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small animal (fourth year) > Dermatology > Flashcards

Dermatology Flashcards

1
Q

what is immune mediated skin disease?

A

immune system fails to tolerate self-antigens and mounts a response against them

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2
Q

what are the two types of immune mediated skin disease?

A

primary - idiopathic
secondary - exogenous trigger

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3
Q

why are primary lesions usually to detect?

A

much narrower list of differentials than secondary lesions

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4
Q

what are the main diagnostics tests for immune mediated skin disease?

A

lesion cytology
skin biopsy/histopathology
haematology, biochemistry
urinalysis
diagnostic imaging

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5
Q

what are the advantages of cytology for diagnosis of immune mediated skin disease?

A

easy, cheap, rapid
differentiate sterile from septic (infectious disease)
determine inflammation type

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6
Q

what are the two different sample techniques for cytology of immune mediated skin disease?

A

direct impression smear (apply slide, dry, diff quik)
FNA

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7
Q

what lesions are direct impression smears useful for?

A

pustules, exudative lesions, draining tracts

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8
Q

what is needed for a diagnostic sample using skin biopsy/histopathology?

A

> 3 biopsies
primary lesions
range of lesions samples
entire lesion sampled if possible
avoid ulcerated lesions

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9
Q

what are the most common primary skin lesions seen with immune mediated skin disease?

A

pustules
plaques/nodules
erythematous macules/patches
hypopigmented macules/patches

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10
Q

are erosions, ulcers and crust primary or secondary lesions?

A

secondary

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11
Q

what pathology causes erosions/ulcers?

A

keratinocyte death
loss of keratinocyte adhesions
self trauma (pruritic)
secondary bacterial infection

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12
Q

what are crusts?

A

dried exudate on skin surface

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13
Q

what can crusts arise from?

A

pus (pustules)
exudate (erosions/ulcers)
blood

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14
Q

what are the list of differentials for a pustule?

A

bacterial infection
pemphigus foliaceus
superficial pustular drug reaction (rare)
superficial pustular dermatophytosis (rare)

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15
Q

what immune mediated skin diseases cause pustules?

A

pemphigus foliaceus
superficial pustular drug reaction (rare)

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16
Q

what is the distribution of lesions for pemphigus foliaceus?

A

muzzle
eyes
ears
footpads
(generalised)

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17
Q

what are acantholytic keratinocytes?

A

large rounded epithelial cells (limited number of diseases associated with these)

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18
Q

what skin diseases are acantholytic keratinocytes associated with?

A

pemphigus foliaceus
rare infectious diseases

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19
Q

why do acantholytic keratinocytes form with pemphigus foliaceus?

A

auto-immune antibodies target desmosomes that link keratinocytes which causes separation and loss of cell structure

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20
Q

what is the most common autoimmune skin disease of dogs?

A

pemphigus foliaceus

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21
Q

what is the signalment of dogs effected with pemphigus foliaceus?

A

middle aged
breeds - spaniel, dachshund, chow chow, akita…

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22
Q

is pemphigus foliaceus pruritic?

A

variable pruritis (tends to have more if eosinophils are present)

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23
Q

what is the history/signalment for eosinophilic furunculosis of the face?

A

young adults
rapid onset and intense pruritis

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24
Q

what is the lesion morphology for eosinophilic furunculosis?

A

eroded/ulcerated plaques and nodules

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25
Q

what is the signalment and history of sterile granulomatous dermatitis and lymphadenitis?

A

puppies (sporadic adult cases)
acute onset, non-pruritic, painful, pyrexia, lethargy

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26
Q

what is the morphology of sterile granulomatous dermatitis and lymphadenitis lesions?

A

follicular nodules/plaques
alopecia
diffuse swelling
lymphadenomegaly

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27
Q

what is the main cause of non-immune mediated causes of hypopigmentation, erythematous macules and patches?

A

hypersensitivity reactions

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28
Q

what are the different variants of cutaneous lupus erythematosus?

