Dermatology Flashcards
what is immune mediated skin disease?
immune system fails to tolerate self-antigens and mounts a response against them
what are the two types of immune mediated skin disease?
primary - idiopathic
secondary - exogenous trigger
why are primary lesions usually to detect?
much narrower list of differentials than secondary lesions
what are the main diagnostics tests for immune mediated skin disease?
lesion cytology
skin biopsy/histopathology
haematology, biochemistry
urinalysis
diagnostic imaging
what are the advantages of cytology for diagnosis of immune mediated skin disease?
easy, cheap, rapid
differentiate sterile from septic (infectious disease)
determine inflammation type
what are the two different sample techniques for cytology of immune mediated skin disease?
direct impression smear (apply slide, dry, diff quik)
FNA
what lesions are direct impression smears useful for?
pustules, exudative lesions, draining tracts
what is needed for a diagnostic sample using skin biopsy/histopathology?
> 3 biopsies
primary lesions
range of lesions samples
entire lesion sampled if possible
avoid ulcerated lesions
what are the most common primary skin lesions seen with immune mediated skin disease?
pustules
plaques/nodules
erythematous macules/patches
hypopigmented macules/patches
are erosions, ulcers and crust primary or secondary lesions?
secondary
what pathology causes erosions/ulcers?
keratinocyte death
loss of keratinocyte adhesions
self trauma (pruritic)
secondary bacterial infection
what are crusts?
dried exudate on skin surface
what can crusts arise from?
pus (pustules)
exudate (erosions/ulcers)
blood
what are the list of differentials for a pustule?
bacterial infection
pemphigus foliaceus
superficial pustular drug reaction (rare)
superficial pustular dermatophytosis (rare)
what immune mediated skin diseases cause pustules?
pemphigus foliaceus
superficial pustular drug reaction (rare)
what is the distribution of lesions for pemphigus foliaceus?
muzzle
eyes
ears
footpads
(generalised)
what are acantholytic keratinocytes?
large rounded epithelial cells (limited number of diseases associated with these)
what skin diseases are acantholytic keratinocytes associated with?
pemphigus foliaceus
rare infectious diseases
why do acantholytic keratinocytes form with pemphigus foliaceus?
auto-immune antibodies target desmosomes that link keratinocytes which causes separation and loss of cell structure
what is the most common autoimmune skin disease of dogs?
pemphigus foliaceus
what is the signalment of dogs effected with pemphigus foliaceus?
middle aged
breeds - spaniel, dachshund, chow chow, akita…
is pemphigus foliaceus pruritic?
variable pruritis (tends to have more if eosinophils are present)
what is the history/signalment for eosinophilic furunculosis of the face?
young adults
rapid onset and intense pruritis
what is the lesion morphology for eosinophilic furunculosis?
eroded/ulcerated plaques and nodules
what is the signalment and history of sterile granulomatous dermatitis and lymphadenitis?
puppies (sporadic adult cases)
acute onset, non-pruritic, painful, pyrexia, lethargy
what is the morphology of sterile granulomatous dermatitis and lymphadenitis lesions?
follicular nodules/plaques
alopecia
diffuse swelling
lymphadenomegaly
what is the main cause of non-immune mediated causes of hypopigmentation, erythematous macules and patches?
hypersensitivity reactions
what are the different variants of cutaneous lupus erythematosus?
rapid onset -vesicular
chronic onset - facial discoid lupus erythematosus, generalised, mucocutaneous, exfoliative
what is the most common cutaneous lupus erythematosus?
facial discoid lupus erythematosus
what breeds are predisposed to facial discoid lupus erythematosus?
German shepherds
what are the lesions of facial discoid lupus?
loss of cobblestone nasal planum
hypo pigmented macules/patches
erosions, ulcers, crusting
black to blue to pink pigment change
what are the most common two forms of erythema multiforme?
major and minor
what is the history associated with erythema multiforme?
acute onset, non-pruritic with possible systemic signs
possible trigger - drug, virus, vaccine, neoplasia…
what is the primary lesion of erythema multiforme?
annular erythematous macule
what is the distribution of erythema multiforme?
usually ventral abdomen (can be generalised)
what disease are target lesions associated with?
erythema multiforme
what are target lesions?
erythematous macules that spread peripherally producing an annular pattern
central erythema then ring of clear oedema then ring of erythema
what is seen on cytology of erythema multiforme?
sterile non-specific inflammation (can’t use this to diagnose it)
what is the main histopathological finding of erythema multiforme?
keratinocyte apoptosis (this determines the severity)
what age dogs are effected by hyperkeratotic erythema multiforme?
older
what are the types of erythema multiforme?
minor
major
Steven-johnson syndrome
toxic epidermal necrolysis
(in order of severity)
what is the signalment and history of uveodermatologic syndrome?
young to middle aged
acute bilateral uveitis and non-pruritic
what breed is predisposed to uveodermatologic syndrome?
