Dermatology 3 Flashcards

Approach to pustule, papule, scale and crust,

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1
Q

What history is needed when working up a case presented for pustules/papules/scale/crust?

A
  • Breed, age of onset
  • In contacts/human affected
  • Pruritus presence/abscence, severity,before or after lesion)
  • Course of disease
  • Seasonality
  • Response to past treatment incl, parasiticides
  • Results of prior tests
  • Concurrent systemic signs
  • Travel abroad
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2
Q

In what conditions is pyoderma of the face more likely to occur?

A
  • Autoimmune
  • Drematophytosis
  • Chronic disease
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3
Q

In which conditions are large, green pustules more common?

A

Pemphigus and HAC

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4
Q

What would pustular lesions that come in waves be suggestive of?

A

Pemphigus

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5
Q

Explain the importance of determining the variety of lesions present (early vs late)

A
  • Mixture of pustules at different stages suggests bacterial pyoderma
  • If all are at the same stage, more suggestive of pemphigus
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6
Q

What diagnostic tests should be carried out when investigating pustules/papules/crusts/scale?

A
  • Tests for ectoparasites, dermatophytosis
  • Stained acetate tape strips, impression smears for cytology
  • Cytology of fresh pustule contents if available
  • +/- bacterial culture/sensitivity testing
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7
Q

If you have no strong suspicion of pemphigus foliaceous, what investigation plan should be followed?

A
  • Thorough parasite control program, including treatment for sarcoptic mange and fleas
  • Eliminate secondary infection (bacterial pyoderma/Malassezia dermatitis)
  • Re-evaluate after 3-6 weeks
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8
Q

If you have a strong suspicion of pemphigus foliaceous, what investigation plan should be followed?

A

Eliminate secondary microbial infection then biopsy

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9
Q

If, following treatment for microbial infection and ectoparasites, the pustules/papules have resolved but the animal is still pruritic, what would be the next approach?

A

Work up as for hypersensitivities

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10
Q

If, following treatment for microbial infection and ectoparasites, the pustules/papules have resolved but there is rapid relapse, what would be the next approach?

A
  • Consider if: initialtherapy too short, owner compliance, adequate antibiotic dose
  • Check re. underlying health/endocrine/metabolic disease
  • If all normal, consider primary bacterial pyoderma, although likely to have unidentified underlying cause
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11
Q

If, following treatment for microbial infection and ectoparasites, the pustules/papules have not changed or are worse, what would be the next approach?

A
  • repeat skin scrapings re. Demodex
  • Repeat impression smears
  • Culture intact pustule (resistance)
  • Biopsy (pemphigus foliaceous)
  • Serum biochem, haematology, urinalysis (systemic disease)
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12
Q

What is scale caused by?

A

Hyperkeratosis, due to increased or disrupted epidermal turnover, leading to increased depth of cornified layer

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13
Q

What are the 2 types of scale?

A

Parakeratotic and orthokeratotic

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14
Q

Describe parakeratotic hyperkeratosis (appearance and cause)

A
  • Cells have nuclei
  • May be inflammation and high turnover of epidermis e.g. Malassezia dermatitis, zinc responsive deramtosis, superficial necrolytic dermatitis
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15
Q

Describe orthokeratotic hyperkeratosis (appearance and cause)

A
  • Increase in normal keratinocytes
  • Common inflammatory disorders, keratinisation disorders
  • No nuclei
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16
Q

What are crusts often associated with?

A
  • Surface squames, hair, topical medications
  • scaling
  • Pustular diseases
  • Ulcerative diseases
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17
Q

Why should steroids not be used in the treatment of crusts prior to diagnosis?

A

Need to see if lesions are pruritic following treatment for ectoparasites and microbial infections

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18
Q

Outline the diagnostic approach to scaling or crusting

A
  • History, signalment, general/derm examination
  • Rule out ectoparasites using routine tests, treatment trials
  • rule out microbial infection using cytology, cultures, response to treatment
  • If lesions remain, are they pruritic?
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19
Q

If crusting or scaling lesions are pruritic following treatment for ectoparasites and microbial infection, what are the next steps?

