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Dermatology > Atopic Dermatitis > Flashcards

Atopic Dermatitis Flashcards

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1
Q

What is atopic dermatitis?

A
  • Genetically predisposed inflammatory and pruritic skin disease
  • Tendency to develop IgE-mediated allergy against environmental allergens
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2
Q

Risk factors for atopic dermatitis?

A
  • Strong hereditary tendencies
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3
Q

What factors work into the pathophysiology of atopic dermatitis?

A
  • Genetic
  • Barrier function
  • Immunologic factors
  • Allergens
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4
Q

What type of hypersensitivity is atopic dermatitis?

A
  • Type I
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5
Q

What is the second most common hypersensitivity disorder in dogs?

A
  • Atopic dermatitis
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6
Q

Role of cutaneous itch-selective neurons in atopic dermatitis?

A
  • Skin held quite tightly together
  • If you have allergens that penetrate through cracks in the skin
  • Langerhans process them and present them to T helper cells –> release of cytokines
  • More inflammatory substances and mast cell degranulation (vicious cycle)
  • Cytokines go to afferent nerve pathways and dorsal root ganglion, then perceived in the brain to start itching
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7
Q

What are genetic factors in humans that are implicated in atopic dermatitis?

A
  • Filaggrin gene mutations
  • Abnormal epidermal differentiation
  • Defective defense mechanisms predispose to AD
  • In veterinary studies, nothing has been shown like this
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8
Q

What are the major lipids of the stratum corneum, and which are the most important?

A
  • Cholesterol
  • FFAs
  • Ceramides
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9
Q

How does transepidermal water loss play a role in atopic dermatitis?

A
  • Cracks allow moisture to evaporate through

- Allergens can get in

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10
Q

What is the major entry route in dogs for atopic dermatitis?

A
  • Percutaneous absorption (PRIMARY)

- Also Inhalation

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11
Q

Which cytokine do individuals with atopy produce greater amounts of?

A
  • IL-4
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12
Q

IL-4 cascade

A
  • IL-4 pushes the immune system into a T-lymphocyte helper 2 (Th2) direction
  • Th2 is associated with allergic diseases and release of more IL-4, as well as IL-5, IL-13, and IL-31
  • IL-31 recently identified as a major cause of pruritus
  • Th2 response results in a significant increase in production of IgE antibody
  • Other antibody classes may be involved in the pathogenesis of atopy (short term sensitizing IgG or IgD)
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13
Q

What type of allergens can contribute to or exacerbate atopic dermatitis?

A
  • Environmental allergens***
  • Food allergens (triggers AD)
  • Bacterial antigens (Staph pseudintermedius)
  • Yeast antigens (Malassezia pachydermatis)
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14
Q

Which bacterial antigens contribute to AD?

A
  • Staphylococcus pseudintermedius
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15
Q

Which yeast antigens contribute to AD?

A
  • Malassezia pachydermatis
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16
Q

Signalment of dogs with AD

A
  • 1-3 years of age (not younger than 6-9 months usually and uncommon in middle age to older animals)
  • Breeds: Terriers, boxers, labs
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17
Q

Seasonality of AD?

A
  • Seasonal but can be year round
  • Often spring and summer
  • Chronic disease, and continued sensitization can lead to more progressive, year-round symptoms
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18
Q

Which sites are affected with AD?

A
  • Ventral hairless areas
  • Face
  • Feet
  • Peri-anal
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19
Q

Atopy and sensitization

A
  • Requires prior sensitization wherein IgE and IgGd antibody then fix to tissue mast cells and basophils
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20
Q

When do clinical signs develop with atopy?

A
  • Secondary challenge
  • Allergen cross-links cell-fixed IgE results in degranulation of mast cells releasing pharmacologically active substances
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21
Q

How does abnormal barrier function contribute to atopic dermatitis/

A
  • Ceramides are an important lipid component
  • Abnormal barrier function leads to increased trans-epidermal water loss, dry and itchy skin, and allows for penetration of allergens and pathogens
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22
Q

Secondary infections with AD

A
  • Atopic patients have higher rates of colonization of normal microflora (e.g. staph and malassezia)
  • Can be induced from scratching/pruritus and excoriations
  • Pyoderma
  • Yeast dermatitis
  • Otitis externa
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23
Q

Diagnosis of atopic dermatitis?