Akita
what is the most common lesion seen with uveodermatologic syndrome?
hypopigmented macules
what are some immune mediated disease that cause alopecia?
sebaceous adenitis
alopecia areata
dermatomyositis
ischaemic dermatopathy
what should be done to rule out demodicosis or dermatophytosis as a cause of alopecia?
trichography
what are the lesions associated with sebaceous adenitis?
partial alopecia and generalised poor coat quality
follicular casts/scale
what is the histopathological changes seen with sebaceous adenitis?
pyogranulomatous inflammation targeting sebaceous glands
what is the lesion morphology of alopecia areata?
foal/multifocal patches of alopecia with possible erythema
what is the classic histopathological finding of alopecia areata?
lymphocytic destruction of hair bulbs
where is the typical distribution of alopecia areata?
head/face
what is canine atopic dermatitis?
genetically predisposed inflammatory and pruritic allergic skin disease associated with IgE antibodies most commonly to environmental allergens
what are the four factors that contribute to the pathogenesis of CAD?
cutaneous inflammation and pruritis
defective skin barrier
microbial colonisation
other flare factors
what is CAD?
canine atopic dermatitis
how does the defective skin barrier contribute to CAD?
increased transepidermal water loss
wide intercellular spaces between corneocytes
disorganised/fragmented lipid matrix
decreased protein/lipids
why does microbial colonisation occur in cases of CAD?
increased binding sites from inflammation
reduced barrier function from lipid/protein
damaged skin surface (self trauma)
dysbiosis
what is dysbiosis associated with CAD?
changed patterns of bacterial colonisation on the skin creating reduced diversity and imbalance of commensals
what are the most common secondary microbial colonisations for dogs with CAD?
Staphylococcal
Malassezia dermatitis
what is the recurrent microbial colonisation of CAD cases called?
atopic flares (causes further inflammation and pruritis)
what are common causes of atopic flares?
bacterial and yeast infection
seasonal increases/changes in allergens
ectoparasite infection
reduction of therapy
what is the typical history of CAD patients?
pruritis (seasonal, perennial, with) - itch that rashes
<3 years old (<1 for food allergy)
breed predispositions
what are the compatible clinical signs of CAD?
pruritis - licking, chewing, grooming…
erythema and papules
what is used to measure pruritits?
pruritis visual analogue scale (grades the itch)
what are secondary skin lesions of CAD usually due to?
self trauma
what secondary skin lesions are associated with CAD?
otitis
alopecia
excoriations
salivary staining
lichenification
pustules, epidermal collarettes, crusts
hyperpigmentation
what is the distribution of CAD lesions?
face/chin
periorbital areas
ears
elbow creases
feet
ventral abdomen
perianal area
what are favrots criteria?
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
how is favrots criteria used?
the more signs the higher the chance of CAD
what are some differentials for pruritis in dogs?
ectoparasites
allergic skin disease (CAD, contact dermatitis)
microbial infection
Malassezia dermatitis
others - Pemphigus foliaceus…
is atopic dermatitis an outside in or an inside out disease?
inside out
what is done to rule out ectoparasites in cases of suspected CAD?
diagnostic tests and treatment trials
why are treatment trials needed to exclude ectoparasites from your differential diagnosis list for CAD?
some parasites live in the environment or are rare to find on the patient
what drug group is used for treatment trials for ectoparasites?
isoxazoline
what are some hints that CAD might be food induced?
concurrent GI signs
non-seasonal
very young dogs
pruritis is poorly responsive to steroid
what is the only way to diagnose a food allergy inducing CAD?
elimination novel diet trial
what are the two options of diet trials?
home cooked
commercial hydrolysed diet
what are some problems associated with home cooked diets for novel diet trials?
identifying appropriate
unsuitable for longterm for growing animals
labour intensive
palatability issues
GI upset
cost
how do hydrolysed protein diets work for food trials?
assumes there is a type 1 hypersensitivity so protein is chopped up so small the allergen doesn’t create a reaction
how long should a diet trial be done for?
minimum of 6-8 weeks
what should be used for 2-3 weeks at the start of a food trial?
steroids or oclacitinib
why would steroids or oclacitinib be used at the start of a food trial?
reduce secondary inflammation to reduce the length of the diet trial
why does care need to be taken when worming during a diet trial?
the wormers could be flavoured
what are the three things CAD therapy treats?
pruritis
inflammation
secondary infection/overgrowth
what guides the therapy for CAD?