A

rapid onset -vesicular
chronic onset - facial discoid lupus erythematosus, generalised, mucocutaneous, exfoliative

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29
Q

what is the most common cutaneous lupus erythematosus?

A

facial discoid lupus erythematosus

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30
Q

what breeds are predisposed to facial discoid lupus erythematosus?

A

German shepherds

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31
Q

what are the lesions of facial discoid lupus?

A

loss of cobblestone nasal planum
hypo pigmented macules/patches
erosions, ulcers, crusting
black to blue to pink pigment change

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32
Q

what are the most common two forms of erythema multiforme?

A

major and minor

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33
Q

what is the history associated with erythema multiforme?

A

acute onset, non-pruritic with possible systemic signs
possible trigger - drug, virus, vaccine, neoplasia…

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34
Q

what is the primary lesion of erythema multiforme?

A

annular erythematous macule

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35
Q

what is the distribution of erythema multiforme?

A

usually ventral abdomen (can be generalised)

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36
Q

what disease are target lesions associated with?

A

erythema multiforme

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37
Q

what are target lesions?

A

erythematous macules that spread peripherally producing an annular pattern
central erythema then ring of clear oedema then ring of erythema

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38
Q

what is seen on cytology of erythema multiforme?

A

sterile non-specific inflammation (can’t use this to diagnose it)

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39
Q

what is the main histopathological finding of erythema multiforme?

A

keratinocyte apoptosis (this determines the severity)

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40
Q

what age dogs are effected by hyperkeratotic erythema multiforme?

A

older

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41
Q

what are the types of erythema multiforme?

A

minor
major
Steven-johnson syndrome
toxic epidermal necrolysis
(in order of severity)

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42
Q

what is the signalment and history of uveodermatologic syndrome?

A

young to middle aged
acute bilateral uveitis and non-pruritic

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43
Q

what breed is predisposed to uveodermatologic syndrome?

A

Akita

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44
Q

what is the most common lesion seen with uveodermatologic syndrome?

A

hypopigmented macules

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45
Q

what are some immune mediated disease that cause alopecia?

A

sebaceous adenitis
alopecia areata
dermatomyositis
ischaemic dermatopathy

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46
Q

what should be done to rule out demodicosis or dermatophytosis as a cause of alopecia?

A

trichography

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47
Q

what are the lesions associated with sebaceous adenitis?

A

partial alopecia and generalised poor coat quality
follicular casts/scale

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48
Q

what is the histopathological changes seen with sebaceous adenitis?

A

pyogranulomatous inflammation targeting sebaceous glands

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49
Q

what is the lesion morphology of alopecia areata?

A

foal/multifocal patches of alopecia with possible erythema

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50
Q

what is the classic histopathological finding of alopecia areata?

A

lymphocytic destruction of hair bulbs

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51
Q

where is the typical distribution of alopecia areata?

A

head/face

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52
Q

what is canine atopic dermatitis?

A

genetically predisposed inflammatory and pruritic allergic skin disease associated with IgE antibodies most commonly to environmental allergens

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53
Q

what are the four factors that contribute to the pathogenesis of CAD?

A

cutaneous inflammation and pruritis
defective skin barrier
microbial colonisation
other flare factors

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54
Q

what is CAD?

A

canine atopic dermatitis

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55
Q

how does the defective skin barrier contribute to CAD?

A

increased transepidermal water loss
wide intercellular spaces between corneocytes
disorganised/fragmented lipid matrix
decreased protein/lipids

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56
Q

why does microbial colonisation occur in cases of CAD?

A

increased binding sites from inflammation
reduced barrier function from lipid/protein
damaged skin surface (self trauma)
dysbiosis

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57
Q

what is dysbiosis associated with CAD?

A

changed patterns of bacterial colonisation on the skin creating reduced diversity and imbalance of commensals

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58
Q

what are the most common secondary microbial colonisations for dogs with CAD?

