer tear test.

Qualitative tear film deficiency

Issue with tear film stability, leading to premature evaporation, shows normal Schirmer tear test.

Treatment for KCS

Lifelong management: tear stimulants (expensive) or replacements. Surgical options possible such as parotid duct transposition (mainly obsolete) or cyclosporine implant.

Tests conducted during neuro-opthalmic examination

Palepbral (V / VII)

Menace (II / VII)

Pupillary light reflex (II / III)

Dazzle (subcortical reflex. II, VII)

Function of the direct opthalmoscope

Used to observe ocular surface and internal structures, as well as for Fluorescein stain testing and aqueous flare. The field of view is small, so must be within 2cm of the patient’s face.

Indirect opthalmoscopy

Utilises a hand lens, allows for a larger field of view and visualisation of the anterior chamber / fundus. However, it has less magnification, and requires drug-induced mydriasis for use.

Schrimer tear test

Assesses the production of the aqueous portion of tear film by placing a small strip in the lower fornix for 1 minute. Indicated to perform if the eye is red or has mucoid discharge. Do after exam, but before other tests.

Fluorescein stain

Used for red / blue eye, blepharospasms, discharge, or corneal defects. Hydrophilic, lipophobic stain (adheres to stroma but not epithelium). Enhanced with blue light examination (wood lamp, direct opthalmoscope).

Jones test

Assesses nasolacrimal duct patency by applying fluorescein to the eyes and detecting when it appears in the nares (variably 30s – 30m). May be unreliable in brachycephalics.

Tonometry

Checks intraocular pressure (indicated by red / blue eye, blepharospasms, conjuntival hyperemia, pupillary changes, etc.), can be done rebound (momentary contact, no anesthetic) or applanation (topical anesthetic).

Layers of the globe

Fibrous (sclera, cornea), uvea (iris, ciliary body, choroid), nervous (retina, optic nerve).

Chambers of the globe

Anterior chamber (aqueous), posterior chamber (aqueous), vitreous.

Cornea – structure and function

Avascular, mostly dehydrated structure with four layers: epithelium (non-keratinised), stroma, Descemet’s membrane, endothelium.  Works to transmit and refract light.

Corneal innervation

Sensory innervation via the opthalmic divison of the trigeminal nerve – decreased sensitivity can affect healing, as in brachycephalics (less nerve branches).

Corneal edema

Appears as a blue opacity, usually due to endothelial or epithelial damage such as ulceration, uveitis, or glaucoma.

3 responses of the cornea to damage

Vascularisation: due to keratitis, starts at limbus after 1 week, grows 1mm per day.

Pigmentation: secondary to chronic irritation.

Cellular infiltration: due to infected corneal ulcer or neoplasia.

Corneal ulceration

Corneal lesion resulting in loss of epithelium and sometimes stroma, diagnosed by direct exam and fluorescein stain. May be caused by trauma, eyelash or lid abnormalities, neuropathy, or extension of systemic illness.

Simple corneal ulcer

Superficial (only epithelial loss), not infected, no underlying condition, and heals within about 7 days.

Complex corneal ulcer

Deep (epithelial and stromal loss), may be infected, have underlying conditions, and take over 7 days to heal.

Symptoms of corneal ulceration

Blepharospasms, epiphora, corneal edema, conjunctival hyperemia.

Melting corneal ulcer

Seen with invading leukocytes or specific bacterial / fungal infection – ulcer complicated by the release of collagenases and matrix metalloproteinases (MMPs), which causes rapid stromal loss. The cornea feels soft and liquified.

Treatment for superficial ulcers

Abx (to prevent infection), analgesia, e-collar to prevent rubbing. Recheck in 7 days (2 for brachycephalics).

Treatment for complex ulcers

May need referral, or even surgical grafting. Abx and serum q2hr based on sensitivity profile, analgesia, e-collar, frequent rechecks.

Indolent corneal ulcer

Chronic, superficial non-healing ulcer (>2 weeks), with loose edge of epithelium. Some breeds are predisposed (boxers, French bulldogs). Treated with debridement, keratotomy.