(pathogenesis)
skin barrier dysfunction
skin inflammation
allergen sensitivity
microbial colonisation
what are the aims of improving skin barrier function in CAD cases?
reduce transepidermal water loss
reduce exposure to environmental allergens/irritants
reduce microbial colonisation
what treatments are used to improve skin barrier function?
non-irritating shampoos
topical moisturisers and emollients
oral/topical essential fatty acids
what should shampoos for CAD cases contain?
emollient (bring/trap water)
anti-seborrheic (grease/scaling)
antiseptic (prevent infection)
what is the aim of using essential fatty acids in CAD treatment?
improve barrier function of the skin
what does allergen immunotherapy do in CAD cases?
desensitises dog to environmental allergens by inducing tolerant T cells
how is allergen immunotherapy carried out?
administration of gradually increasing quantities of an allergen extract to an allergic subject to decrease the severity of clinical signs from subsequent exposure
how long does allergen immunotherapy need to be given for?
minimum of 12 months
what are the side effects to allergen immunotherapy?
very few - itching…
what are the aims of anti-inflammatory and anti-pruritic therapy?
long term reduction of inflammation
avoid flare ups of inflammation
restore normal skin environment and prevent microbial overgrowth
what are some possible drug types used anti-inflammatory and anti-pruritic therapy of CAD?
glucocorticoids
calcineurin inhibitors
janus kinase inhibitors
biologics
antihistamines
what systemic glucocorticoids can be used for CAD?
prednisolone and methylprednisolone
what are the possible side effects of glucocorticoid use in CAD patients?
polyphagia, PUPD, panting, behaviour changes, iatrogenic hyperadrenocorticism and increased UTI risk
what is the ideal way to use systemic glucocorticoids in CAD cases?
as “crisis busters” in flare ups
when are systemic glucocorticoids given in flare ups?
as early as possible
what topical glucocorticoids can be used for CAD?
hydrocortisone aceponate
what is the major risk of prolonged topical glucocorticoid use in CAD cases?
skin thinning on abdomen
what is the oral calcineurin inhibitor used for CAD?
ciclosporin
what is the function of oral calcineurin inhibitors?
inhibit T lymphocyte function by blocking calcineurin
what are the possible adverse effects of oral calcineurin inhibitors?
GI signs
gingival hyperplasia
viral papillomas
hirsutism (excessive hair)
what is the janus kinase inhibitor used for CAD?
oclacitinib
what is the function of janus kinase inhibitors?
inhibit JAK1 enzymes which signal transduction of pro-inflammatory, pro-allergic and pruritogenic cytokines
what is blood monitoring recommended when giving janus kinase inhibitors?
minor effect of JAK2 enzymes that effect the haematopoetic system
what are the contraindications for oclacitinib?
<12 months old
<3kg bodyweight
breeding dogs
severe infection, neoplasia or immunesuppression
how does lokivetmab work?
it is a monoclonal antibody that target/neutralises canine IL-31 (pruritogenic cytokine)
what is the advantage of lokivetmab?
highly targeted so minimal impact on normal immune function and can be used with other drugs
what is the main antihistamine used for CAD?
chlorphenamine
to what degree do ciclosporins control inflammation and itch?
moderate control of itch, inflammation and infection
to what degree does oclacitinib control inflammation and itch?
moderate inflammatory control and very good itch control
to what degree does lokivetmab control inflammation and itch?
poor at inflammation
excellent at itch
what is the aim of phase one CAD treatment?
induce remission
what is the aim of phase two CAD treatment?
prevent recurrences (proactive therapy)
what needs to be done to reach the pruritic threshold set for CAD patients?
remove flare factors (parasites, infection…)
what supports the vertical and horizontal canal of the ear?
auricular and annular cartilage
what is the name for the ear drum?
tympanic membrane
what connects the tympanic membrane to the inner ear?
auditory ossicles
what connects the middle ear to the nasopharynx?
eustachian/auditory tube
what is the function of the eustachian/auditory tube?
allow drainage of the middle ear
what is the differences between the tympanic bulla of cats and dogs?
cats - bony shelf that separates it into two halves
dogs - incomplete bony shelf
why is treating disease in the tympanic bulla of cats often difficult?
bony shelf makes accessing the ventral tympanic bulla
how can you tell what the cranial portion of the tympanic membrane is?