A

Staphylococcal
Malassezia dermatitis

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59
Q

what is the recurrent microbial colonisation of CAD cases called?

A

atopic flares (causes further inflammation and pruritis)

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60
Q

what are common causes of atopic flares?

A

bacterial and yeast infection
seasonal increases/changes in allergens
ectoparasite infection
reduction of therapy

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61
Q

what is the typical history of CAD patients?

A

pruritis (seasonal, perennial, with) - itch that rashes
<3 years old (<1 for food allergy)
breed predispositions

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62
Q

what are the compatible clinical signs of CAD?

A

pruritis - licking, chewing, grooming…
erythema and papules

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63
Q

what is used to measure pruritits?

A

pruritis visual analogue scale (grades the itch)

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64
Q

what are secondary skin lesions of CAD usually due to?

A

self trauma

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65
Q

what secondary skin lesions are associated with CAD?

A

otitis
alopecia
excoriations
salivary staining
lichenification
pustules, epidermal collarettes, crusts
hyperpigmentation

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66
Q

what is the distribution of CAD lesions?

A

face/chin
periorbital areas
ears
elbow creases
feet
ventral abdomen
perianal area

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67
Q

what are favrots criteria?

A

onset of signs is under three years old
mainly indoor dogs
glucocorticoid responsive pruritis
itch before lesions
affected front feet/ear pinnae
non-affected ear margins
non-affected dorso-lumbar area

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68
Q

how is favrots criteria used?

A

the more signs the higher the chance of CAD

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69
Q

what are some differentials for pruritis in dogs?

A

ectoparasites
allergic skin disease (CAD, contact dermatitis)
microbial infection
Malassezia dermatitis
others - Pemphigus foliaceus…

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70
Q

is atopic dermatitis an outside in or an inside out disease?

A

inside out

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71
Q

what is done to rule out ectoparasites in cases of suspected CAD?

A

diagnostic tests and treatment trials

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72
Q

why are treatment trials needed to exclude ectoparasites from your differential diagnosis list for CAD?

A

some parasites live in the environment or are rare to find on the patient

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73
Q

what drug group is used for treatment trials for ectoparasites?

A

isoxazoline

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74
Q

what are some hints that CAD might be food induced?

A

concurrent GI signs
non-seasonal
very young dogs
pruritis is poorly responsive to steroid

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75
Q

what is the only way to diagnose a food allergy inducing CAD?

A

elimination novel diet trial

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76
Q

what are the two options of diet trials?

A

home cooked
commercial hydrolysed diet

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77
Q

what are some problems associated with home cooked diets for novel diet trials?

A

identifying appropriate
unsuitable for longterm for growing animals
labour intensive
palatability issues
GI upset
cost

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78
Q

how do hydrolysed protein diets work for food trials?

A

assumes there is a type 1 hypersensitivity so protein is chopped up so small the allergen doesn’t create a reaction

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79
Q

how long should a diet trial be done for?

A

minimum of 6-8 weeks

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80
Q

what should be used for 2-3 weeks at the start of a food trial?

A

steroids or oclacitinib

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81
Q

why would steroids or oclacitinib be used at the start of a food trial?

A

reduce secondary inflammation to reduce the length of the diet trial

82
Q

why does care need to be taken when worming during a diet trial?

A

the wormers could be flavoured

83
Q

what are the three things CAD therapy treats?

A

pruritis
inflammation
secondary infection/overgrowth

84
Q

what guides the therapy for CAD?

A

(pathogenesis)
skin barrier dysfunction
skin inflammation
allergen sensitivity
microbial colonisation

85
Q

what are the aims of improving skin barrier function in CAD cases?

A

reduce transepidermal water loss
reduce exposure to environmental allergens/irritants
reduce microbial colonisation

86
Q

what treatments are used to improve skin barrier function?

A

non-irritating shampoos
topical moisturisers and emollients
oral/topical essential fatty acids

87
Q

what should shampoos for CAD cases contain?

