Dogs and Cats 4 Flashcards
1
Q
Management with behavioral problems what are the 2 main types and things within
A
- Acute management of self-harming
○ Bandages
○ Muzzle
○ Sedative -> stop from spinning for a short term in order to relieve - Chronic management - reducing stress
○ Remove sources of stress and frustration
○ Request-Response-Reward interactions (RRR)
§ Every time you interact with animal, ask to do what they know “sit”, then get reward when do it right
§ Putting predictability and consistency in its life
○ Training - again give predictability give animal sense of control
○ Consistent routine
○ Daily walks
§ Social interaction
○ Opportunity to control aspects of the environment
§ e.g. meals from food dispensing toys - controlling their food intake
2
Q
Describe 3 main behaviour modifications that are used for behavioural problems
A
1) Response substitution
○ teach an alternative and incompatible behaviour
○ If start to spin around tell to go into safe place such as a crate (need to create a good environment in that crate not associated with the spinning first before can try)
2) Systematic desensitisation
○ reduce fear and anxiety
3) Counter-conditioning
○ reduce fear and anxiety
3
Q
What are the 2 main medications and how to apply when treating behavioural problems
A
- SSRi’s - selective serotonin reuptake inhibitors (fluoxetine, sertraline)
- TCA’s - tri-cyclic antidepressants (clomipramine, doxepin (anti-histamine as well))
- Most effective in early stage
○ Treat early!
○ Wean off after two months of complete clinical resolution
§ 75% dose for 2 weeks, then 50% dose for 2 weeks, then 25% dose for 2 weeks and discontinue
§ Recommence at lowest effective dose if reappears
4
Q
What are important aspects of prognosis with compulsive behavioural problems
A
- Control rather than cure….. relapses with stress
- 2/3 owner satisfied with outcome
- Failures
○ Poor owner compliance
○ Long problem duration
○ Did not attempt treatment
5
Q
Acral lick dermatitis (lick granuloma) what are they, common location, causes and when more common
A
- Ulcerative plaques secondary to chronic licking, biting and chewing
- Carpus, metacarpus > radius, metatarsus, tibia
- Occurs when owner present and absent (often exacerbated)
○ Absent - possible separation anxiety - Occasionally history of trauma to area
- More common in large breeds
- Males 2X > females
6
Q
Acral lick dermatitis differentials and treatment
A
Differentials: dermatological, neurological or displacement behaviour
Treatment: behavioural and dermatological
- Other treatments - probably not as good
○ Cryosurgery
○ Radiation therapy
○ Excisional surgery
○ Laser surgery
○ Acupuncture
Topical medications
7
Q
Acral lick dermatitis what are some causes
A
- Normal
- Anxiety: Uncertain/inconsistent interactions/ relationships
- Inadequate physical, mental social stimulation
- Attention seeking
- Oral and GI disease
- Compulsive disorder
- Displacement behaviour
- Dermatological condition
- Endocrinopathies
- Secondary to pain or irritation, e.g. arthritis
8
Q
Flank sucking what breed most common in, what causes
A
- Dobermans
- Damp ruffled skin to raw open sores
- If doesn’t cause physical damage or interfere with normal functioning then may be acceptable ‘coping’ mechanism?
- In some cases constant sucking when not sleeping or engaged in other activity
9
Q
What are the some causes of tail chasing
A
- Conflict, frustration
- Reinforced
- Epileptic, episodic behaviour
- Neuropathological
- Psychotic/ hallucinary
- Dermatitis
10
Q
Psychogenic alopecia (overgrooming) what is the general history and main clinical sign
A
- History
○ Environmental or social change may be trigger
○ More common in indoor cats
§ Confinement stress?
§ Social stress?
§ Social isolation?