A
  • No definitive test
  • Signalment and seasonality
  • Distribution of pruritus
  • History
  • Clinical signs
  • Exclusion of other pruritic disease (ectoparasites, infections, and allergies)
  • Look for and address all secondary infections (Cytology! Skin, ear, and feet)
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24
Q

Lesions associated with AD

A
  • Typically secondary from self-trauma
  • Erythema (ear/pinnae, interdigital, axillae)
  • Excoriations
  • Crust and scale (rule out pyoderma)
  • Alopecia
  • Hyperpigmentation
  • Lichenification
  • Salivary staining
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25
Q

Breeds with AD association

A
  • Any breed!
  • Terriers
  • Labs
  • Setters
  • Boxers
  • Lhasa apso
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26
Q

Differential diagnoses for Atopic Dermatitis?

A
  • Ectoparasites (Scabies, otodectes, fleas)
  • Seasonal pruritus (consider or rule out flea allergy)
  • None-seasonal (year-round) pruritus: rule out food allergy
  • Not all itchy dogs are atopic!
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27
Q

What are three important concepts for treatment of atopic dermatitis?

A
  1. Threshold phenomenon
  2. Summation effect
  3. Avoidance
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28
Q

Threshold phenomenon

A
  • A certain allergen load can be tolerated by individuals without manifesting in disease, but a small increase in that load may push them over that threshold and result in clinical signs
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29
Q

Summation effect

A
  • A subclinical hypersensitivity in combination with pyoderma or yeast dermatitis may lead to severe pruritus
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30
Q

Avoidance

A
  • Not always possible
  • Decrease in overall contributing antigen load may be helpful (e.g. flea allergy)
  • This is why flea control is very important in atopic patients
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31
Q

Antihistamine MOA

A
  • Prevent release of histamine but do nothing for the cytokines or TH2 associated with atopic dermatitis
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32
Q

How useful are antihistamines?

A
  • Can be useful or helpful in mild, non-acute pruritus
  • Tend to be mediocre for more severely pruritic patients
  • Sedative effects may be a reason they can be helpful
  • Clinical trials show no significant benefits
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33
Q

Where are antihistamines metabolized?

A
  • Liver
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34
Q

Drug examples of antihistamines

A
  • Hydroxyzine (1st gen)
  • Diphenhydramine
  • Cetirizine (2nd gen)
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35
Q

How are antihistamines most useful?

A
  • Given as a preventative
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36
Q

Glucocorticoids - how effective?

A
  • VERY useful short term
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37
Q

How selective are glucocorticoids?

A
  • Not, they act at multiple sites
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38
Q

How do glucocorticoids work?

A
  • Prevent release of inflammatory mediators from TH2 cells
  • Impact mast cells
  • neutrophils and eosinophils with extravasation which causes the cascade
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39
Q

Side effects of corticosteroids

A
  • PU/PD
  • Polyphagia
  • Panting
  • Behavioral changes/aggression
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40
Q

Examples of oral glucocorticoids

A
  • Prednisone
  • Prednisolone
  • Methylprednisolone
  • Temaril P (combined with antihistamine)
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41
Q

Long-acting formulations of glucocorticoids - recommended?

A
  • Solumedrol
  • Vetalog
  • Few RCTs proving efficacy
  • Greater potency
  • Greater risk of adverse effects
42
Q

What are life-threatening side effects of steroids used inappropriately?

A
  • Diabetes mellitus
  • Calcinosis cutis
  • Exacerbate kidney disease and proteinuria
  • Lead to CHF
  • Iatrogenic Cushing’s disease
  • Steroid hepatopathy
  • Pancreatitis
  • Predispose to infections (Skin, UTIs)
  • Muscle wasting/atrophy
43
Q

Free fatty acids for atopic dermatitis

A
  • Many formulations including topical, diets, and supplements
44
Q

How are topical free fatty acids thought to help AD?

A
  • Thought that they restore barrier function
  • May prevent release of hsitamine from mast cells and prevent neutrophils from extravasating
  • He doesn’t like
  • Inhibits production of pro-inflammatory mediators of prostaglandin PG2 and leukotriene (LT4 series)
45
Q

Topical therapy for AD

A
  • Shampoos bathing 1-3x a week (shouldn’t dry them too much)
  • Regular sprays and wipes
  • Avoid potent glucocorticoids
46
Q

What does dermal atrophy or miliary dermatitis in dogs suggest?