A

emollient (bring/trap water)
anti-seborrheic (grease/scaling)
antiseptic (prevent infection)

88
Q

what is the aim of using essential fatty acids in CAD treatment?

A

improve barrier function of the skin

89
Q

what does allergen immunotherapy do in CAD cases?

A

desensitises dog to environmental allergens by inducing tolerant T cells

90
Q

how is allergen immunotherapy carried out?

A

administration of gradually increasing quantities of an allergen extract to an allergic subject to decrease the severity of clinical signs from subsequent exposure

91
Q

how long does allergen immunotherapy need to be given for?

A

minimum of 12 months

92
Q

what are the side effects to allergen immunotherapy?

A

very few - itching…

93
Q

what are the aims of anti-inflammatory and anti-pruritic therapy?

A

long term reduction of inflammation
avoid flare ups of inflammation
restore normal skin environment and prevent microbial overgrowth

94
Q

what are some possible drug types used anti-inflammatory and anti-pruritic therapy of CAD?

A

glucocorticoids
calcineurin inhibitors
janus kinase inhibitors
biologics
antihistamines

95
Q

what systemic glucocorticoids can be used for CAD?

A

prednisolone and methylprednisolone

96
Q

what are the possible side effects of glucocorticoid use in CAD patients?

A

polyphagia, PUPD, panting, behaviour changes, iatrogenic hyperadrenocorticism and increased UTI risk

97
Q

what is the ideal way to use systemic glucocorticoids in CAD cases?

A

as “crisis busters” in flare ups

98
Q

when are systemic glucocorticoids given in flare ups?

A

as early as possible

99
Q

what topical glucocorticoids can be used for CAD?

A

hydrocortisone aceponate

100
Q

what is the major risk of prolonged topical glucocorticoid use in CAD cases?

A

skin thinning on abdomen

101
Q

what is the oral calcineurin inhibitor used for CAD?

A

ciclosporin

102
Q

what is the function of oral calcineurin inhibitors?

A

inhibit T lymphocyte function by blocking calcineurin

103
Q

what are the possible adverse effects of oral calcineurin inhibitors?

A

GI signs
gingival hyperplasia
viral papillomas
hirsutism (excessive hair)

104
Q

what is the janus kinase inhibitor used for CAD?

A

oclacitinib

105
Q

what is the function of janus kinase inhibitors?

A

inhibit JAK1 enzymes which signal transduction of pro-inflammatory, pro-allergic and pruritogenic cytokines

106
Q

what is blood monitoring recommended when giving janus kinase inhibitors?

A

minor effect of JAK2 enzymes that effect the haematopoetic system

107
Q

what are the contraindications for oclacitinib?

A

<12 months old
<3kg bodyweight
breeding dogs
severe infection, neoplasia or immunesuppression

108
Q

how does lokivetmab work?

A

it is a monoclonal antibody that target/neutralises canine IL-31 (pruritogenic cytokine)

109
Q

what is the advantage of lokivetmab?

A

highly targeted so minimal impact on normal immune function and can be used with other drugs

110
Q

what is the main antihistamine used for CAD?

A

chlorphenamine

111
Q

to what degree do ciclosporins control inflammation and itch?

A

moderate control of itch, inflammation and infection

112
Q

to what degree does oclacitinib control inflammation and itch?

A

moderate inflammatory control and very good itch control

113
Q

to what degree does lokivetmab control inflammation and itch?

A

poor at inflammation
excellent at itch

114
Q

what is the aim of phase one CAD treatment?

A

induce remission

115
Q

what is the aim of phase two CAD treatment?

A

prevent recurrences (proactive therapy)

116
Q

what needs to be done to reach the pruritic threshold set for CAD patients?

A

remove flare factors (parasites, infection…)

117
Q

what supports the vertical and horizontal canal of the ear?

A

auricular and annular cartilage

118
Q

what is the name for the ear drum?

A

tympanic membrane

119
Q

what connects the tympanic membrane to the inner ear?