A
  • Exclusion diet trial
  • If effective, is food induced atopy
  • If negative, probably environmental atopy, but biopsy if clinical signs do not fit
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20
Q

If crusting or scaling lesions are not pruritic following treatment for ectoparasites and microbial infection, what are the next steps?

A
  • Evaluate for metabolic/endocrine disease
  • If positive, may be hypoT, HAC, sex/adrenal hormone imbalance, DM, superficial necrolytic dermatitis
  • If negative, biopsy
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21
Q

If there is no evidence of metabolic or endocrine disease in the investigation of crusting or scaling lesions that are not pruritc following ectoparasite and microbial infection treatment trials, what conditions may be found on biopsy?

A
  • Primary keratinisation disorders
  • Neoplasia: cutaneous lymphoma, paraneoplastic syndromes
  • Immune mediate: pemphigus, lupus
  • Nutritional: zinc-responsive dermatosis, EFA deficiency, generic dog food disease
  • Other underlying disorders: Leishmaniasis, FeLV, FIV, superficial necrolytic dermatitis, adverse drug reactions
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22
Q

What are primary keratinisation disorders?

A
  • The only primary causes of scale
  • Defects in normal keratinisation process
  • Either due to abnormal formation of keratinocytes, or abnormal sebaceous gland function
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23
Q

Describe the occurrence, diagnosis and treatment of primary keratinisation disorders

A
  • Rare
  • Often breed related and occur in younger animals (genetic)
  • Diagnosis by exclusion
  • Treat symptomatically, care not to miss other disorders that can be cured
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24
Q

List the primary keratinisation disorders of dogs

A
  • Primary idiopathic keratinisation disorder (“idioathic seborrhoea”)
  • Nasodigital hyperkeratosis
  • Icthyosis
  • Vitamin-A responsive dermatosis
  • Schnauzer comedo syndrome
  • Ear margin dermatosis
  • Footpad hyperkeratosis
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25
Q

Which breeds are predisposed to primary idiopathic keratinisation disorder?

A
  • Cocker/Springer spaniels
  • Irish setter
  • Basset
  • Sharp-pei
  • Doberman
  • WHWT
  • GSD
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26
Q

Which breeds are predisposed to nasodigital hyperkeratosis?

A
  • Cocker/English springer spaniels

- Old dogs of any breed, more commonly related to age

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27
Q

Which breeds are predisposed to ichthyosis?

A
  • WHWT

- Golden retrieer

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28
Q

Which breeds are predisposed to Vitamin-A responsive dermatosis?

A

Cocker spaniels

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29
Q

Which breeds are predisposed to Ear Margin Dermatosis?

A
  • Dachshund
  • Doberman
  • Short-haired breeds
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30
Q

Which breeds are predisposed to Footpad hyperkeratosis?

A
  • Irish terrier

- Dogue de Bordeaux

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31
Q

Describe the appearne of primary idiopathic keratinisation disorder in spaniels and other breeds

A
  • Scaling, often thick and adherent
  • Erythema, greasy scale of lips, periocular skin, ventral neck/body, feet, tail
  • Often otitis externa
  • Secondary pyoderma and Malassezia dermatitis common
  • Can appear similar to allergic animal
  • Other breeds often dry truncal scale
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32
Q

Describe the appearance of ichthyosis in Golden retrievers

A
  • Fish scale appearance

- Often young dogs, no other clinical signs unless secondarily infected

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33
Q

Describe the appearance of nasodigital hyperkeratosis

A

Frond like hyperkeratosis that may fissure and become infected

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34
Q

What is the key part of treatment for nasodigital hyperkeratosis?

A

Need to stop foot pad fissuring

  • Warm water soaks (warm damp flannel held against lesion),
  • Topical salicylic acid
  • Poprylene glucol
  • 0.5% tretinoin
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35
Q

What conditions can nasodigital hyperkeratosis develop secondary to?

