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Dermatology 2 > Autoimmune and Immune mediated skin diseases 2 > Flashcards

Autoimmune and Immune mediated skin diseases 2 Flashcards

Autoimmune, immune mediated, allergy, management of allergic skin disease

1
Q

Explain the use of tetracyclines in the treatment of CLE/DLE (modes of action)

A
  • Inhibits neutrophil and leukocyte chemotaxis
  • Inhibits degranulation and phagocytosis
  • Inhibits lymphoblast formation/proliferation/antibody production
  • Inhibits activation of complement C3
  • Increases prostaglandin synthesis
  • Inhibits lipases and collagenases
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2
Q

What are the treatment options for plasma cell pododermatitis?

A
  • Resolution without therapy
  • Glucocorticoids
  • Gold salts
  • Chlorambucil
  • Surgery
  • Doxycycline
  • Ciclosporin, but not documented
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3
Q

How are glucocorticoids used in the treatment of plasma cell pododermatitis?

A

Prednisolone 4mg/kg/day initially, subject to change

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4
Q

How long until gold salts show an effect in the treatment of plasma cell pododermatitis

A

Can take up to 12 weeks to full effect

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5
Q

Outline the use of chlorambucil in the treatment of plasma cell pododermatitis

A

In combination with other drugs, especially steroids

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6
Q

Discuss the role of surgery in the treatment of plasma cell pododermatitis

A
  • Effective in severe cases, esp. where bleeding may be a major problem
  • Pad tissue regrows after the srugery
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7
Q

Discuss the use of doxycycline in the treatment of plasma cell pododermatitis (dose, long term use, mode of action)

A
  • 5mg/kg BID for up to 3 weeks
  • May have initial improvement allowing pulse therapy or low dose continuous therapy
  • Mode of action presumed immune mediate effects
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8
Q

Outline the management of idiopathic symmetric lupoid onychodystrophy when the nails start to lift off

A
  • Sedate/anaesthetise
  • Remove all loose nails
  • Bandage and antibacterial therapy combined with NSAIDs for pain relief
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9
Q

Describe the long term treatment of ILSO

A
  • Will have recurrent bouts of nail loss
  • Pentoxifylline (Trental), or tetracycline and niacinamide
  • Severe cases: glucocorticoids, ciclosporin
  • Keep nails short to avoid catching and ripping (main management)
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10
Q

Outline the treatment of vasculitis

A
  • Remove underlying cause
  • Outcome dependent on organs affected
  • Glucocorticoids are mainstay of treatment using immunosuppressive doses
  • Alternate therapies: pentoxifylline, sulphasalazine, dapsone
  • Sulphasalazine and dapsone not commonly used
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11
Q

What is pentoxifylline?

A

Methylxanthine derivative and phosphodiesterase inhibitor

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12
Q

What is the key risk owners need to be aware of when usinng pentoxifylline?

A

Risk of kidney failure

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13
Q

What are the effects of pentoxifylline?

A
  • Immunomodulatory (inhibits pro-inflammatory cytokines, upregulates anti-inflammatory IL-10)
  • Stimulates wound healing by stimulating collagenase production
  • interferes with adhesion of inflamm. cells to endothelial cells and keratinocytes
  • Decreases blood viscosity by inhibition of platelet aggregation
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14
Q

What conditions is pentoxifylline used for?

A
  • Vasculitis
  • Contact allergic dermatitis
  • Erythema multiforme
  • Dermatomyositis
  • Ulcerative dermatitis syndrome of rough collies
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15
Q

What are the 3 main groups of conditions that will cause pruritus?

A
  • Infections
  • Allergic skin disease
  • Ectoparasites
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16
Q

List potential differentials for pruritus/allergic skin disease

A
  • Ectoparasites hypersensitivities
  • Environmental atopy
  • Cutaneous adverse food reactions (CAFR) (dietary allergens and intolerance)
  • Contact allergy
  • Drug reactions
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17
Q

Define atopy

A

Inherited predisposition to develop a type I hypersensitivity reaction to environmental allergens

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18
Q

What is atopy-like dermatitis/intrinsic atopy?