A

auditory ossicles

120
Q

what connects the middle ear to the nasopharynx?

A

eustachian/auditory tube

121
Q

what is the function of the eustachian/auditory tube?

A

allow drainage of the middle ear

122
Q

what is the differences between the tympanic bulla of cats and dogs?

A

cats - bony shelf that separates it into two halves
dogs - incomplete bony shelf

123
Q

why is treating disease in the tympanic bulla of cats often difficult?

A

bony shelf makes accessing the ventral tympanic bulla

124
Q

how can you tell what the cranial portion of the tympanic membrane is?

A

C shaped structure (auditory ossicle) points cranially

125
Q

what are the two parts of the tympanic membrane?

A

pars flaccida
pars tensa

126
Q

what is the function of the pars flaccida?

A

contains blood vessels that supply the pars tensa

127
Q

what histological features are different in the ear canal skin compared to normal skin?

A

small hairs
ceruminous glands
sebaceous glands

128
Q

what is the lining of the middle ear?

A

modified respiratory epithelium

129
Q

what are the histological features the lining of the middle ear?

A

simple squamous to cuboidal epithelium
few ciliated cells
mucous secreting goblet cell
(modified respiratory epithelium)

130
Q

what are the mechanisms that allow self cleaning of the external ears?

A

cerumen - catches material, keratinocytes, microbes and contains antimicrobial peptides and lysosomes
epithelial migration - living keratinocytes carry cerumen from tympanic membrane to external ear

131
Q

what are the mechanisms that allow self cleaning of the middle ear?

A

mucous from goblet cells trap microbes and debris and drains via the Eustachian tube to be swallowed

132
Q

what is the main type of bacteria found in the normal flora of the external ear canal?

A

gram positive cocci - Staphylococci

133
Q

what is otitis?

A

inflammation of the ear

134
Q

what mnemonic can be used for the differential of otitis?

A

(VIP MEGA FAME)
Viral
Immune mediated
Parasites
Mycoses
Endocrine
Glandular
Allergy
Foreign body
Autoimmune
Miscellaneous
Epithelialisation disorders

135
Q

what is the most common parasites effecting the ear?

A

Otodectes cynotis

136
Q

what are the most common differentials for otitis in dogs?

A

Foreign bodies
Allergen
Bugs (parasites)

137
Q

what are the most common differentials for otitis in cats?

A

Flu (viral)
Allergens
Bugs (parasites)

138
Q

how would the wax of a dog with Otodectes cynotis be described?

A

dark coffee ground appearance

139
Q

why do most patients present very pruritic with Otodectes cynotis?

A

they have a hypersensitivity reaction to the mites

140
Q

why are Otodectes cynotis mites difficult to see with a otoscope?

A

they are photophobic (run away from light)

141
Q

what is used to treat Otodectes cynotis?

A

selamectin/moxidectin spot-on
steroid for intense hypersensitivity reaction

142
Q

what are the main causes of secondary otitis?

A

microbial infection
topical medication reaction
inappropriate cleaning

143
Q

what are some predisposing causes of otitis?

A

obstructive ear disease
conformation - hairy, narrow, waxy canals
environment
systemic disease

144
Q

what are the most common causes of obstructive ear disease?

A

polyp
ceruminous gland neoplasia

145
Q

what is the order of progressive pathological changes of the ear?

A

failure of epithelial migration
progressive epithelial hyperplasia and oedema
glandular dilation/hyperplasia
canal stenosis
rupture of tympanum
calcification of pericartilaginous tissue
osteomyelitis
para-aural abscessation

146
Q

what are the clinical signs of otitis externa?

A

otic pruritis
pain
discharge/malodour
loss of hearing
secondary changes - scaling, lichenification, pyotraumatic dermatitis

147
Q

what is usually the disease progression of otitis externa?

A

Malassezia overgrowth
change to external ear canal due to inflammatory changes which increases humidity (good environment for pathogens)
gram negative infection (Pseudomonas) infection
progresses to otitis media

148
Q

what are the clinical signs of otitis media and interna?