A
  • HypoT
  • Pemphigus foliaceous
  • Cutaenous lupus
  • Necrolytic Migratory Erythema (MNE)
  • Distemper
  • ZN-responsive dermatosis
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36
Q

What are calluses and how do they develop? What is the main concern with these?

A
  • Areas of hyperkeratosis and acanthosis
  • Develop on bony prominences in heavy dogs on hard surfaces, normal protection mechanism
  • Usually no concern but may fissure and become infected
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37
Q

Describe the treatment for calluses

A
  • Do not excise, will not heal due to pressure that caused initial lesion
  • Warm water soaks, topical salicylic acid, propylene glycol, o.5% tretinoin
  • Control infection if present
  • Encourage lying on soft bedding
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38
Q

List primary keratinisation disorders of cats

A
  • Stud tail/tail gland hyperplasia
  • Feline ace
  • Fleine seborrhoea
  • Idiopathic facial dermatitis
  • Sebaceous adenitis
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39
Q

Describe the predisposition, appearance and treatment of stud tail in cats

A
  • Entire males mainly
  • Greasy, scaly tail
  • Neutering is treatment
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40
Q

Which breeds are predisposed to feline seborrhoea?

A
  • Persian
  • Himalayan
  • Exotic short-haired
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41
Q

Which breeds are predisposed to feline Idiopathic facial dermatitis?

A

Persian and Himalayan

42
Q

Describe the appearance of feline acne

A

Dark waxy scaleson chin

43
Q

Outline the investigation of feline acne

A
  • May be primary or secondary

- Need to rule out causes for this being secondary i.e. scrapes, plucks, culture for dermatophytosis

44
Q

What are common outcomes of feline acne?

A

Develop secondary Malassezia, pyoderma and furunculosis

45
Q

Outline the treatment of feline acne

A
  • Treat underlying cause if present, if not then symptomatic treatment (mainly options 1 and 2)
    1: Chlorhexidine (+/- miconazole) washes
    2: Antiseborrheic washes to dissolve crust and scale
  • topical antibiotics if secondarily infected (fusidic acid)
  • Neutering
  • Benzoyl peroxide product (no longer available as veterinary products)
  • 0.5% tretinoin topical retinoid
46
Q

Give examples of neoplasias that may cause secondary keratinisation disorders

A
  • Thymoma, leading to exfoliative dermatitis (paraneoplastic syndrome)
  • Epitheliotropic lymphoma
47
Q

Outline immune mediated disorders as causes of secondary keratinisation disorders

A
  • E.g. cutaneous lupus, pemphigus foliaceous
  • All look the same, follow diagnostic protocol and biopsy
  • Biopsy is only method of distinguishing these
48
Q

Which breeds are predisposed to sebaceous adenitis

A
  • Standard poodle
  • Akita
  • Samoyed
  • Viszla
  • English Springer Spaniel
  • Occasionally others
49
Q

Describe the pathogenesis of sebaceous adenitis

A

Inflammation of sebaceous glands leads to gland destruction

50
Q

Describe the appearance of sebaceous adennitis

A
  • Tightly-adherent frond-like scale, follicular casts
  • Hair loss
  • Generalised, focal or multifocal
  • Often secondarily infected leading to pruritus
51
Q

How is sebaceous adenitis diagnosed?

A
  • Rule out and eliminate secondary infection first

- Multiple biopsies usually required

52
Q

Describe the treatment of sebaceous adenitis

A
  • Ciclosporin
  • If not, then symptomatic control
  • Euthanasia if cannot get condition under control
53
Q

Describe the presentation of sebaceous adenitis in Viszlas

A
  • Present as serpiginous alopecia (snake-like alopecia and erythema)
  • Heat present, uncommon for pyoderma
54
Q

What are the potential underlying causes of superficial necrolytic dermatitis/necrolytic migratory erythema?

