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
Breeds with AD association
- Any breed! - Terriers - Labs - Setters - Boxers - Lhasa apso
26
Differential diagnoses for Atopic Dermatitis?
- 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!
27
What are three important concepts for treatment of atopic dermatitis?
1. Threshold phenomenon 2. Summation effect 3. Avoidance
28
Threshold phenomenon
- 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
29
Summation effect
- A subclinical hypersensitivity in combination with pyoderma or yeast dermatitis may lead to severe pruritus
30
Avoidance
- 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
31
Antihistamine MOA
- Prevent release of histamine but do nothing for the cytokines or TH2 associated with atopic dermatitis
32
How useful are antihistamines?
- 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
33
Where are antihistamines metabolized?
- Liver
34
Drug examples of antihistamines
- Hydroxyzine (1st gen) - Diphenhydramine - Cetirizine (2nd gen)
35
How are antihistamines most useful?
- Given as a preventative
36
Glucocorticoids - how effective?
- VERY useful short term
37
How selective are glucocorticoids?
- Not, they act at multiple sites
38
How do glucocorticoids work?
- Prevent release of inflammatory mediators from TH2 cells - Impact mast cells - neutrophils and eosinophils with extravasation which causes the cascade
39
Side effects of corticosteroids
- PU/PD - Polyphagia - Panting - Behavioral changes/aggression
40
Examples of oral glucocorticoids
- Prednisone - Prednisolone - Methylprednisolone - Temaril P (combined with antihistamine)
41
Long-acting formulations of glucocorticoids - recommended?
- Solumedrol - Vetalog - Few RCTs proving efficacy - Greater potency - Greater risk of adverse effects
42
What are life-threatening side effects of steroids used inappropriately?
- 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
Free fatty acids for atopic dermatitis
- Many formulations including topical, diets, and supplements
44
How are topical free fatty acids thought to help AD?
- 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
Topical therapy for AD
- Shampoos bathing 1-3x a week (shouldn't dry them too much) - Regular sprays and wipes - Avoid potent glucocorticoids
46
What does dermal atrophy or miliary dermatitis in dogs suggest?
- excessive corticosteroid use
47
Dose of steroids used for AD
- 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
What active ingredients are drying?
- Benzoyl peroxide or dawn dish detergent
49
What focal pruritus sprays/wipes, or mousses should you use?
- Avoid potent steroids sprays like triamcinolone or betamethasone - Use hydrocortisone based products
50
What is it important to do before testing for allergen-specific desensitization?
- Important to have made clinical diagnosis or ruled out other causes (e.g. flea allergy, food allergy, and/or ectoparasites) before testing
51
What is allergy testing technically testing for?
- What the patient is reactive too | - Based on intradermal testing and serum blood testing
52
What is the gold standard for allergy diagnosis?
- Intradermal testing
53
How does the intradermal test work?
- Inject into skin and see immediate reaction | - Results in mast cell degranulation
54
Causes of false negatives for intradermal skin testing?
- Medications (steroids) - Diseases - Timing (peak season) - Technique
55
In vitro serum test - What is it measuring?
- IgE
56
In vitro serum test - How good of an indicator of allergic disease is it?
- Poor | - Never completely sensitive nor specific
57
Correlation of serum testing with IDT?
- Poor
58
Reproducibility of serum testing?
Poor
59
Is serum testing affected by medications?
No
60
What drugs can alter IDT?
- Antihistamines | - Corticosteroids
61
What are the significance of the reactions with IDT?
- 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
What should results from in vitro serum testing correlate with?
- sesaonality
63
Seasonal allergens
- Grasses - Trees - Weeds
64
Year round allergens
- Dust mites
65
Mechanism of allergen immunotherapy
- Maybe blunts T helper and reduces mast cells as well as eosinophils? - Unknown exactly how it works
66
Response to desensitization therapy - rate and timeline?
- Can be effective in up to 75% of patients | - Response can be seen within 4 months to 1 year
67
How is desensitization therapy administered?
- Shots every 7-21 days and should be tailored to patient's response - Sublingual drops 1-2x a day
68
Sublingual immunotherapy - response rate?
- Novel therapy | - 60% response rate
69
Where are allergy drops giveN?
- Under the tongue - Absorbed by oral mucosa - q12-24hrs EVERY day
70
Allergy drops for shot failures - how many of those respond?
- 50% response
71
Reactions to allergy drops
- 3% may develop mild to moderate pruritus, hives, and GI signs
72
How long should you continue with desensitization therapy?
- 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
Shots vs drops - how to decide one over the other?
- No clear advantage (similar cost) - Drops are novel - Client schedule and convenience (Aversion to needles?) - Shot failure? - Adverse effects are rare
74
Mechanism of atopica
- 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
Other uses of cyclosporine
- IMmune mediated diseases | - Organ transplant rejection therapy in humans
76
Downstream pathways of calcineurin (i.e. the pathways inhibited by cyclosporine)
- 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
What enzyme metabolizes cyclosporine, and where is it metabolized?
- Cytochrome P450 - Liver - Small intestine
78
How can you utilize drug interactions to reduce the amount of cyclosporine you use?
- They can increase bioavailability - Ketoconazole inhibits Cytochrome P450 - Fluconazole inhibits CYP3a in vitro
79
How quickly does cyclosporine work?
- Slow onset - Takes about 2-4 weeks - Treatment may be refractory
80
Is skin testing affected by Cyclosporine?
- No
81
Treatment trial for cyclosporine
- 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
Side effects of cyclosporine (+ what's the big one)?
- 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
Oclacitinib labeled use
- Control of allergic dermatitis and cAD - Dogs at least 12 months of age - Not for cats
84
What diseases may oclacitinib predispose to?
- Demodicosis - Infections - Neoplasia
85
Jak-Stat - how many members in each?
- JAK has 4 members | - STAT has 7 members
86
Which JAK proteins does apoquel target?
- JAK 1 and 2 - JAK-1 (IL-31 and pruritus) - JAK2: Polycythemia vera; myelofibrosis; rheumatoid arthritis?; neutropenia, thrombocytopenia; anemias)
87
What is JAK1 responsiblefor?
- Pruritus
88
JAK2 responsible for what?
Hematopoiesis
89
JAK3 responsible for what?
- Expressed in lymphocytes and regulates the immune system
90
Tyrosine kinase 2 responsible for what?
- Regulates immune system
91
JAK-STAT signaling
- 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
How quickly should dogs stop itching with oclacitinib, and how long should it last?
- Stop itching in 2-3 hours | - Last for about 24 hours
93
Mechanism of action of Lokivetmab (Cytopoint)?
- 90% caninized monoclonal antibody - Neutralizes IL-31 - Inhibits binding to IL-31 receptors
94
Why doesn't lokivetmab work on cats?
- It's a primarily caninized antibody | - Murine portions added
95
Side effects of oclacitinib
- GI upset (rare) - Susceptibility to opportunistic infections (demodicosis, dermatophytosis) - Possible risk of neoplasia - Bone marrow supression? - Immune-suppression?
96
Route of cytopoint?
- Subcutaneous injection
97
How long does lokivetmab work?
- 4-8 weeks, but approximately 30 days for most patients
98
Metabolism of lokivetmab?
- Does not depend on normal liver and kidney function
99
Primary effect of lokivetmab?
- Anti-pruritic | - No known anti-inflammatory or immune-suppression
100
Safety for lokivetmab - what age of patient can use it?
- All ages (vs apoquel which is over 12 months
101
Side effects of lokivetmab?
- Pain/discomfort when administering | - Possible recurring skin/ear infections
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