A

Atopy with no IgE demonstrable (atopy usually associated with IgE)

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19
Q

What 2 defects are required in order for canine atopic dermatitis to develop?

A
  • Epidermal barrier function defect, allowing entry of percutaneous allergens from the environment
  • Polarisation of lymphocytes towards Th2, instead of Th1, routes
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20
Q

What steps are involved in the pathogenesis of canine atopic dermatitis?

A
  • Sensitisation and epidermal barrier defect
  • Re-exposure to the allergen
  • Direct neuronal stimulation
  • Chronicity
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21
Q

Explain the sensitisation and epidermal barrier defect step in the pathogenesis of canine atopic dermatitis

A
  • Percutaneous exposure to allergen leads to allergen capture and processing by Langerhans cells -> presented to naiive T lymphocytes, production of Th2 lymphocytes
  • Production of IL-4, IL-5, IL-13, activate skin immune system, stim, class switchin gin B cells = prod. of allergen specific IgE
  • Tissue mast cells bind IgE, sensitised to allergen
  • Additional IgE on basophils, langerhans cells and in circulation
  • Period of sensitisation before allergy
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22
Q

What is expressed by mast cells that allows binding to the allergen specific IgE in canine atopic dermatitis?

A

High-affinity Fc Epsilon receptors

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23
Q

Describe the re-exposure to allergen step in the pathogenesis of canine atopic dermatitis

A
  • Cross linking of mast cell surface IgE by allergen -> degran. of MCs -> released of preformed mediators and new synthesis -> cytokines from keratinocytes, activated T cells
  • Recruitment of inflamm. cells to dermis
  • Inflamm cells activate and proliferate via Janus Kinase (JAK) pathways on cell surface
  • Leads to inflammation, itch and scratch, worsen epidermal barrier, epidermal hyperplasia, worsening of epidermal barrier function
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24
Q

Explain the direct neuronal stimulation step in the pathogenesis of canine atopic dermatitis

A
  • On re-exposure, LC recognises allergen, migrates to dermis, presents allergen to primed Th2 cells
  • Pro-inflamm cytokines e.g. IL-31 released, bind to receptors on surface of neurons, trigger activation of JAK enzymes, stimulate nerve
  • Leads to itch then scratch
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25
Q

Explain the role of chronicity in the pathogenesis of canine atopic dermatitis

A
  • Scratching, toxins from secondary microbial infections, continued exposure to allergens all lead to progression of atopy
  • Activate keratinocytes and other immune cells e.g. macrophages
  • IL-12 released
  • Polarisation to ?Th1 phenotype => release of IFN-y increases monocyte/macrophage recruitment and activation
  • Leads to thickening of epidermis, stratum corneum etc.
  • Further worsening of epidermal barrier function
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26
Q

What are the 3 phases of inflammation seen in canine atopic dermatitis?

A
  • Acute phase
  • Late phase
  • Chronic phase
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27
Q

Describe the acute phase of inflammation in canine atopic dermatitis

A
  • Th2 cytokine profile
  • 15-20 mins after initiation
  • Inflammatory mediators released from mast cells (e.g. histamine, serotonin, PGs)
  • Effect is local vasodilation, tissue oedema, influc of inflammatory cells
  • Often pruritus
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28
Q

Describe the late phase of inflammation in canine atopic dermatitis

A

Eosinophil dominated, seen after 6-12 hours

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29
Q

Describe the chronic phase of inflammation in canine atopic dermatitis

A
  • Subsequent infiltration of lymphocytes

- Th1 dominated or unpolarised cytokine profile

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30
Q

Compare feline and canine atopic dermatitis

A
  • Poorly defined in cats
  • Not simple Th2 bias in lesional skin in cats
  • Cats referred to as “non-flea, non-food induced hypersensitivity dermatitis” i.e. hypersensitivity proven to not be food or fleas and therefore assume environmental
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31
Q

Describe the typical presentation for feline atopic dermatitis

A
  • Chronic, relapsing disease
  • May be seasonal or perennial
  • Hypersensitivity proven to not be food or fleas
  • May present at young age (6mo-3yr)
  • Genetic predilection recognised by some reports, esp. purebreds
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32
Q

What is allergic respiratory and cutaneous disease recognised for in horses?