A

pain
horners syndrome
hearing loss
vestibular disease

149
Q

what is the usual cause of primary otitis media in dogs and cats?

A

dogs - brachycephalic
cats - nasopharyngeal polyps
(Eustachian tube dysfunction)

150
Q

what is primary secretory otitis media?

A

build up of mucous in the middle ear causing pain, deafness and bulging of tympanic membrane

151
Q

what system is used to determine a cause for otitis?

A

primary causes (differentials)
secondary causes
predisposing factors
perpetuating factors
(PSPP)

152
Q

what is the preferred imaging modality for otitis cases without neurological signs?

A

CT (computed tomography)

153
Q

what colour should the tympanic bull appear on CT?

A

black - air filled

154
Q

when would MRI be used to image otitis cases?

A

if there is neurological involvement (good soft tissue imaging)
if para-aural abscess is present with chronic otitis external

155
Q

what is a myringotomy?

A

creating a hole in the tympanic membrane (can allow sampling/cleaning of middle ear)

156
Q

which quadrant should the hole be made in for myringotomy?

A

caudoventral quadrant of tympanic membrane (as far away from C shape)

157
Q

what are the indications for myringotomy?

A

bulging eardrum on otoscope with pain/neurological signs
imaging results show bulla changes and intact ear drum
evidence of tissue/fluid behind eardrum
medically unresponsive vestibular disease with an intact eardrum
chronic otitis externa failing to respond to treatment

158
Q

why does cleaning the ear usually help otitis cases?

A

remove infectious debris
disrupts microbial biofilms
allows visualisation of tympanic membrane
exposes polyps/tumours
enhances action of topical therapy

159
Q

how does ear cleaning need to be carried out in chronic otitis cases with copious amounts of discharge?

A

general anaesthetic
cuffed ET tube (infection material drained by Eustachian tube)
analgesia (paracetamol)
prednisolone pretreatment - open ear canal

160
Q

what are biofilms?

A

microbes stuck together in extracellular matrix forming a protected environment making treatment of infection more difficult

161
Q

what treatments can be used to help break up/disrupt biofilms?

A

N-acetylcysteine
polyhexanide

162
Q

how is N-acetylcysteine used to break up biofilms?

A

lavage ear with water and then leave product in the ear for 5 minutes
thoroughly flush with water

163
Q

what anti-inflammatory drugs are best for ears?

A

glucocorticoids (anti-inflammatory dose)

164
Q

what glucocorticoids can be used for otitis as anti-inflammatory treatment?

A

prednisolone
dexamethasone
betamethasone

165
Q

what sampling technique is used for the external ear canal?

A

indirect impression smear (cotton bud and role onto slide then Diff-Quik

166
Q

what otic infections is chlorhexidine effective against?

A

gram positive cocci
gram negative rods
Malassezia

167
Q

what otic infections are clotrimazole, miconazole and nystatin effective against?

A

Malassezia

168
Q

what otic infections are florfenicol and fucidic acid effetive against?

A

gram positive cocci

169
Q

what criteria is used to select topical antimicrobial proprietary treatments?

A

glucocorticoids (more potent for severe PPC)
concurrent disease (immune suppression by glucocorticoid)
spectrum of antimicrobial activity
potential for ototoxicity
patient/owner compliance

170
Q

what treatment is licensed for patients with a ruptured eardrum?

A

none

171
Q

if the eardrum isn’t visible (unsure if ruptured) what treatment should be given to otitis cases?

A

systemic prednisolone for 1-2 weeks then recheck
clean ear then recheck
treat with safe water based product and recheck
(or a combination of the above)

172
Q

why is culture not very useful for otitis diagnose?

A

the site isn’t sterile to begin with before otitis

173
Q

what are the indications for culture and sensitivity for otitis cases?

A

if confirmed with cytology and needing to speciate bacteria
if systemic antimicrobials are required
if cases aren’t responding to appropriate treatment

174
Q

what is a common gram negative rod that effects the ear?