○ Excessive grooming, chewing, pulling out hair
§ Away from owner if previously punished - Hairloss
○ Focal, partial, bilateral
○ Common in groin, ventrum, medial and caudal thighs
○ Skin normal to erythematous and/or abraded
11
Q
Overgrooming in cats what is the main cause, breed most common and treatment
A
○ Large percentage of cases have underlying medical problems
§ Allergy, Endocrine
§ Infections: parasitic, fungal, bacterial
§ Trichogram important to determine cause is grooming
□ But still multiple aetiologies
→ Diagnosis of exclusion
○ Most common in Burmese and Siamese
○ Most common in Burmese and Siamese
○ Ingestive compulsive disorder
§ Rule out gastro-intestinal disease, nutritional deficiencies, metabolic disease, CNS
○ Treatment
§ Alternative oral stimulation -> Bulky, dry, chewy, fibre, bones
§ Reduce anxiety and conflict
§ TCA, SSRI
12
Q
Feather picking list the 3 main groups of causes and treatment options
A
1) pathological
2) behavioural
3) genetics
Treatment
- Limit self-trauma
○ E. collar
- Increased space and option of flight
- Structured interactions and training
- 12 hours dark, quiet sleep
- Adding mate/removing incompatible mate
- Toys and other environmental enrichment
- Videos, radio, water spray to encourage natural grooming
- Work for varied diet
○ Food dispensing toys
- Medications
○ TCA, SSRI
13
Q
List some pathological causes of feather picking
A
○ Nutritional deficiencies
§ Poor diet
§ Chronic disease → abnormal skin and feather development
○ Toxins
○ Infections e.g. PBFD, fungal, viral, bacterial
○ Ectoparasites, e.g. lice, mites
○ Endoparasites, e.g. giardia in cockatiels
○ Organ pathology
○ Feather cysts (Golden macaws, canaries)
○ Dermatitis
§ Hypersensitivities
□ Irritant dermatitis
14
Q
List some behavioural causes of feather picking
A
○ Confinement ○ Limited stimulation ○ Stress / frustration (e.g. sexual) ○ Attention seeking ○ Crowding (social stress) ○ Dominance (social stress) ○ Environmental § Low humiditiy § Lack of sun, fresh air § Abnormal and inconsistent light/dark cycle § Noisy and unpredictable
15
Q
List 3 main genetic causes of feather picking
A
○ Female Amazons
○ Parallel to trichotillomania in women
○ Trigger by stress associated with sudden, unpredictable stimuli
16
Q
Skin crusting what are the 3 main colours and generally what they mean
A
○ White/grey crusts = scaling disorders
○ Yellow crusts (pus) = pustular disease
○ Dark crusts (dry blood) = erosive and ulcerative disease
17
Q
List 4 main causes of white/grey skin crusting
A
a. Scabies
b. Keratinisation defects - skin cells higher turnover that accumulate
c. Endocrinopathies
d. Sebaceous adenitis - defect in sebaceous glands resulting in dehydrated scaly skin
18
Q
List 2 main causes of yellow (honey coloured) skin crusts
A
pustules a. Bacterial infections - staphylococcus b. Immune mediated (pemphigus, drug eruptions) -> if present in areas without follicles (nose) know that it is THIS ○ Diagnosis § Cytology -> skin scraping
19
Q
List 2 main causes of dark skin crusts
A
Dark (serum/blood) = ulcers /erosions a. Self-trauma (itchy diseases) - important in cats b. Immune mediated - causes cell death § DLE - discoid lupus erythematosus § EM § Vasculitis § Cutaneous lymphoma #
20
Q
Sebaceous adenitis how common, what occurs, main risk factor and clinical presentation
A
- Relatively common
- In dogs, cats and rabbits
- Immune destruction of sebaceous glands
Risk factors
1. Breed - maltase terrier, Samoyed, goldern retriever
Clinical presentation - Scaly dry skin
○ Skin becoming dry due to defect in sebaceous glands and their excretions that are meant to hydrate the skin
○ Skin then tries to repair itself by making more lipid, only way is to make more skin cells -> higher turnover (hyper-proliferative) -> scaling - Dull coat - lack of sebum
- Alopecia -> sebum needed to keep hair within shaft
21
Q
Sebaceous adenitis what is the clinical presentation in short vs long coated dogs and diagnosis in these cases
A
1) Short coated -> nodules on the skin -> hair loss -> multiple dry scaly circular lesions
§ Looks like folliculitis -> dermatophytosis, demodex
§ Diagnosis -> cytology -> sticky tap prep or Trichograms (follicular casting will be present - also present in demodex)
□ Next step -> biopsy
2) Long coated -> present with advanced clinical disease as owners generally don’t notice early signs above
§ Large amount of diffuse hair loss and scaly dry skin
§ Diagnosis -> cytology, biopsy
□ Need to tell pathologist about distribution of lesions, breed, and possible sebaceous adenitis
22
Q
Sebaceous adenitis treatment for the different stages and what is important for future of animal
A
- Early stage (short coated) - Cephalosporin -> specifically targets the T cells which is the issue in these cases
- End stage (long coated) - hair will never come back normally as destroyed sebaceous glands
○ oil soaks
§ Cover baby oil/conconut oil 30 mins
§ Wash off and descale with Palmolive detergent
§ Phytosphingosine shampoo/mousse/conditioner
§ Repeat as needed -> monthly to normalise skin and weekly phytosphinogosine