A
  • Aka hepatocutaneous syndrome, metabolic epidermal necrosis
  • secondary to end-stage liver disease
  • Pancreatic atrophy
  • glucagonomas
  • Diabetes mellitus
55
Q

Describe the appearance, diagnosis and prognosis of Necrolytic Migratory Erythema

A
  • Affects joints, pressure-points, lips and feet
  • Erythematous plaques/erosions covered with thick adherent scale
  • Uncommon
  • Diagnosed based on biopsy
  • Grave prognosis due to underlying liver or pancreatic disease
56
Q

List the options for symptomatic management of scaling/crusting diseases

A
  • Anti-seborrheic shampoos
  • Emollients
  • Moisturisers
  • Essential fatty acids
  • topical/systemic antimicrobials
  • Retinoids
  • Ciclosporin
57
Q

What are the main types of antiseborrheic shampoos available? What is their function?

A
  • Keratolytic: reduce cohesion between cells of stratum corneum
  • Keratoplastic: restore normal epidermal epithelialisation and keratinisation reduce skin turnover
  • Degreasing: remove excess grease but want to minimise drying effect so use mildest available and follow with moisturiser if needed
58
Q

List the common ingredients in anti-seborrhoeic shampoos, giving their mechanism of action (KL = keratolytic, KP = keratoplastic, DG = degreasing) and any additional properties

A
  • Sulphur (KL, KP): antimicrobial, antipruritic
  • Salicyclic acid (KL, KP): bacteriostatic, antipruritic
  • Selenium sulphide (KL, KP, DG): antifungal, can be drying, foundin seleen, not for dry dogs
  • Ammonoium lactate (KL, KP)
  • Benzoyl peroxide (human products) (KL, DG): only human acne products, can be drying/irritant, antibacterial, toxic to cats, long term bleaching
59
Q

Describe the mechanism of action, role of and give examples of emollients

A
  • Soften and soothe skin
  • Reduce trans-epidermal water loss but need to put water in first
  • e.g. vaseline, lanolin, paraffin, vegetable and animal oils
60
Q

Describe the mechanism of action of moisturisers

A

Increase water content of stratum corneum but drawin gin water (hydropic effect) e.g. urea, sodium lactate, colloidal oatmeal, glycerine, propylene glycol, lactic acid, ammonium lactate

61
Q

When are essential fatty acids particularly useful?

A

In treatment of dry scale

62
Q

When are topical/systemic antimicrobials typically used in the treatment of scale/crust?

A
  • To treat or prevent secondary microbial infections, if required
  • Use shampoo where possible to avoid use of antimicrobials
63
Q

What are the effects of retinoids?

A
  • Anti-proliferative
  • Anti-inflammatory
  • Immune modulatory
64
Q

Discuss the use of retinoids in the treatment of scale and crust

A
  • Have vitamin A activity
  • Not routinely
  • Expensive
  • Only used under consultant dermatologist guidance
65
Q

Discuss the use of systemic retinoids

A
  • Vitamin A: for vitamin A responsive dermatosis

- Isotretinoin, acitretin: significant side effect, only for use under consultant dermatologist’s guidance

66
Q

What are the side effects of isotretinoin and acitretin?

A
  • Highly teratogenic
  • KCS
  • Joint pain
  • Vomiting
  • Diarrhoea
  • Dry skin
  • Hyperostosis
67
Q

What is the topical formulation of retinoids?

A

Tretinoin 0.5%, unlicensed

68
Q

What crusting/scaling condition is ciclosporin used for?