Function of the uvea

Modifies external and internal light (iris – modifies pupil size, ciliary body – alters lens focal power), nourishes eye interior (ciliary body – produces aqueous humor and drains it to manage pressure), removes waste.

Uveitis (ocular vasculitis)

Can be primary (idiopathic, ulcers, cataracts, tumours, trauma, pigmentary uveitis), or secondary to systemic disease (infection, metabolic, immune disease, metastatic neoplasia).

Symptoms of uveitis

Pain, conjunctival hyperemia, decreased IOP, miosis, edema, and a very long list of other symptoms… basically if it’s an eye symptom it can happen.

Iris bombe

Synechiae (adhesions) between the iris’s pupillary margin and the anterior lens capsule, resulting in aqueous humour accumulating in the posterior chamber, causing iridial ballooning and obstructing the iridocorneal angle (causing glaucoma).

Diagnosis of uveitis

Detection of low intraocular pressure (due to reduced aqueous humour), along with the physical and opthalmic exams.

Glaucoma

Disease characterised by increased intraocular pressure, resulting in damage to the optic nerve or ganglia. May be congenital, primary (as in iridocorneal angle issues), or secondary to things like uveitis or neoplasia.

Signs of glaucoma

Acute: pain, corneal edema, episcleral injection, pupillary dilation, blindness.

Chronic: bupthalmia, lens luxation, blindness.

Diagnosis and treatment of glaucoma

Intraocular pressure increased over 25mmHg with concurrent clinical signs. Treatment changes based on whether it is primary / secondary, acute / chronic, but the goal is lowering intraocular pressure. Usually requires intensive medication and long term prognosis is relatively poor.

Lens luxation

May be posterior (lens falls into vitreous chamber) or anterior (emergency due to glaucoma risk, requires referral or enucleation), and occur due to primary (hereditary) or secondary (glacuoma, truama, uveitis) causes.

Cataracts

Cloudiness of the lens, blocking vision. Usually hereditary (in dogs) or secondary to uveitis (cats), sometimes due to diabetes, trauma, toxins, or age. Treated surgically.

Lenticular sclerosis

Normal, bisymmetrical age-related hardening of the lens fibres with minimal vision impact. Pathognomic feature is tapetal reflection (not present with cataracts).

Observing fundus

Optic disc has variable size and shape, but should be whitish and in the same plane as the retina (no bulging). Count, analyse and observe the vessels and where they cross (many variations of normal). The tapetum is in the dorsal fundus and may vary in colour between species, or not be present in dilute or albino animals.

 Hypertensive retinopathy

Displays as retinal hemorrhage and bullous retinal detachment, possibly with associated tapetal hyperreflectivity. Secondary to systemic hypertension (often due to CKD, cushings).

Periodontal disease

Insidious, progressive inflammatory disease of the peritoneum, eventually leading to attachment loss.

Gingivitis

First stage of periodontal disease: inflammation of free gingival margin. Can occur within two weeks of having untreated plaque (gingival epithelium replaces every 4 – 12 days).

Periodontitis

Inflammation of support structures of tooth, resulting in irreversible attachment loss.

Four phases of plaque formation

1 - Immediate (<1 hour), prescence of salivary glycoproteins and formation of dental pellicle.

2 - Within a few hours, Gram + bacteria colonise the pellicle to form a biofilm.

3 - 24 hours, bacteria produce polysaccharides and form an immature plaque.

4 - >24 hours, anaerobic bacteria colonise and form calculus.

Calculus formation

Plaque mineralises from saliva into calculus, which is mechanically irritating and provides a supportive environment for more plaque and anaerobic organism colonisation. The bacterial toxins and metabolic products cause inflammation.

Inflammatory cascade

Biofilms resist desiccation and immune response / antimicrobials. No blood supply to tooth surface (inability to deliver inflammatory cells, oxygen). Calculus is impenetrable by host immune cells. This all leads to increased host osteoclastic activity and proteolytic enzyme production, resulting in tissue attachment destruction (edentulism).

Prevalence of periodontal disease

80-85% of animals >2 have periodontal disease, and the incidence is increasing.