DO NOT BREED -> genetic disease
23
Q
keratinisation defect what breeds common in, how diagnose
A
Breeds
- Cocker spaniel
- Irish setter
- Gold retriever - most common
- Others
DIAGNOSIS BY BREED AND HISTOPATHOLOGY -> young animal, generalised scale
- DNA testing Goldern Retriever - respond well to phytosphingosine
24
Q
what is the difference berween auto-immune and immune mediated and give an example
A
- Auto-immune - no trigger found, loss of self-tolerance
- Immune mediated (immune response cause injury but may have removable trigger
○ Eg: drug reaction -> most common drug is penicillins - first time on the drug then wont occur (needs to take 7-10days)
25
Pemphigus causes
- Breed related
○ Jack Russell's, akita, alaskan malamute, Samoyed - CAN BE ANY BREED
○ Cats -> Siamese derivations
- Drug induced/triggered -> penicillin common -> can be treated by removing this trigger
- Secondary to chronic skin disease
26
Pemphigus pathogensis and presentation
Pathogenesis
- Auto-antibodies present against desmosomal proteins which help with normal intercellular adhesions between skin cells
○ Can be transmitted to offspring through milk and transfer of auto-antibodies
- Results in blisters - skin cells separate - acantholysis -> triggers release of cytokines that attract neutrophils -> pus
Presentation
- Face - eyelids, nose, ears
- Feet
- Cat -> nail bed -> squeeze and pus comes out
○ Area of high mechanical
○ Rely on cytology here
Truncal -> less commo
27
Pemphigus diagnosis what are the 2 mechanisms
1) cytology -> neutrophils + keratinocytes (larger rounded cells)
2) Biopsy
○ Should biopsy INTACT pustule -> punch biopsy
§ 4mm punch if pustule is small enough as don't want to rupture
§ 8mm punch if larger pustule need to ask for multiple resections
○ Should do before just start treating -> otherwise if doesn't work need to stop treatment, wait and then biopsy
○ Farm dogs -> dermatophytosis can mimic pemphigus so should do it
28
What looks like pemphigus in cats and how to differentiate
Mosquito hypersensitivity in cats
| - Looks like pemphigus -> bites around the nose HOWEVER - eosinophils present without acanthocytes also seasonal
29
Discoid lupus erythematosus what breeds common in and presentation
Breeds - border collies, scotch collies, Shetland sheep dogs, maremma, kelpie
Presentation
- Depigmentation and crusting on the nasal planum
- Loss of architecture - flattening of the skin
30
Discoid lupus erythematosus pathogenesis, diagnosis and treatment
Pathogenesis
- UV induced -> causes movement of cellular proteins on surface of cell that immune system then recognises them as foreign and mounts immune response -> antibody and cell mediated immune systems
○ Cell damage leads to further release of these proteins -> self-propagating
Diagnosis
- Biopsy -> area where pigment is fading
Treatment
- REMOVE FROM THE SUNLIGHT
31
What 2 diseases look like discoid lupus erythematosus
1) mucocutaneous pyoderma
| 2) nasal hyperkeratosis
32
Lupoid onychodystrophy what is it, presentation and treatment
- Most common immune mediated but NOT CRUSTING
- Idiopathic?
Presentation
- Acute onset of multiple nails falling off
- Loose nails, splitting nails
- Adult dogs
Treatment
- Results in dystrophic nails if don't treat early - REFER
33
What are 3 functions of the hair coat
1. Environmental protection
2. Maintenance of skin microclimate
3. Psychosocial functions
34
Hair follicle cycle what are the 3 phases when prolonged
1. Telogen - resting
○ Prolonged in winter coated animals - huskies
§ Therefore can maybe not regrow hair for a long time
2. Anagen - growth - metabolic
○ Prolonged in longer coated dogs
3. Catagen
35
What are the 2 main facotrs that affect the hair follicle cycles and factors within
Intrinsic factors
- Epithelial-mesenchymal interactions
Extrinsic factors
- Photoperiod, temperature, nutrition, endocrine - IMPORTANT FOR DISEASE
○ When dogs lose their hair coat may grow back pigmentated -> melanin production due to temperature
○ Shave Siamese cats may regrow dark pigmented
36
What are the 3 main mechanisms of alopecia and mechanisms within
1. Excessive loss
○ Mechanical - trauma
○ Folliculitis - would see anagen hair but broken on Trichograms
2. Failure to grow
○ Follicular arrest -> severe physiological stress
○ Folliculopathy
3. No follicles
○ Scarring
○ Congenital alopecia -> ectodermal dysplasia (Will also have no teeth)
37
List 4 important steps in the diagnostic approach to a bald dog
1) signalment
2) history
3) physical examination
4) diagnostic test
38
What is important with signlament in terms of a diagnosis of a bald dog
```
○ Age (0-12 months)
○ Breed
§ Associated with breeding
○ Gender
§ Male -> testicular tumours
□ Sertoli cell tumour -> feminisation -> atrophy of one testicle
§ Female -> hyper-oestrogenism
```
39
What are important factors to consider with history when diagnosing a bald dog
○ Excessive loss -> scratching where on the body
○ Failure to grow -> generally slow progressive, diet - nutrition
§ Cosmetic (Cushing or thyroid) or not?