A

Culicoides/insect bite hypersensitivity and atopic dermatitis

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33
Q

Give examples of allergens implicated in equine atopic dermatitis

A
  • Dust mites, forage mites (>90%)
  • Dust extracts, epidermals, feathers
  • Mould spores
  • Tree, grassweed pollens
  • Concurrent insect-bite hypersensitivity
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34
Q

What is meant by cutaneous adverse food reaction?

A

Inappropriate reactions to elements of diet

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35
Q

Compare food intolerance and dietary hypersensitivity

A
  • Intolerance: non-immunological mechansism

- Hypersensitivity: immunological mechanisms, not just type I hypersensitivity

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36
Q

What are the potential manifestations of CAFR?

A
  • GI disease
  • GI + cutaneous disease
  • Cutaneous disease alone
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37
Q

Compare the prevalence of atopic dermatitis and CAFR in dogs and cats

A
  • CAFR uncommon in dogs, whereas AD is common

- CAFR may be as common as AD in cats

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38
Q

Compare the clinical appearance of atopic dermatitis and CAFR

A

Are clinically indistinguishable

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39
Q

Outline the development of CAFR

A
  • Require sensitisation, generally over long period of time
  • Must be exposed to diet before
  • Clinical signs generally when diet has been eaten long term
  • Allergens poorly characterised and geographical differences likely
  • May react more to one protein
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40
Q

Describe the onset of clinical signs of CAFR

A
  • Can be within minutes of exposure

- More often 4-24 hours after ingestion

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41
Q

In what ways may chemicals and biologicals cause cutaneous skin disease on contact?

A
  • Irritant nature of substance: not hypersensitivity, contact irritant dermatitis
  • Or true allergy: type IV hypersensitivity reactions, contact hypersensitivity, delayed type
42
Q

Give examples of substances that may cause allergic contact dermatitis

A
  • Plants: pollen and sap
  • topical drugs and shampoos
  • Chemicals in furniture, carpet dyes, polishes, cleaners, rubber, plastic, leather, metal
43
Q

Describe the cutaneous manifestations of drug reactions

A
  • Can manifest as almost any type of cutaneous lesion or reaction pattern
  • Variable pruritus
  • May involve any hypersensitivity mechanisms
44
Q

Which drugs most frequently cause cutaneous reactions?

A

Antibiotics, esp. potentiated sulphonamides

45
Q

Describe the clinical signs of canine atopic dermatitis

A
  • Chronic relapsing dermatitis
  • Seasonal intially, progress to perennial
  • Onset young adult, 6mo to 3yr
  • Glucocorticoid responsive
  • Pruritus
  • Otitis externa
  • erythema, papules, wheals, alopecia, lichenification, hyperpigmentation
  • Secondary pyoderma/Malassezia dermatitis
46
Q

List breeds that are predisposed to canine atopic dermatitis

A
  • Terriers
  • Retrievers
  • english setters
  • Boxers
  • GSDs
  • French bulldog
47
Q

Describe the pruritus that may occur with canine atopic dermatitis

A
  • Face, feet, inguinum, axillae, flexural surfaces of limb, pinnae
  • Face rubbing and foot licking
  • Acral lick granulomas
  • May be the only sign initially
48
Q

What is the significance for having 5 out of 8 of Favrot’s criteria, and 6 out of 8?

A
  • 5: sensitivity 85%, specificity 79.1% for AD

- 6: sensitivity 58%, specificity 89% for AD

49
Q

What is unusual about AD in WHWT?

A
  • Usually AD does not cause dorsal pruritus

- But in Westies, AD, Demodex injai and fleas all cause dorsal pruritus

50
Q

Compare the onset of CAFR and AD

A

CAFR usually very early or later than expected for AD

51
Q

Compare the responsiveness to steroids in CAFR and AD

A

Pruritus less often responsive to steroids in CAFR than AD

52
Q

Explain the allergic threshold principle

A
  • AD may coexist with other allergic diseases
  • Secondary infections common which add to pruritus
  • Pruritic threshold below which have no clinical signs
  • Need to address all compounding concurrent or secondary pruritic disease to reduce pruritus to below threshold and stop itching and reduce chance of secondary infections
53
Q

What are the 4 cutaneous reaction patterns of cats?