A
  • excessive corticosteroid use
47
Q

Dose of steroids used for AD

A
  • Anti-inflammatory induction dose (0.5-1 mg/kg/day for 3-7 days) then taper
  • If necessary for long-term use: find the lowest effective anti-inflammatory dose and only use EVERY OTHER DAY or less frequently even
48
Q

What active ingredients are drying?

A
  • Benzoyl peroxide or dawn dish detergent
49
Q

What focal pruritus sprays/wipes, or mousses should you use?

A
  • Avoid potent steroids sprays like triamcinolone or betamethasone
  • Use hydrocortisone based products
50
Q

What is it important to do before testing for allergen-specific desensitization?

A
  • Important to have made clinical diagnosis or ruled out other causes (e.g. flea allergy, food allergy, and/or ectoparasites) before testing
51
Q

What is allergy testing technically testing for?

A
  • What the patient is reactive too

- Based on intradermal testing and serum blood testing

52
Q

What is the gold standard for allergy diagnosis?

A
  • Intradermal testing
53
Q

How does the intradermal test work?

A
  • Inject into skin and see immediate reaction

- Results in mast cell degranulation

54
Q

Causes of false negatives for intradermal skin testing?

A
  • Medications (steroids)
  • Diseases
  • Timing (peak season)
  • Technique
55
Q

In vitro serum test

  • What is it measuring?
A
  • IgE
56
Q

In vitro serum test

  • How good of an indicator of allergic disease is it?
A
  • Poor

- Never completely sensitive nor specific

57
Q

Correlation of serum testing with IDT?

A
  • Poor
58
Q

Reproducibility of serum testing?

A

Poor

59
Q

Is serum testing affected by medications?

A

No

60
Q

What drugs can alter IDT?

A
  • Antihistamines

- Corticosteroids

61
Q

What are the significance of the reactions with IDT?

A
  • Important to interpret in light of patient’s clinical signs (e.g. year round pruritus and only 1-2 reactions??)
  • Tells you animal has allergen specific IgE but does NOT tell you allergen is CAUSING clinical signs
62
Q

What should results from in vitro serum testing correlate with?

A
  • sesaonality
63
Q

Seasonal allergens

A
  • Grasses
  • Trees
  • Weeds
64
Q

Year round allergens

A
  • Dust mites
65
Q

Mechanism of allergen immunotherapy

A
  • Maybe blunts T helper and reduces mast cells as well as eosinophils?
  • Unknown exactly how it works
66
Q

Response to desensitization therapy - rate and timeline?

A
  • Can be effective in up to 75% of patients

- Response can be seen within 4 months to 1 year

67
Q

How is desensitization therapy administered?

A
  • Shots every 7-21 days and should be tailored to patient’s response
  • Sublingual drops 1-2x a day
68
Q

Sublingual immunotherapy - response rate?

A
  • Novel therapy

- 60% response rate

69
Q

Where are allergy drops giveN?

A
  • Under the tongue
  • Absorbed by oral mucosa
  • q12-24hrs EVERY day
70
Q

Allergy drops for shot failures - how many of those respond?

A
  • 50% response
71
Q

Reactions to allergy drops

A
  • 3% may develop mild to moderate pruritus, hives, and GI signs
72
Q

How long should you continue with desensitization therapy?

A
  • If effective, continue long-term (if possible)
  • UP to 1 year; if no improvement, consider discontinuing
  • May need to consider use of anti-pruritic treatments during desensitization process
  • Attempt to taper/reduce dependency of anti-pruritic meds to determine efficacy of desensitization therapy
73
Q

Shots vs drops - how to decide one over the other?

A
  • No clear advantage (similar cost)
  • Drops are novel
  • Client schedule and convenience (Aversion to needles?)
  • Shot failure?
  • Adverse effects are rare
74
Q

Mechanism of atopica

A
  • Cyclosporine binds cyclophilin, which inhibits calcineurin
  • Inhibition works upstream, blocking pro-inflammatory cytokines such as IL-2
  • Targets T cells
  • Prevents T cell activation and release of pro-inflammatory cytokines (IL-2, IL-4, IL-5)
  • Inhibits histamine release (blocks degranulation of mast cells)
75
Q

Other uses of cyclosporine

A
  • IMmune mediated diseases

- Organ transplant rejection therapy in humans

76
Q

Downstream pathways of calcineurin (i.e. the pathways inhibited by cyclosporine)

A
  • NFAT (Nuclear factor of activated T-cells) dephosphorylated
  • Goes into the cell leading to RNA polymerase transcription of DNA
  • Translation of mRNA produces proteins
  • Function of the cell is changed
77
Q

What enzyme metabolizes cyclosporine, and where is it metabolized?