□ Hyper A - PU/PD, activity levels, appetite, panting, recurrent skin infections
□ Hypothyroidism - weight gain, heat seeking behaviour, muscle weakness, decreased fertility
○ At what age did this occur
○ Time of year
○ Drug history
○ Goal -> Differentiate between HyperA/hypothyroidism AND telogen effuvium/drug induced/post clipping
40
Physical examination what are some clinical signs to look for when diagnosing a bald dog
○ Dull coat
○ Bronzing -> melanin transfer stops as not growing -> oxidation from UV light
○ Hyper A -> abdominal enlargement, hepatomegaly, temporal muscle wastage, skin changes, increased panting
○ Hypothyroidism - Common -> lethargy, pyoderma, greasy scaly skin
○ Frictional hair loss
○ Peeling skin infection - staphylococcus
○ Calcinosis cutis
41
Diagnostic tests list the 3 main important ones for diagnosing a bald dog
1) trichogram
2) biopsy
3) haematology/biochemistry
42
Trichograms what is important to look for when diagnosing a bald dog
```
□ Traumatic (breaking), which phase within, folliculitis (demodex), follicular dysplasia
Folliculitis (demodex)
1. Anagen alopecia
- Excess loss
- Pattern baldness
- Early follicular dysplasia
2. Telogen alopecia
- Endocrinopathies
- Alopecia X
- Late FD
```
43
Biopsy where take from with bald dog and what is important to identify
edge of lesions, lesions and from bald areas
- Cut parallel to the skin and line with permanent marker, get lab to cut parallel to see the whole hair shaft
□ Histopathology
® Pattern baldness
® Early follicular dysplasia
® Inflammatory "non-inflammatory alopecia"
44
Haematology/biochemistry what important to diagnose with bald dogs and results that support this
```
For HyperA and hypothyroidism
1) HyperA -> LDDST, ACTH stim
2) HypoT -> if clin and clin path support then asses - BUT MOST COMMON OVER-DIAGNOSIS IN VET MEDICINE
◊ Haemogram Changes
- Mild non-regenerative anaemia (30-50%)
◊ Serum Biochemistry Changes
- Hypercholesterolaemia (75%)
- CPK elevation
- Mild increases in liver enzymes
◊ Endogenous TSH and free T4
```
45
What microbes cause otitis externa and what is important about them and therefore how does infection occur
Top 3 are present as normal flora within the ear - opportunistic
- Staphylococcus spp 22-40%
- Streptococcus spp 10%
- Malassezia spp 80%
- Pseudomonas spp 20% - exceptions to normal flora
○ Ubiquitous in water and environment
- Proteus mirabilis 11%
- Others (occasional)
INFECTION - change in micro-climate (swimming, scratching, inflammation etc.)
46
List 6 things that increase inflammation/humidity changing the microclimate of the ear leading to infection
1) allergies
2) shampoos
3) foriegn bodies
4) parasites
5) ear cleaners - overuse
6) plucking ears
47
ear cleaners what are they meant to do, most common and function
○ Removes wax from ear canal -> if too much wax (inflammation) then need to treat the inflammation not wax
§ Paws gentle ear cleaner - only one that removes wax -> IF CAN'T SEE EAR DRUM THEN CANNOT GIVE EAR CLEANERS -> toxic to middle ears
○ Most common ear cleaner -> odiflush - makes antibiotics work better BUT DOESN'T REMOVE WAX
□ Safe for middle ear if ear drum ruptured
48
What are important ocnsiderations when plucking ears
○ Plucking causes inflammation - change in microclimate - infection
○ If can place cotton bud into ear canal then DON'T NEED TO PLUCK - patent ear canal
○ Sedate dog to pluck if need be and then steroid to stop inflammation post plucking
49
List the 3 main reasons why treatment fails
1) failure of drug penetration
2) incorrect medication
3) failure of inflammation control
50
What occurs to contribute to failure of drug penetration
○ Wax present and stopping drug penetration
○ May need clean the ear canal mechanically under anaesthetic -> wax clumping
○ Owner compliance -> test for crystals present in the ear (vehicle in which drug is administered) if so then penetrating but possible resistance issues
○ Need to give them the right dose
51
What are important considerations with giving medications for ear infections to prevent incorrect medication
○ Can give oral steroids
○ Oral glucocorticoids best pain relief
○ Ruptured ear drum -> MIDDLE EAR SAFE
○ May need to give a long lasting one under general anaesthetic if unpleasant dog
○ Reliant on cytology- BUT NEED TO CLEAN THE EAR FIRST
○ Culture and sensitivity -> sensitivity based on laboratory not in the EAR CANAL - only used in certain situations
52
What is important to remember about antibiotics polymxin and gentamycin in the ear
Polymyxin - pseudomonas will develop resistance RAPIDLY - just need to know
- Use fluoroquinolone
Gentamycin - inactivated by pus
53
Culture and sensitivity with ear infection why bad, therefore when do and don't use
○ Culture and sensitivity -> sensitivity based on laboratory not in the EAR CANAL
§ Culture -> passenger bugs not important except if grown in pure culture
§ WHY BAD -> antimicrobial synergism, effects of cleaners, vehicles, antibiotic activity in different environments
§ DON'T CULTURE with pseudomonas
§ WHEN DO YOU USE
□ Otitis media -> as using oral antibiotics
□ Where resistance is suspected especially with cocci infection (MRSP)
® Uniform population
® Failure to respond
ALL other causes for failure ruled out
54