A
  • Head and neck excoriations
  • symmetrical self-induced alopecia
  • Miliary dermatitis
  • Eosinophilic granuloma complexes (granulomas/ulcers/plaques)
54
Q

In what conditions do the 4 cutaneous reaction patterns of cats occur?

A
  • Flea bite hypersensitivity
  • Non-flea non-food induced hypersensitivity/feline atopy
  • Food induced hypersensitivity dermatitis
  • Other diseases e.g. parasitic, viral, bacterial, fungal, autoimmunem neoplastic
55
Q

What are Favrot’s criteria for the diagnosis of non-flea hypersensitivity dermatitis (i.e. food induced and/or non-food induced hypersensitivity dermatitis)?

A
  • At least 2 body sites affected
  • At least 2 of the cutaneous reaction patterns
  • Presence of symmetrical alopecia
  • Presence of any lesions on lips
  • Presence of erosions/ulcerations on chin or neck
  • Absence of lesions on rump
  • Absence of non-symmetrical lesions on rump/tail
  • Absnece of nodule or tumours
56
Q

How many criteria are required to have a 75% sensitivity and 76% specific for the diagnosis of non-flea hypersensitivity dermatitis in cats?

A

5

57
Q

Other than Favrot’s criteria, what are the clinical signs of feline AD?

A
  • +/- sneezing, chronic coughing, asthma
  • Secondary bacterial and yeast infection less common vs. dog but possible
  • +/- blood eosinophilia non-specific finding)
58
Q

Outline the value of histopathology in the diagnosis of allergic diseases

A

Are all indistinguishable from one another so not useful

59
Q

Describe the signalment for equine AD

A
  • Uncertain prevalence
  • Onset most commonly 1.5-6yrs
  • No sex predilection
  • Breed predilection for TB and Arabs
  • Signs seasonal and progress to perrenial, or start non-seasonal
60
Q

Describe the clinical signs of equine AD

A
  • Pruritus and urticaria (urticarial wheal, rugae, angio-oedema)
  • Tail flicking, stamping, rubbing, head shaking
  • Initially no dermatological signs, but self-inflicted damage leads to alopecia, excoriations, lichenification, thickening, hyperpigmentation, secondary infection
  • Rufted papules, may coalesce to form crusts and focal alopecia
  • Nodues
  • Rarely concurrent respiratory disease e.g. COPD, allergic rhinitis/conjunctivitis
61
Q

Describe the presentation of CAFR in dogs

A
  • All signs indistinguishable from AD

- Only distinguishable by age of onset (older and younger animals affected, in AD mainly younger animals)

62
Q

Describe the presentation of CAfR in the cat

A

Any one or more of the 4 cutaneous reaction patterns in cats

63
Q

Describe the presentation of CAFR in horses

A
  • RARE

- Foods often suspected by owners, aka “protein bumps” but not supported by elimination diets or challenge

64
Q

Describe the clinical manifestation of contact hypersensitiity

A
  • Rare, difficult to confirm
  • Patch testing difficult
  • lesion areas related to exposure
  • Often affects more sparsely haired areas
  • Variable pruritus
  • Erythema, papules, plaques, hypo- or hyperpigmentation
65
Q

Discuss the difficulties associated with management of allergic skin disease

A
  • Cannot be cured, only controlled
  • Allergen avoidance ideally
  • Life long therapy required if cannot avoid
66
Q

What is the effect of stress on the development of AD?

A
  • Stress increases pruritus
  • Adds to self trauma and inflammation
  • Worsens barrier defect
  • Increased entrance of allergens
67
Q

What aspects are involved in the treatment of AD?