C shaped structure (auditory ossicle) points cranially
what are the two parts of the tympanic membrane?
pars flaccida
pars tensa
what is the function of the pars flaccida?
contains blood vessels that supply the pars tensa
what histological features are different in the ear canal skin compared to normal skin?
small hairs
ceruminous glands
sebaceous glands
what is the lining of the middle ear?
modified respiratory epithelium
what are the histological features the lining of the middle ear?
simple squamous to cuboidal epithelium
few ciliated cells
mucous secreting goblet cell
(modified respiratory epithelium)
what are the mechanisms that allow self cleaning of the external ears?
cerumen - catches material, keratinocytes, microbes and contains antimicrobial peptides and lysosomes
epithelial migration - living keratinocytes carry cerumen from tympanic membrane to external ear
what are the mechanisms that allow self cleaning of the middle ear?
mucous from goblet cells trap microbes and debris and drains via the Eustachian tube to be swallowed
what is the main type of bacteria found in the normal flora of the external ear canal?
gram positive cocci - Staphylococci
what is otitis?
inflammation of the ear
what mnemonic can be used for the differential of otitis?
(VIP MEGA FAME)
Viral
Immune mediated
Parasites
Mycoses
Endocrine
Glandular
Allergy
Foreign body
Autoimmune
Miscellaneous
Epithelialisation disorders
what is the most common parasites effecting the ear?
Otodectes cynotis
what are the most common differentials for otitis in dogs?
Foreign bodies
Allergen
Bugs (parasites)
what are the most common differentials for otitis in cats?
Flu (viral)
Allergens
Bugs (parasites)
how would the wax of a dog with Otodectes cynotis be described?
dark coffee ground appearance
why do most patients present very pruritic with Otodectes cynotis?
they have a hypersensitivity reaction to the mites
why are Otodectes cynotis mites difficult to see with a otoscope?
they are photophobic (run away from light)
what is used to treat Otodectes cynotis?
selamectin/moxidectin spot-on
steroid for intense hypersensitivity reaction
what are the main causes of secondary otitis?
microbial infection
topical medication reaction
inappropriate cleaning
what are some predisposing causes of otitis?
obstructive ear disease
conformation - hairy, narrow, waxy canals
environment
systemic disease
what are the most common causes of obstructive ear disease?
polyp
ceruminous gland neoplasia
what is the order of progressive pathological changes of the ear?
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
what are the clinical signs of otitis externa?
otic pruritis
pain
discharge/malodour
loss of hearing
secondary changes - scaling, lichenification, pyotraumatic dermatitis
what is usually the disease progression of otitis externa?
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
what are the clinical signs of otitis media and interna?
pain
horners syndrome
hearing loss
vestibular disease
what is the usual cause of primary otitis media in dogs and cats?
dogs - brachycephalic
cats - nasopharyngeal polyps
(Eustachian tube dysfunction)
what is primary secretory otitis media?
build up of mucous in the middle ear causing pain, deafness and bulging of tympanic membrane
what system is used to determine a cause for otitis?
primary causes (differentials)
secondary causes
predisposing factors
perpetuating factors
(PSPP)
what is the preferred imaging modality for otitis cases without neurological signs?
CT (computed tomography)
what colour should the tympanic bull appear on CT?
black - air filled
when would MRI be used to image otitis cases?
if there is neurological involvement (good soft tissue imaging)
if para-aural abscess is present with chronic otitis external
what is a myringotomy?
creating a hole in the tympanic membrane (can allow sampling/cleaning of middle ear)
which quadrant should the hole be made in for myringotomy?
caudoventral quadrant of tympanic membrane (as far away from C shape)
what are the indications for myringotomy?
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
why does cleaning the ear usually help otitis cases?
remove infectious debris
disrupts microbial biofilms
allows visualisation of tympanic membrane
exposes polyps/tumours
enhances action of topical therapy
how does ear cleaning need to be carried out in chronic otitis cases with copious amounts of discharge?
general anaesthetic
cuffed ET tube (infection material drained by Eustachian tube)
analgesia (paracetamol)
prednisolone pretreatment - open ear canal
what are biofilms?
microbes stuck together in extracellular matrix forming a protected environment making treatment of infection more difficult
what treatments can be used to help break up/disrupt biofilms?