A

Sebaceous adenitis, off label use

69
Q

Give an example of a non-dermatological disease that may cause head and neck excoriations in the cat

A

Feline calicivirus

70
Q

List the causes of feline symmetrical alopecia that are due to overgrooming

A
  • Pruritus: parasites, dermatophytosis, hypersensitivities, hyperthyroidism
  • Psychogenic alopecia
  • Pain, neurodermatitis, neuralgia
71
Q

List the causes of feline symmetrical alopecia that are due to spontaneous hair loss

A
  • Endocrinopathies: HAC, DM, hypoT
  • Paraneoplastic alopecia
  • Neoplasia (epitheliotropic T cell lymphoma)
  • Infections/ectoparasites: dermatophytosis, demodicosis
  • Others: trichorrhexis nodosa ec (rare causes)
72
Q

Give examples of breed predispositions that may present as symmetrical alopecia in cats

A
  • Persian cats: dermatophytosis

- Oriental cats: psychogenic alopecia

73
Q

List the common causes of miliary dermatitis in cats

A
  • Fleas
  • Environmental and dietary hypersensitivities
  • Dermatophytosis
  • Pyoderma
  • Pemphigus foliaceous
  • D. gatoi, Cheyletiella, Neotrombila, Otodectes
74
Q

Describe the methods for the diagnosis of feline cowpox

A
  • Clinical signs
  • Cells from biopsy material taken from marginal zones of inflammation
  • Immunofluorescence tests (quick, reliable)
  • Viral isolation using dried exudate
  • Isolation of virus from bronchoalveolar lavage fluid, swabs
  • Inclusion body in cells from FNA of lung
  • Send crusts to Bristol uni, perform PCR
75
Q

Describe the treatment of feline cowpox

A
  • Usually resolves spontaneously after 6-8weeks
  • Antibiotics if secondary infection
  • Steroids and other immunosuppressives must be avoided
76
Q

Describe the clinical signs of cutaneous presentations of feline respiratory diseases

A
  • FHV-1, FCV
  • Skin lesions especially in immunosuppressed animals
  • Usually concurrent URT infection/oral ulceration
  • Often local lymphadenopathy
  • Poorly defined ulcers, discrete crusts
  • Often head/limbs, occasionally generalised
  • +/- mild pruritus
77
Q

List the signs of virulent systemic feline calicivirus

A
  • Cutaneous/systemic vasculitis leading to subcut oedema, skin ulceration
  • Anorexia, pyrexia, lethargy (80%)
  • Oral ulceration (50%)
  • Nasal discharge (30%)
  • Also respiratory distress, ocular discharge, jaundice, GI signs, coagulopathy
78
Q

What are the predisposing factors for the development of virulent systemic feline calicivirus?

A

Crowded high stress environments (but milder signs in these cats than on exposure of naive cats in new homes/veterinary surgery)

79
Q

Describe the diagnosis of virulent systemic feline calicivirus

A

Oropharyngeal swabs and clinical signs

80
Q

Describe the treatment of cats with virulent systemic FCV

A
  • Strict biosecurity
  • High dose interferon
  • Supportive treatment
  • Systemic glucocorticoids as needed
81
Q

Describe the prognosis for cats with virulent systemic FCV

A
  • Up to 50% mortality, even if vaccinated

- Prognosis worse for older than for kittens

82
Q

Describe the presentation of pemphigus foliaceous in cats

A
  • Primary pustules rupture forming multifocal crusts
  • Face, pinnae, nipples, foot pads particularly affected
  • Sometimes caseous purulent exudate of multiple digits (“Philadelphia feet”)
83
Q

Describe the diagnosis of pemphigus foliaceous in cats

A
  • Straightforward if involvement of claw beds
  • Dermatological signs
  • Bacterial swab that shows sterile
  • Tzanck prep of pustule showing acantholytic keratinocytes and neutrophils
  • Skin biopsy
84
Q

Describe the treatment of pemphigus foliaceous in the cat

A
  • Glucocorticoids
  • Cyclosporin
  • Gold salts
  • Chlormbucil
  • Oclacitanib
  • NO azathiprine in cats
85
Q

Describe the cause and presentation for Persian cat facial dermatitis

A
  • Cause unknown
  • Dark waxy debris in facial folds, around eyes, chin
  • +/- erythema, pruritus
  • +/- bacterial/Malassezia infection
  • +/- submandibular lymphadenopathy
86
Q