Local effects of periodontal disease

Halitosis, pain and discomfort, rhinitis (maxillary teeth), nasolacrimal disease (maxillary canines), tooth root / retrobulbar abscessation (uncommon), pathologic jaw fractures (mandibular teeth of small breeds due to small cortical bone), and osteomyelitis.

Distant effects of periodontal disease

Hepatitis, endocarditis, chronic kidney disease, insulin resistance (maybe unsubstantiated?).

Staging of periodontal disease

Done with periodontal probing and intraoral radiography to assess gingivitis and degree of bone loss.

Periodontal stage 0 (PD0)

Clinically normal (no inflammation), showing no attachment loss (bone close to neck of tooth) on radiographs. Excellent prognosis, continue at home oral care.

Periodontal stage 1 (PD1)

Gingivitis only, showing no attachment loss (bone close to neck of tooth) on radiographs. Excellent prognosis, treated with dental scaling and polish + at home oral care.

Periodontal stage 2 (PD2)

Gingivitis, mild periodontitis, showing under 25% attachment loss or furcation on a multirooted tooth. Good prognosis, treated with dental scaling and polish + at home oral care.

Periodontal stage 3 (PD3)

Gingivitis, moderate periodontitis, showing 25-50% attachment loss or stage 2 furcation of multirooted tooth. Poor or guarded prognosis, treated with tissue regeneration and extractions.

Periodontal stage 4 (PD4)

Gingivitis, advanced periodontitis, showing >50% attachment loss or stage 3 furcation of multirooted tooth. Grave to grim prognosis, treated with extraction.

Dental antimicrobial use recommendations

Generally, only indicated if there is preexisting risk factors. Transient bacteremia is a result of professional dental cleaning, for systemically healthy patients this can be ignored.

Dental antimicrobial use protocols

Intra-operative: for severely immunocompromised patients, those with cardiac disease or severe hepatitis, renal disease, and oral infection, give 30-60 mins before and then every 90 during the procedure.

Pre or post-operative: if severe soft tissue involvement or osteomyelitis, start 5-7 days before (soft tissue) or 28 days before (osteomyelitis).

Scaling

Cleaning the teeth above (supragingival) and below (subgingival) the gumline.

Guided tissue regeneration

Facilitates regeneration of lost periodontal tissue.

Closed periodontal therapy

GTR, uses ultrasonic and hand instruments on pocks under 4mm to remove the superficial layer of the cementum and perform gingival curettage, requires at home care.

Open periodontal therapy

GTR, uses ultrasonic and hand instruments on pocks over 4mm to remove the superficial layer of the cementum and perform gingival curettage, requires mucoperiosteal flap.

Local antimicrobial therapy

GTR, using low-dose doxycycline for injection or commercial doxirobe gel in the gingival sulcus to form a protective matrix (biodegradable).

Bone grafting / implants

Replaces lost bone and facilitates regrowth. Can be autogenous (from patient), alloplasts (synthetic), allographs (from same species), xenographs (from other species).

Cementum

Outer layer of tooth root, acting functionally as its periosteum. Is also considered part of the periodontal support apparatus.

Dentin

Continually produced tissue that forms the main component of the tooth, consisting of multiple tubules and sensory nerve fibres, covered by cementum (root) and enamel (crown).

Attached gingiva

Gingiva attached to periosteum of alveolar bone, extending to mucogingival junction (where gingiva and oral mucosa meet).

Free gingiva

Portion of gingiva not attached to tooth, but closely adapted to its surface.

Periodontal support apparatus (periodontium)

Consists of alveolar bone (cancellous bone around roots), lamina dura (dense, cortical bone forming alveolar wall next to tooth), the periodontal ligament, cementum, and gingiva.

Canine dental formula

3130, total 28 teeth (decidious).

3142/3143, total 42 teeth (adult).

Feline dental formula

3130/3120, total 26 teeth (decidious).

3131/3121, total 30 teeth (adult).

Teeth eruption timing

Dogs get their decidious teeth between 3-10 weeks, and their permanent teeth between 3-7 months (incisors, canines earliest).

Cats get their decidious teeth between 2-6 weeks, and their permanent teeth between 3-6 months (incisors, canines earliest).