A
  • Allergen avoidance
  • Control of secondary infection
  • Anti-inflammatory/antipruritic agents
  • Address barrier function
  • Allergen specific immunotherapy
68
Q

List examples of products that may support the cutaneous barrier function

A
  • Oral essential fatty acids
  • EFA shampoos
  • Topical skin lipid complex/essential oils
  • Topical moisturisers
69
Q

List examples of anti-inflammatory/anti-pruritic agents that can be used inn the treatment of atopy

A
  • Glucocorticoids (systemic/topical)
  • Ciclosporin
  • Oclacitanib
  • Lokivetmab
  • Antihistamines, Tacrolimus, PEA-UM
70
Q

Explain the importance of controlling secondary infections in the treatment of atopy

A
  • Will reduce pruritus andminimise self trauma

- Allows healing of barrier function if self trauma is reduced

71
Q

Outline the method of control of secondary infections associated with atopy

A
  • Assess if pyoderma +/- Malassezia present using clinical presentation, in house cytology, culture and susceptibility if history of recurrent pyoderma
  • Treat infections but avoid immunosuppressives
72
Q

Explain why the use of immunosuppressives should be avoided when treating atopy with concurrent secondary infection

A

Immunosuppression causes superficial and deep pyoderma, so administration of glucocorticoids or oclacitanib will worsen the disease

73
Q

Outline the treatment of bacterial pyoderma with concurrent atopy

A
  • Topical: antimicrobial shampoo/wipes.foams, esp/ chlorhexidine 2-4%, use in preference to antibiotics where possible
  • Systemic antibiotics if necessary: adequate length of time for superficial or deep
74
Q

Outline the treatment of Malassezia dermatitis with concurrent atopy

A

Topical antifungals usually, occasionally systemic

75
Q

How may allergens be avoided?

A
  • Rarely possible to eliminate
  • Can reduce house dust mites by steam cleaning, freezing bedding after washing etc
  • Regular shampooing to remove allergens from coat
76
Q

Outline the role of barrier function in the treatment of AD

A
  • Impaired barrier function allows entry of allergen into the skin
  • Need to reduce trans-epidermal water loss
  • Important in long term control but slow to take effect
  • Use in combination with other therapies
77
Q

Explain how topical moisturisers aid barrier function

A
  • Restore barrier function and reduce pruritus
  • May contain urea, glycerine, linoleic acid, colloidal oatmeal
  • Draw moisture into skin by osmosis or act as emolients and trap water
  • Cooling effect reduces pruritus
78
Q

Explain the role of glucocorticoids in the treatment of atopy

A
  • Anti-inflammatory, non-specific action that will also stop itch
  • Rapid onset of action, inexpensive
79
Q

Outline a treatment plan for glucocorticoids in the treatment of AD

A
  • Pred or methylpred (Mpred has no mineralocorticoid action but more expensive)
  • Start daily at antiinflamm dose of 0.5-1mg/kg pred SID, then reduce to lowest effective alternate day dose to protect adrenal axis
  • Aim for <0.5mg/kg pred EOD
  • Taper gradually
  • Owner must aware of side effects
80
Q

Describe the short and long term side effects of glucocorticoids

A
  • Most side effects of all AD treatments
  • Short: PUPD, polyphagia, panting
  • Long: live problems, bladder infection, diabetes mellitus, muscle wasting, gastric ulcers, pancreatitis, hair loss, skin thinning, pyoderma
81
Q

When is the use of systemic glucocorticoids int he treatment of AD indicated?

A
  • ONly when necessary
  • Short term treatment of severe pruritic flare up
  • In early stages of immunotherapy
  • Seasonal pruritus requiring only 3-4months treatment/year
  • When other treatments are inadequate or financially prohibited
82
Q

Discuss the use of long acting injectable glucocorticoids in the treatment of AD

A
  • High risk of HPA axis suppression
  • Poorer dose control
  • Induces diabetes mellitus relatively frequently
  • Rarely used except in fractious cats
83
Q

When are topical glucocorticoids indicated in the treatment of AD?

A
  • Pyotraumatic dermatitis (surface pyoderma), eyes, ears

- Short term flare ups affecting small areas

84
Q

Discuss the considerations regarding the use of topical glucocorticoids in the treatment of AD

A
  • Must wear gloves
  • Some may contain antibiotics and should only be used short term
  • Consider potency of glucocorticoid: higher ok short ter,, but lower preferred long term
  • Side effects possible, including skin thinning
85
Q

How does the potentcy of hydrocortisone aceponate compare to that of other glucocorticoids?