What can contribute to failing to control inflammation in ear infections
○ Foreign bodies -> especially grass seeds
○ Parasites -> ear mites
○ Ear cleaners
55
Primary secretory otitis media what occurs, result in , prognosis and what breed common in
- Mucous in their middle ear -> don't drain properly -> pressure in middle ear -> neurological signs, hearing loss
- Bulging ear drum
- If get early can regain hearing - referral
- COMMON IN CAVELIERS
56
List 6 things that result in eosinophilic recruitment
1. Allergies - NOT JUST ALLERGIES
2. Viral infection
3. Fungal infection
4. Furunculosis
5. Tissue necrosis
6. Neoplasia
57
List 8 clinical patterns of eosinophilic granuloma complex and what is important about this complex
- Miliary dermatitis
- Oral granuloma
- Palatine ulcers
- Indolent lip ulceration
- Lower lip granuloma
- Eosinophilic plaque
- Eosinophilic granuloma
- Linear granuloma
Multiple lesion types may be present in same cat
ECG is a reaction pattern NOT A DIAGNOSIS
58
Milary dermatitis what apart of, define and list 5 differential list
Eosinophilic granuloma complex
- Multifocal crusted papules (hard to differentiate follicular from no follicular)
Differential list
a. Folliculitis (dermatophytosis, bacterial)
b. Allergy (flea, atopy, food, mosquito)
c. Ectoparasites (Otodectes, Cheyletiella)
d. Immune mediate (Pemphigus)
e. Nutritional (EFAs, biotin def)
59
List some historical and clinical clues in miliary dermatitis and what causes they suggest
```
Historical clues
a. Nutritional (diet)
b. Fleas, Cheyletiella, Otodectes (current flea control)
c. Food allergy (if seasonal)
d. Atopy/Fleas (seasonal)
e. Persians (dermatophytosis)
f. Cattery (dermatophytes, Cheyletiella)
Clinical clues
a. Head (atopy, food allergy, Otodectes)
b. Neck (fleas, atopy, food allergy)
c. Pre-auricular (atopy, food)
d. Limbs/paws (atopy, food)
e. Tail base, caudal thighs (fleas)
f. Nasal planum (pemphigus, herpes, mossies)
g. Footpads, pinnae (pemphigus, mossie)
h. Nail beds (atopy, pemphigus)
```
60
What are 7 diagnostic approaches to determine the cause of miliary dermatitis
1) wood's lamp
2) fungassay
3) cytology.antimicrobial trial
4) biopsy (if nasal planum/pads)
5) insect elimination trail
6) food trial
7) intradermal skin testing/allercept serum testing
61
Wood's lamp in diagnosis of miliary dermatitis cause when should perform and what cause determining
§ Easy and should always be done
§ Positive fluorescence is the HAIR SHAFT not skin scales
□ If fluorescence check for broken hairs and send for fungal assay -> most likely Microsporum canis
□ Negative fluorescence doesn't rule out!
62
Fungaassay what need to do and what means positive when determing cause of miliary dermatitis
§ Check daily to assess colony growth and colour change
§ Discard after 14 days if no growth
§ The colour changed from YELLOW TO RED SIMULTANEOUS with the appearance of the colony
63
Cytology and antimicrobial trial when determining the cause of miliary dermatitis what need to do and what cause most likely with 1. neutriphils + cocci, 2. eosinophils without cocci, 3. acanthylotic cells
§ Lift the crusts and take a direct impression smear from beneath the crusts
§ Neutrophils, eosinophils and acantholytic cells
§ Neutrophilic/eosinophilic inflammation + cocci = infection secondary to underlying eosinophilic disease
§ Eosinophilic inflammation without cocci = eosinophilic dermatoses
§ Acantholytic cells - pemphigus foliaceous and diagnostic if in pustules on pads, nasal planum or nail beds
64
Biopsy what used for when determing cause for miliary dermatitis in cats
§ Used to confirm eosinophilic dermatitis and rule out dermatophytosis
§ Except with nasal planum and footpads where pemphigus foliaceous is a differential
65
Indolent ulcer reaction what is it, define and the 3 main differential diagnosis
```
Part of eosinophilic granuloma complex
Define - erosion/ulceration of the upper lip adjacent the canines and philtrum
Differential diagnosis
1. Hypersensitivity
- Flea allergy
- Atopy
- Food allergy
- Over-grooming
- Idiopathic
2. Squamous cell carcinoma
3. Feline sarcoid
```
66
What are the 4 tests in the diagnostic approach for indolent ulcer reaction in cats
1. Cytology (eosinophilic, neutrophilic, intracellular bacteria)
2. Antibiotic trail
3. Histopathology indicated if severe and progressive especially in older cats
4. Allergy investigation as per miliary dermatitis
67
Eosinophilic plaque reaction pattern what part of, define and the 3 main differential diagnosis and causes within
```
Eosinophilic granuloma complex
Definition - flat topped plaques
Differential diagnosis
1. Hypersensitivity
2. Infectious granulomatous
○ Mycobacteriosis
○ Nocardia/actinomycetes
○ Fungal granulomas
3. Xanthoma
○ Congenital hyperlipidaemia
○ Diabetes
○ HyperA
```
68
Eosinophilic plaque reaction pattern clinical clues and 6 tests within the diagnostic approach
```
Clinical clues
- Lick accessible areas
- Very pruritic
- Erythematous, yellow foci
Diagnostic approach
1. Cytology (surface and FNA)
2. Antimicrobial trial (oral and topical)
3. Biopsy ( if poorly responsive)
4. Insect elimination trial
5. Food trial
6. Intradermal skin testing/Allercept serum testing
```
69
Oral granuloma/ulcer what apart of, differential diagnosis, clinical clues and diagnostic approach