N-acetylcysteine
polyhexanide
how is N-acetylcysteine used to break up biofilms?
lavage ear with water and then leave product in the ear for 5 minutes
thoroughly flush with water
what anti-inflammatory drugs are best for ears?
glucocorticoids (anti-inflammatory dose)
what glucocorticoids can be used for otitis as anti-inflammatory treatment?
prednisolone
dexamethasone
betamethasone
what sampling technique is used for the external ear canal?
indirect impression smear (cotton bud and role onto slide then Diff-Quik
what otic infections is chlorhexidine effective against?
gram positive cocci
gram negative rods
Malassezia
what otic infections are clotrimazole, miconazole and nystatin effective against?
Malassezia
what otic infections are florfenicol and fucidic acid effetive against?
gram positive cocci
what criteria is used to select topical antimicrobial proprietary treatments?
glucocorticoids (more potent for severe PPC)
concurrent disease (immune suppression by glucocorticoid)
spectrum of antimicrobial activity
potential for ototoxicity
patient/owner compliance
what treatment is licensed for patients with a ruptured eardrum?
none
if the eardrum isn’t visible (unsure if ruptured) what treatment should be given to otitis cases?
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)
why is culture not very useful for otitis diagnose?
the site isn’t sterile to begin with before otitis
what are the indications for culture and sensitivity for otitis cases?
if confirmed with cytology and needing to speciate bacteria
if systemic antimicrobials are required
if cases aren’t responding to appropriate treatment
what is a common gram negative rod that effects the ear?
Pseudomonas
what are some possible treatments for hypersensitivity (atopic) otitis?
triamicolone
HCA - hydrocortisone anencephaly
dexamethasone
what are some possible signs that would given an otitis case a guarded-poor prognosis?
solid/non-pliable external ear canal
severe stenosis and fibrosis
marked mineralisation
neoplasia/polyps
para-aural abscessation
what are the most common skin infections?
superficial pyoderma
Malassezia dermatitis
surface overgrowth (not true infection as there are no neutrophils)
what are hot spots?
localised material overgrowth (extremely pruritic and painful)
how are hot spots treated?
sedate and clip/clean
topical anti-inflammatories
analgesia (paracetamol)
what are the two main types of bacterial overgrowths?
hot spots
fold dermatitis
what is the usual cause of superficial pyoderma?
Staphylococcus pseudointermedius
what is the most important factor of treatment in superficial pyoderma cases?
topical treatment
what is topical therapy for superficial pyoderma usually based on?
chlorhexidine
how is Malassezia dermatitis treated?
shampoo - chlorhexidine and miconazole
systemic antifungals - itraconazole
allergy vaccine (if hypersensitive)
what are most skin antiseptics based on?
chlorhexidine
what is the protocol for treating deep pyoderma?
topical antiseptics and antibiotics
systemic antibiotics based on culture on widespread
biopsy fresh tissue to guide treatment
what duration of treatment is needed for superficial pyoderma?
2-3 weeks
what duration of treatment is needed for deep pyoderma?
> 4 weeks
what are the two main factors of treating immune-mediated skin disease?
remove/treat external triggers
control inappropriate immune response
what are some possible triggers of immune mediated skin disease?
drugs, UV light, confirmed infections, underlying neoplasia
what is done during the induction of remission phase of treating immune mediated skin disease?
initial bloods/monitor to ensure no underlying disease
aggressive therapy whilst trying to avoid severe adverse effects
needs regular monitoring and modification
what phase of treatment follows induction of remission of immune mediated skin disease?
transition
what is done in the transition phase of treating immune mediated skin disease?
taper drugs to lowest effective dose
less frequent monitoring with time and reduction of adverse effects
taper treatment to stop if no relapse
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?
maintenance (for cases that relapse in the transition phase)
what is done during the maintenance phase for immune mediated skin disease?
this is lifetime treatment with the lowest effective dose and monitor for adverse effects
what is done during the maintenance phase for immune mediated skin disease?
this is lifetime treatment with the lowest effective dose and monitor for adverse effects
how often is a patient with immune mediated skin disease monitored in the induction treatment period?
every 7-14 days
what are some common adverse effects seen with steroids?
PUPD
polyphagia
muscle weakness
breathlessness/panting
weight gain
alopecia
secondary bacterial infection
what are the possible adverse effects of ciclosporin?
vomiting and diarrhoea
increased hair/gum growth
immunosuppression (shouldnt be vaccinated)
papiloma growth
what are the possible adverse effects of ciclosporin?
vomiting and diarrhoea
increased hair/gum growth
immunosuppression (shouldn’t be vaccinated)
papiloma growth
what are the aims for treating sebaceous adenitis?
remove the thick scales
rehydrate the skin