Describe the treatment of persian cat facial dermatitis

A
  • Partial improvement in some with corticosteroids or itraconazole
  • Ciclosporin effective in others
  • No consistently effective treatment, guarded prognosis
87
Q

Describe shiny cat syndrome

A
  • Rare conditionaffecting cats <10yo
  • Marker for underlying malignancy, most commonly pancreatic tumour
  • Alopecia developing over weeks/months
  • Usually ventrum first then spreads to limbs, head often spared
  • +/- focal erythema, shiny skin
  • +/- crust, waxy debris (Secondary Malassezia infection)
  • +/- systemic signs e.g. weight loss
88
Q

Describe the presentation of feline thymoma-associated exfoliative dermatitis

A
  • Non-pruritic scaling and mild erythema
  • Head/pinnae then spread to more generalised scaling/alopecia
  • +/- crusts, ulcers, brown waxy exudate
  • +/- secondary Malassezia dermatitis leading to pruritus
89
Q

Describe the diagnosis of feline thymoma-associated exfoliative dermatitis

A
  • histopath of skin
  • Demonstration of anterior mediastinal mass, +/- pleural effusion on radiography
  • Ultrasound guided cytology/histopathology can confirm thymoma
  • CT scan to stage mass
90
Q

Describe the treatment for feline thymoma-associated exfoliative dermatitis

A
  • Surgical removal of mass curative, median survival nearly 2 years
  • Radiation therapy for non-resectable tumours reported
91
Q

Give examples of neuropathic dermatological diseases of cats

A
  • Feline idiopathic ulcerative dermatitis

- Feline orofacial pain syndrome (FOPS)

92
Q

Describe the presentation of feline idiopathic ulcerative dermatitis

A
  • Non-healing ulceration between scapulae or dorsal neck
  • Violent episodes of self trauma, with variable pain/pruritus between
  • May follow injection/spot on but many with no obvious inciting cause
93
Q

Describe the diagnosis of feline idiopathic ulcerative dermatitis

A
  • Eliminate infectious, allergic, ectoparasitic causes, trauma or burn
  • Biopsy shows linear sub-epidermal fibrosis in chronic cases
94
Q

Outline the prognosis for feline idiopathic ulcerative dermatitis

A
  • Guarded as underlying cause unknown

- Relapse common

95
Q

Describe the management of feline idiopathic ulcerative dermatitis

A
  • Treat secondary infeciton
  • Prevent self trauma until healed
  • If recurs, consider medical treatment: systemic corticosteroids after resolution of infection, surgical incision (some recur), off label use of gabapentin or topiramate effective in some cases (supports involvement of neuropathy)
96
Q

What is the cause of feline orofacial pain syndrome?

A

Neuropathy, similar to trigeminal neuralgia

97
Q

Describe the presentation of feline orofacial pain syndrome

A
  • Self-trauma to tongue, lips, buccal mucosa
  • Exaggerated licking/pawing at mouth
  • Predisposed to by oral lesions/dental disease/dental eruption (may be triggered by dental procedure)
  • stress involvement
98
Q

Describe the diagnosis of feline orofacial pain syndrome

A
  • Appropriate clinical signs

- Elimination of other diagnoses for head and neck excoriations

99
Q

Describe the treatment of feline orofacial pain syndrome

A
  • Prevent self-mutilation
  • Treat any dental disease
  • Environmental changes to reduce stress
  • Feline anti-stress pheromone preparations
  • Anecdotal reports of successful treatment with phenobarbital, gabapentin, amitriptyline
100
Q

Describe the typical presentation of mast cell tumours in the cat

A

Usually internal and often affect the spleen, may see oedema that comes and goes without explanation

101
Q

When sedating an animal for intradermal skin testing, what is a key consideration regarding the choice of drug?

A

Some interfere histamine release and so should be avoided: propofol (stimulate release), pethidine (stimulate release), acepromazine (depresses release)