```
Eosinophilic granuloma complex
Differential diagnosis
1. Hypersensitivities
- Flea bite hypersensitivity
- Atopy
- Food allergy
- Idiopathic
2. Infectious granulomas
3. Neoplasia
Clinical clues
- Yellow foci
Diagnostic approach
- As per indolent ulcers although antibiotics rarely helpful in oral lesions but good with lip lesions
```
70
Eosinophilic granuloma complex management what are the 2 main ways and what is poor response
```
Specific
- Flea control
- Dietary manipulation
- Immunotherapy
Non-specific
- Glucocorticoids
- Cyclosporine
- Apoquel NOT registered in cats <30% efficacy in cats at dog dosese
Poor response re-assess diagnosis not just treatment
```
71
List 2 other diseases that look like eosinphilic granuloma complex
1) feline cutaneous herpes
| 2) mosquito hypersensitivity
72
Feline cutaneous herpes clinical presentation and management
```
Clinical presentation
- Eosinophilic inflammation - looks like eosinophilic dermatitis
- Intra-nuclear inclusion bodies
- Ulcerative dermatitis face or nasal planum
- Re-activation of latent infection
Management
- Lysine (not helpful)
- IFN
- Famciclovir
- Sun avoidance possibly
```
73
Mosquito hypersensitivity what are the historical and clinical clues
Historical clues
- Strong seasonal history (warm weather)
- Access to outdoors at evening
Clinical clues
- Location on the LATERAL aspects of the pads
- Dorsal nasal bridge and pinna
74
Mosquito hypersensitivity diagnostic approach and treatment options
Diagnostic approach
- Cytology (eosinophilic and no acantholytic cells)
- Response to indoor housing
Treatment
- Indoor housing best treatment
- Vit B? - shown to decrease severity in people
- Repellents - can be effective HOWEVER DEET toxicity is a risk in cats resulting in tremors, increased salivation, ataxia, vomiting, loss of appetite
75
Non-inflammatory alopecia what is one reason and how to diagnose
Over grooming
- Why groom? -> stimulation of pressure activate A fibres, release Beta endorphins
- Clinical presentation - alopecia in lick areas
- Diagnosis
○ Trichograms - trauma
○ woods lamp
76
What is the first thing you need to do with a cloudy eye and how to achieve
Locate cloudiness -> cornea, anterior chamber, lens or vitreous body
Detect -> with retro-illumination -> assess sizse, shape and depth of cloudiness
do before and after pupillary dilation
77
What are the 4 main reasons for a cloudy cornea and what do each look like
1. Corneal Oedema
○ = light scatter -> bluish tone to the cloudiness
○ Focal superficial oedema = epithelial loss
○ Diffuse, severe oedema = endothelial dysfunction
2. Fibrosis - bright white - healing corneal ulcer so fluroescein stain negative
3. white cell infiltrate - yellow looking due to puss
4. lipid/calcium - again bright white but crystal looking
78
Aqueous flare what is it and main causes, what can chronic uveitis lead to
- Cloudiness in between focal reflections on the cornea and iris/lens
- 50% immune-mediated
- 25% neoplasia
- 25% infectious disease
- Chronic uveitis frequently associated with cataract formation, secondary glaucoma or retinal detachment
79
List the 3 reasons for a cloudy lens
1) cataracts
2) senile nuclear sclerosis
3) lens luxation
80
Cataracts what is it, how common and treatment
○ Any opacity of the lens or its capsule
○ Most common cause of treatable vision loss
○ Approx. 1-5% of dogs may develop cataracts
○ Treatment = surgery -> can place a prostatic lens
81
Senile nuclear sclerosis what does it lead to, when common and cause
cloudy lens
○ Starts at 6-8 years in dogs
○ Due to continued growth of lens, lens expansion and compression of lens centre
○ Becomes obvious at 10-12 years
82
Lens luxation causes and why then become cloudy
Causes
○ Lens displacement due to zonular disruption
○ Primary in terrier breeds
○ Secondary to chronic uveitis, glaucoma, trauma (damage the zonules itself)
○ Cause cloudiness by:
§ Corneal oedema (elevated IOP +/- lens contact with corneal endothelium)
§ Cataract formation
83
What is the main reason for the vitreous to be cloudy, cause, presentation, and vision
○ Age related
○ Bilateral but not symmetrical
○ Retroillumination
○ When advanced will impact vision
84
What are 3 important tests for perform on cloudy eyes
1. Perform tonometry
2. Fundus
○ Can be difficult to perform through a cloudy eye
○ Indirect ophthalmoscopy seems to be more effective
3. Fluorescein stain
○ Fluorescein stain should be placed in dorsal bulbar conjunctiva
Don't touch cornea
85
What are 5 aspects of treatment for corneal ulcers
- Topical broad spectrum AB therapy
- Topical atropine? Only if uveitis present
- Oral doxycycline? May be of benefit
- Oral NSAIDS - definitely
- +/- bandage contact lens - eye drop will penetrate
○ 50% will fall out within the first week
86
Corneal foreign bodies how to remove and then post-removal treatment options
1) Removal
○ DON'T USE FORCEPS -> only push it in further
○ 10ml syringe with broken-off 25g needle -> removal with hydropulsion if superficial
○ If deeper may need general anaesthetic and removal with surgery microscope and go within the eye
2) Need to then help heal the ulcer that will result from foreign body
○ Topical broad spectrum antibiotics eye drop or ointment
○ Oral NSADIS, atropine?, doxycycline?