A
  • Hydrocortisone usually lower

- Hydrocortisone aceponate is exception, similar potency to betamethasone (i.e. higher)

86
Q

What is are the main advantages of using hydrocortisone aceponate?

A
  • Similar potency to betamethasone, but less systemic absorption so less effect on HPA suppression
  • less skin thining vs other topicals of similar potency
  • Spray
  • Licensed for 7 day use
87
Q

Which treatments are licensed in the treatment of atopic dermatitis in dogs and cats?

A
  • Ciclosporin in both
  • Glucocorticoids in both
  • Oclacitanib only licensed in dogs
  • Lokivetmab only in dogs
88
Q

Describe the mechanism of action of ciclosporin

A
  • Calcineurin inhibitor
  • Blocks release of inflammatory mediated molecules e.g. cytokines, ILs
  • Inhibit cells of allergic reaction e.g. T lymphocytes, eosinophils, mast cells
  • T cell suppression non-specific
89
Q

What is required prior to use of ciclosporin n cats?

A

Need to test for FeLV, FIV and toxoplasmosis

90
Q

How may ciclosporin have drug interactions?

A

Via cytochrome P450 or P-glycoprotein

91
Q

Explain how ciclosporin may have drug interactions via CYP450

A
  • CYP450 metabolises ciclosporin to inactive/weakly active metabolites
  • Drugs also metabolised by CYP450 may therefore increase ciclosporin bioavailability e.g erythromycin
  • Enzyme inducers may reduce ciclosporin bioavailability e.g. phenobarbitone
92
Q

Explain how ciclosporin may have drug interactions via P-glycoprotein

A
  • Drugs inhibiting efflux pump increase ciclosporin bioavailability, leading to increased brain penetration and potential toxicity
  • e.g. ketoconazole
  • If giving systemic anti-fungals, halve dose of ciclosporin given
93
Q

Describe the efficacy of ciclosporin in the treatment of AD

A
  • Effective in ~80% of cases
  • Slower to effect vs glucocorticoids
  • Changes in 1st month,but 2-3 months to full effect
  • Taper to q48h or twice weekly dosing in many
94
Q

Desribe the side effects of ciclosporin treatment for AD

A
  • Often initial V/D but settles
  • In dogs, occasional reversible anorexia, hirsuitism, gingival hyperplasia, papillomatosis
  • Some risk of immunosuppression leading to bacterial infection, demodicosis, dermatophytosis
95
Q

What are the contraindications for ciclosporin use in the treatment of AD?

A
  • Avoid use 2 weeks either side of vaccination
  • If gingival hyperplasia occurs
  • in dogs <6mo or <2kg body weight
  • Breeding, pregnant, lactating animals
  • Animals with history of malignant disorders
  • Diabetics (may affect circulating insulin, use with caution)
96
Q

What is the mechanism of action of oclacitanib?

A

JAK1 inhibitor, prevents direct stimulation of nerves by IL-31 causing pruritus, and also reduces inflammation

97
Q

What is the indication for use of oclacitanib?

A

Pruritus associated with allergic skin disease, particularly clinical manifestations of atopic dermatitis

98
Q

What are the key advantages of oclacitanib over the other treatments for AD?

A
  • Rapid onset (as fast as pred in most)
  • Side effects less than pred
  • Does not interfere with intradermal testing/IgE serology (corticosteroids do)
  • Can vaccinate during treatment
  • Minimal interactions with other drugs
  • Useful short and long term
  • Cheaper than ciclosporin
99
Q

Describe the typical dosing regime of oclacitanib for the treatment of AD

A
  • Dose 2x daily for 2 weeks
  • Then once daily (may get intial increase in pruritus but will settle)
  • Must see efficacy at once daily administration to continue use
100
Q

What are the contraindications for the use of oclacitanib?

A
  • Dogs <1yo, <3kg
  • Immunosuppressed (may increase susceptibility to infection)
  • Progressive neoplasia
  • Pregnancy, lactation, breeding males

Dermatology 2 (23 decks)

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