A

Pseudomonas

175
Q

what are some possible treatments for hypersensitivity (atopic) otitis?

A

triamicolone
HCA - hydrocortisone anencephaly
dexamethasone

176
Q

what are some possible signs that would given an otitis case a guarded-poor prognosis?

A

solid/non-pliable external ear canal
severe stenosis and fibrosis
marked mineralisation
neoplasia/polyps
para-aural abscessation

177
Q

what are the most common skin infections?

A

superficial pyoderma
Malassezia dermatitis
surface overgrowth (not true infection as there are no neutrophils)

178
Q

what are hot spots?

A

localised material overgrowth (extremely pruritic and painful)

179
Q

how are hot spots treated?

A

sedate and clip/clean
topical anti-inflammatories
analgesia (paracetamol)

180
Q

what are the two main types of bacterial overgrowths?

A

hot spots
fold dermatitis

181
Q

what is the usual cause of superficial pyoderma?

A

Staphylococcus pseudointermedius

182
Q

what is the most important factor of treatment in superficial pyoderma cases?

A

topical treatment

183
Q

what is topical therapy for superficial pyoderma usually based on?

A

chlorhexidine

184
Q

how is Malassezia dermatitis treated?

A

shampoo - chlorhexidine and miconazole
systemic antifungals - itraconazole
allergy vaccine (if hypersensitive)

185
Q

what are most skin antiseptics based on?

A

chlorhexidine

186
Q

what is the protocol for treating deep pyoderma?

A

topical antiseptics and antibiotics
systemic antibiotics based on culture on widespread
biopsy fresh tissue to guide treatment

187
Q

what duration of treatment is needed for superficial pyoderma?

A

2-3 weeks

188
Q

what duration of treatment is needed for deep pyoderma?

A

> 4 weeks

189
Q

what are the two main factors of treating immune-mediated skin disease?

A

remove/treat external triggers
control inappropriate immune response

190
Q

what are some possible triggers of immune mediated skin disease?

A

drugs, UV light, confirmed infections, underlying neoplasia

191
Q

what is done during the induction of remission phase of treating immune mediated skin disease?

A

initial bloods/monitor to ensure no underlying disease
aggressive therapy whilst trying to avoid severe adverse effects
needs regular monitoring and modification

192
Q

what phase of treatment follows induction of remission of immune mediated skin disease?

A

transition

193
Q

what is done in the transition phase of treating immune mediated skin disease?

A

taper drugs to lowest effective dose
less frequent monitoring with time and reduction of adverse effects
taper treatment to stop if no relapse

194
Q

if treatment can’t be tapered to nothing due to them having idiopathic immune mediated skin disease, what stage of treatment do they enter after transition?

A

maintenance (for cases that relapse in the transition phase)

195
Q

what is done during the maintenance phase for immune mediated skin disease?

A

this is lifetime treatment with the lowest effective dose and monitor for adverse effects

196
Q

what is done during the maintenance phase for immune mediated skin disease?

A

this is lifetime treatment with the lowest effective dose and monitor for adverse effects

197
Q

how often is a patient with immune mediated skin disease monitored in the induction treatment period?

A

every 7-14 days

198
Q

what are some common adverse effects seen with steroids?

A

PUPD
polyphagia
muscle weakness
breathlessness/panting
weight gain
alopecia
secondary bacterial infection

199
Q

what are the possible adverse effects of ciclosporin?

A

vomiting and diarrhoea
increased hair/gum growth
immunosuppression (shouldnt be vaccinated)
papiloma growth

200
Q

what are the possible adverse effects of ciclosporin?

A

vomiting and diarrhoea
increased hair/gum growth
immunosuppression (shouldn’t be vaccinated)
papiloma growth

201
Q

what are the aims for treating sebaceous adenitis?

A

remove the thick scales
rehydrate the skin

small animal (fourth year) (26 decks)

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