○ bandage contact lens, third eyelid flap (only use when know there is no infection -> comfort)
§ Will not speed up healing
87
Third eyelid flap what do the provide and the 2 types
- Bandages cornea -> places conjunctiva in close proximity to cornea
- No window for medical treatment - NOT WHEN INFECTED
- Precise suture placement necessary
- Types
○ 1. suture third eyelid to upper dorsal eyelid -> try to include third eyelid cartilage, don't want it to go through and touch the cornea
○ 2. third eyelid sutured to the conjunctiva -> more comfortable as whole eyeball can move however harder to do and can move
88
Distichiasis, trichiasis, ectopic cilia treatment
- Referral and transconjunctival excision of hair
- Post-op treatment - treatment of the ulcer
○ Topical broad spectrum antibiotics eye drop or ointment
○ Oral NSADIS
○ Atropine? Doxycycline?
Bandage contact lens or third eyelid flap if need be
89
Indolent ulcer treatment
- Sterile debridement and grid keratotomy
○ Heavy sedation, topical anaesthesia + GA?
○ Removal of the zone that is preventing attachment of the endothelium -> allows attachment
- Bandage contact lens, third eyelid flap, TT (temporary tarsonomy)
- Oral or injectable NSAIDS
- Topical AB eye drops
90
Infected cornea what treatment options
- Topical fluoroquinolone antibiotics .. Ocuflox
- Topical atropine - ointment better in cats
- Oral doxycycline.. Vibravet
- Oral NSADIS
- OR - can send for a graft -> to assist healing
Similar to corneal ulcer
91
FHV keratoconjunctivitis treatments
- Oral antivirals.. Famciclovir
- Oral doxycycline… vibravet
- Oral NSADIS… metacam
- Topical antiviral… Cidofovir
- Topical lubricants… celluvisc
92
Primary glaucoma treatments and why important
- Carbonic anhydrase inhibitors: trusopt (dorzolamide) or azopt (brinzolamide)
○ Required to make aqueous humour so if block inhibit this production
- Prostaglandin analogues: Xalatan
○ Increase outflow of aqueous humour
- Topical corticosteroids
○ Anti-inflammatory
- Oral anaglesia
- Surgery: laser, anterior chamber shut (alternative outflow of the aqueous humour)
- PROPHYLAXIS FOR OPPOSITE EYE -> need to prevent this from occurring to the other eye
93
Anterior lens luxation how important treatment and why, what is treatment, other treatment needed and what not to use
= emergency - AS CAN LEAD TO GLUACOMA
- Early lens removal surgery may help preserve vision
- Due to complications eg. Retinal detachment and glaucoma, complications higher than cataract surgery
- Medical management whilst awaiting surgery
○ Topical corticosteroids - prednefrin forte or maxidex
○ Oral corticosteroids or NSAIDS
○ Topical atropine
○ Topical azopt or trusopt -> carbonic anhydrase inhibitors
○ DO NOT APPLY XALATAN -> side effect -> mitotic pupil -> make it harder for flow of aqueous humour -> glaucoma
94
Treatment of posterior lens luxation
- Trap lens in posterior segment with xalatan - not worries about blocking aqueous flow
- Long term prognosis if managed well is similar to surgery of anterior lens luxation
- Enucleation or intraocular prosthesis best for chronic lens luxation and blindness
Involves removal of all ocular tissues and leaves a corneal shell -> still moves like normal eye however cannot see -> cosmetically more appealing then removing the eye however can still get corneal ulcers
95
Evaluation of vision what are the 2 main types of tests and tests within
1) distance
1. menace response
2. PLR
3. dazzle
4. visual placing reflex
5. tracking moving objects
6. obstacle course
2) ancillary vision test
1. Electroretinogram
○ Tests electrical function of the retina
○ To diagnose SARDS and PRA (progressive retinal atrophy)
○ Screen retinal function prior to cataract surgery
2. CT/MRI
○ Allows imaging of the optic nerves behind the eye and the brain
96
List 4 congenital/developmental causes of vision loss
1. Optic nerve hypoplasia
2. Collie eye anomaly
3. Retinal dysplasia
4. Multiple ocular defects
○ Multiple ocular problems inc microphthalmia (very small globe) , cataract, retinal dysplasia/detachments, ON hypoplasia
97
Optic nerve hypoplasia what results in, common in and fundus examination results
- Abnormal development of the ON (optic nerve)
○ Decreased number of retinal ganglion cells
- Unilateral or bilateral
- Miniature and toy poodles
- Fundus exam:
○ ONH small and more grey than usual
○ Normal retinal blood vessels
98
Collie eye anomaly and retinal dysplasia cause and fundus exam results
2. Collie eye anomaly
- Inherited
○ Shetland sheepdogs, Australia shepherds, collies
- Fundus exam
○ Choroidal hypoplasia - see more sclera
○ ON (optic nerve) colobomas
3. Retinal dysplasia
- Retinal folds
- Only severe forms cause vision problems
○ Can lead to retinal detachment
99
List 5 causes of sudden vision lss in clear eyes
1. Optic neuritis
2. Sudden acquired retinal degeneration syndrome (SARDS)