A
  • Cytochrome P450
  • Liver
  • Small intestine
78
Q

How can you utilize drug interactions to reduce the amount of cyclosporine you use?

A
  • They can increase bioavailability
  • Ketoconazole inhibits Cytochrome P450
  • Fluconazole inhibits CYP3a in vitro
79
Q

How quickly does cyclosporine work?

A
  • Slow onset
  • Takes about 2-4 weeks
  • Treatment may be refractory
80
Q

Is skin testing affected by Cyclosporine?

A
  • No
81
Q

Treatment trial for cyclosporine

A
  • Try for 30-60 days
  • Taper to every other day
  • SHould work for the first 30 days or not
  • Should work for patients with true environmental allergens
82
Q

Side effects of cyclosporine (+ what’s the big one)?

A
  • Most are GI related (up to 25%)
  • Gingival hyperplasia (more likely with daily dosing)
  • Cutaneous papillomatosis
  • Hypertrichosis
  • Susceptibility to opportunistic infections (e.g. systemic fungal infections
  • POSSIBLE risk of neoplasia
83
Q

Oclacitinib labeled use

A
  • Control of allergic dermatitis and cAD
  • Dogs at least 12 months of age
  • Not for cats
84
Q

What diseases may oclacitinib predispose to?

A
  • Demodicosis
  • Infections
  • Neoplasia
85
Q

Jak-Stat - how many members in each?

A
  • JAK has 4 members

- STAT has 7 members

86
Q

Which JAK proteins does apoquel target?

A
  • JAK 1 and 2
  • JAK-1 (IL-31 and pruritus)
  • JAK2: Polycythemia vera; myelofibrosis; rheumatoid arthritis?; neutropenia, thrombocytopenia; anemias)
87
Q

What is JAK1 responsiblefor?

A
  • Pruritus
88
Q

JAK2 responsible for what?

A

Hematopoiesis

89
Q

JAK3 responsible for what?

A
  • Expressed in lymphocytes and regulates the immune system
90
Q

Tyrosine kinase 2 responsible for what?

A
  • Regulates immune system
91
Q

JAK-STAT signaling

A
  • Cytokines convey information by binding to specific receptors (JAK) on the cell membrane that induce biological responses
  • Cytokine bninds its receptor to activate JAK
  • JAK activates the intracellular proteins called STAT
  • STATs go to the nucleus and activate gene transcription (of IL-31 and inflammation)
  • Apoquel blocks the JAK protein from activating intracellular STAT proteins
92
Q

How quickly should dogs stop itching with oclacitinib, and how long should it last?

A
  • Stop itching in 2-3 hours

- Last for about 24 hours

93
Q

Mechanism of action of Lokivetmab (Cytopoint)?

A
  • 90% caninized monoclonal antibody
  • Neutralizes IL-31
  • Inhibits binding to IL-31 receptors
94
Q

Why doesn’t lokivetmab work on cats?

A
  • It’s a primarily caninized antibody

- Murine portions added

95
Q

Side effects of oclacitinib

A
  • GI upset (rare)
  • Susceptibility to opportunistic infections (demodicosis, dermatophytosis)
  • Possible risk of neoplasia
  • Bone marrow supression?
  • Immune-suppression?
96
Q

Route of cytopoint?

A
  • Subcutaneous injection
97
Q

How long does lokivetmab work?

A
  • 4-8 weeks, but approximately 30 days for most patients
98
Q

Metabolism of lokivetmab?

A
  • Does not depend on normal liver and kidney function
99
Q

Primary effect of lokivetmab?

A
  • Anti-pruritic

- No known anti-inflammatory or immune-suppression

100
Q

Safety for lokivetmab - what age of patient can use it?

A
  • All ages (vs apoquel which is over 12 months
101
Q

Side effects of lokivetmab?

A
  • Pain/discomfort when administering

- Possible recurring skin/ear infections

Dermatology (15 decks)

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