3. Retinal detachment
4. Central blindness
5. Ivermectin toxicity
100
Optic neuritis clinical signs, causes, diagnosis, treatment and prognosis for vision
- Mydriasis
- No PLR - optic nerve inflamed
- ON (optic nerve) elevated, hyperaemic or normal
- Causes
○ Infectious -> viral, fungal, protozoal
○ Inflammatory -> granulomatous meningoencephalitis (GME)
○ Idiopathic
- Diagnosis
○ CBC, Biochem, urinalysis, MRI, CSF tap
- Treatment
○ Directed at underlying cause
○ Systemic corticosteroids if rule out infection or neoplasia
- Prognosis for vision
○ Can be preserved if identified and treated early
○ Longer standing cases have poorer prognosis - damage to more optic fibres
101
Sudden acquired retinal degeneration syndrome how common, cause diagnosis and treatment
- A common cause of sudden vision loss in our practice
- More common in female dogs
- Any breed can be affected but small breeds may be predisposed
- Cause currently unknown, may be related to immune mediated retinitis (IMR)
- Diagnose - ERG (electro-retinogram -> will be flatline with no electrical activity)
- No treatment
102
Sudden acquired retinal degeneration syndrome clinical signs
- Clinical signs
○ Vision loss is usually sudden
§ Occasionally occurs over a few days or weeks
○ PLR present but slow and can be imcomplete
○ PU/PD, polyphagia
○ Cushingoid-like symptoms but don't generally have cushing disease
○ Normal ophthalmic examination initially
§ Panretinal atrophy develops slowly (6months)
103
Retinal detachment what lead to, fundus exam and treatment
```
- Large detachments
○ Vision impairment/loss
○ PLR reduced or absent
- Fundus exam
○ Veil hanging from around ON
○ Ballooning towards the posterior lens
- Treatment
○ Treat underlying cause - hypertension, infection
○ Corticosteroids: not with infection
○ Retinal re-attachment surgery
§ Possible in some cases
§ Available in Sydney
```
104
List 6 main causes of retinal detachment and what if bilateral
○ Trauma
○ Hypertension - especially in cats - blood pressure
○ Infection (FIP, cryptococcus, neospora, toxoplasma, aspergillosis)
○ Uveitis
○ Neoplasia - lymphoma
○ Idiopathic
If bilateral -> likely underlying systemic disease
105
Central blindness how to diagnose and presentation
- Diagnosis by elimination
- Ocular examination may be normal - may not see any changes in the fundus exam
- Often multiple neurological deficits present
○ Cranial nerves
○ Seizures
○ Behavioural changes
- Diagnosis
MRI or CT
106
Ivermectin toxicity what common in, why, breed more sensitive and ocular lesions
- Dogs living on farm or horse properties
- Access to large animal anthelminthic preparations
- Collies more sensitive
- Central blindness ro see ocular lesions
○ Retinal oedema and folds
○ Optic nerve head swelling
107
List 5 causes of sudden vision loss in CLOUDY EYE
```
1. Cataracts (clouding of the lens)
○ Diabetes cataracts can develop in weeks
2. Severe bilateral uveitis
3. Bilateral hyphaema
4. Glaucoma
5. Lens luxation
```
108
Hyphaema define, causes and what think cause if bilateral, unilateral young, unilateral old and old cat
- Blood in anterior chamber
- Causes
○ Hypertension
○ Coagulopathy
○ Neoplasia
○ Retinal detachment
○ Trauma
○ Uveitis
○ Glaucoma
- Bilateral - think systemic disease
- Unilateral, young dogs - think trauma
- Unilateral, old dog - think neoplasia
- Older cat - think hypertension
109
List 5 causes of progressive vision loss
1. Progressive retinal atrophy (PRA)
2. Optic nerve atrophy
3. Chronic uveitis - secondary cataract, glaucoma, retinal detachment
○ Acute there is no increase in pressure but chronic can block aqueous flow -> glaucoma etc.
4. Cataracts - when progress slowly
5. Surface ocular disease
110
Progressive retinal atrophy (PRA) how present, what results, fundic changes and secondary changes
- Bilateral and symmetrical
- Inherited in some breeds
- Degenerative condition of photoreceptors
○ Rods then later cones
§ Night vision loss first (Rods)
- Fundic changes
○ Blood vessel thinning
○ Tapetal hyper-reflectivity
○ Optic nerve head becomes grey
- May see secondary cataracts late in disease
111
Optic nerve atrophy and surface ocular disease what result in associated with
Optic nerve atrophy
- Optic disc appears pale, small and grey
- Associated with
○ PRA, chronic glaucoma, trauma, optic neuritis
- Vision loss if severe
Surface ocular disease
- Can lead to extensive corneal scarring which can cause blindness
- Corneal irritation
○ Blood vessel ingrowth
○ Melanosis
112
Treatment for lower eyelid entropion and keratoconjunctivitis sicca (dry eye)
- Medial canthoplasty surgery
○ Repair medial lower eyelid entropion
○ Reduce size of palpebral fissure
- Treat dry eye
○ Cyclosporine (optimmune) or tacrolimus - will not delay healing of ulcers
§ Topical corticosteroids will delay healing of ulcers
○ Artificial tears until STT comes back into normal range
