Atopic Dermatitis Flashcards

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1
Q

Pruritic think…

A

Allergies!

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2
Q

Atopic Dermatitis

Background

A

Genetically predisposed inflammatory and pruritic skin disease; pruritis is a must

Tendency to develop IgE-mediated allergy vs. environmental allergens

Strong hereditary tendencies

Usually a food allergy

More exposure = more reactive

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3
Q

Atopic Dermatitis

Multifactorial components

A

Genetic
Barrier Function
Immunologic Factors
Allergens

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4
Q

Atopic Dermatitis

Cycle

A

Allergen
Langerhans cell stimulates T-cell
T-cell releases cytokines that stimulate sensory nerve fibers –> itch
Get local inflammation (mast cell degranulation, stimulation of other T-cells, more cytokines) –> itch
Local inflammation can also stimulate Dendritic cells which will release their own cytokines and end up contributing to inflammation

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5
Q

Atopic Dermatitis

Genetic Factors

A

Veterinary studies still needed

Suggested to be seen in West Highland Terriers

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6
Q

Atopic Dermatitis

Barrier Function

A

Compromise; allergens can enter, water evaporates, dry skin (may cause pruritis)

Major lipids of SC
Cholesterol
FFA’s
Ceramides (holds everything together!)

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7
Q

Atopic Dermatitis

Immunologic Factors

A

Helper T Lymphocytes release cytokines and stimulate may ILs

Important one:
IL-4 with T-helper 2 cells
IL-4, IL-5, IL-13, IL-31

IL-31 has a targeted therapy

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8
Q

Atopic Dermatitis

Presentation

A

1-3 years
Seasonal pruritus
Breeds: Terriers, Boxers, Labs

Sites:
Ventral hairless areas
Face
Feet
Peri-anal (licks under tail)
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9
Q

Atopic Dermatitis

Diagnosis

A
No definitive test! 
Signalment
History (seasonality?)
Clinical Signs
Diagnosis of exclusion (rule out: ectoparasites, infections, allergies)
Must address secondary infection(s) 

Allergy test in animals is not useful; can appear to have allergens to all things but what is important is what is causing the pruritis

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10
Q

Atopic Dermatitis
Treatment
Symptomatic Rx

A

Antihistamines
Glucocorticoids
Free Fatty Acids
Topical therapy

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11
Q

Atopic Dermatitis
Treatment
Specifc Rx

A

Immunotherapy (shot, sublingual)
Atopica
Apoquel
Cytopoint

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12
Q

Antihistamines

What is the problem with these?

A

Does not target T-helper 2 cells which are the problem cells

Targets mast cells which do contribute to increased inflammation though

Therefore do not see a significant benefit

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13
Q

Antihistamines

Examples

A

First generation:
Hydroxyzine (Benadryl)

Second generation:
Cetirizine (non-sedating)

Can give as a prevenative

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14
Q

Glucocorticoids

A

Commonly used
Very effective (especially for environmental allergens)
Acts at multiple sites along atopic dermatitis cycle
Potent anti-inflammatory effects

Should NOT be used life long

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15
Q

Glucocorticoids

Atopic Dermatitis Cycle

A
Acts on:
T-helper 2 cells
Reduces cytokines released
Mast cells 
Neutrophils
Monocytes
Eosinophils 

Reduces inflammation

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16
Q

Glucocorticoids

What organs does it effect?

A

Everything! So many side affects may be present

Most commonly: PU/PD

Lymph nodes
Heart and blood vessels
Skin and Fur
Adrenal glands
Kidneys
Pancreas (pancreatitis)
Bladder
17
Q

Glucocorticoids
Oral Rx
Dose

A

Prednisone
Prednisolone
Methyprednisolone
Temaril-P (trimeprazine with prednisolone); anti-prurutic and anti-tussive

0.5-1.0 mg/kg/day
Try to do every other day

18
Q

Glucocorticoids

Injectable

A

Should avoid this b/c of longevity

Greater risk of adverese effects

19
Q

Glucocorticoids

Chronic use

A

Erythematous plaque formation (calcinotis cutis)

20
Q

Free Fatty Acids

A

Many formulations
Topical
Enriched diets
Nutritional/herbal supplement

Not very strong by itself

21
Q

Free Fatty Acids

Atopic Dermatitis Cycle

A

Makes tight junctions in epithelial barrier tighter; prevents allergen from entering

Some decrease in mast cell degranulation
Some action on T-Helper cells

22
Q

Topical Therapy

Kinds

A

Shampoo
1-3x/week bathing

Sprays/wipes; once/day or can cause calcinosis cutis b/c most have steroid component

Avoid potent glucocorticoids

23
Q

Allergy Immunotherapy

Intradermal Testing

A

Gold standard

Results in mast cell degranulation (wheals) - Type I hypersensitivity

False negatives due to:
Medications (no antihistamines on board)
Diseases (Cushing's; should be ruled out before this test)
Timing (peak season) 
Technique
24
Q

In vitro serum testing

A

Measure IgE
Poor indicator of allergic disease
Poor reproducibility between samples

25
Q

Atopic Dermatitis

Seasonal think

A

Grass, Trees, Weeds

26
Q

Atopic Dermatitis

Year round think

A

Dust mites

Food allergies

27
Q

Allergy Immunotherapy

Atopic Dermatitis Cycle

A

T-helper cells (blunts response; unsure exact mechanism)
Mast cells
Eosinophils

28
Q

Allergy Shots

A

50-80% improve within 4-12 months

Individualized protocols; usually once/week and hopefully shift to every other week

Reactions are rare

Usually treat for 1 year but can be up to 5 years

Symptomatic treatment will still be necessary

Goal: desensitize to allergen

29
Q

Allergy drops

A

Sublingual
Must be given every day
Thought; many T-helper cells are here

50% response

Not much research has been done in vet med

30
Q

Cyclosporine

What is it?

A

Calcineurin inhibitors
Targets T-lymphocytes
Prevents T-cell activation and release of pro-inflammatory cytokines
Inhibits histamine release

Note: carcinogenic

31
Q

Cyclosporine Activity

Atopic Dermatitis Cycle

A

Blocks pro-inflammatory cytokines such as IL-2 and pro-inflammatory pathways

Acts on: 
Langerhans cell
T-cells
Mast cells
Eosinophils 
Dendritic cells
32
Q

Cyclosporine

Drug interactions

A
Cytochrome P450 (liver and SI)
Anything that blocks this will increase longevity of cyclosporine 

Ketoconazole inhibits CYP450 and P-GP; so can give less of Cyclosporine b/c will stay in system longer

33
Q

Cyclosporine

Onset

A

Slow onset of action (up to 2 months)

Treatment can be refractory

Should only use for allergies against environmental allergens => if not working most likely is not environmental issue

34
Q

Oclacitinib

What is it?

A

Novel treatment
Apoquel

Allergic dermatitis and atopic dermatitis

Dogs must be at least 12 months of age

Can increase susceptibility to:
Demodicosis
Infections
Neoplasia (low risk)

NOT effective in cats

Usually have to give daily

35
Q

Oclacitnib

What does it target?

A

Apoquel

Targets IL-31 (specific IL for pruritis) by blocking JAK-STAT signaling

JAK-STAT needed to stimulate nucleus for gene transcription to make IL-31

36
Q

Cytopoint

What is it?

A

Lokivetmab
SQ injection
Lasts 4-8 weeks

90% caninized mono-clonal antibody (do NOT use in cats or will cause serum sickness)

Neutralizes IL-31
Inhibits binding to IL-31 receptors => do not register the pruritis b/c IL-31 never binds

Does not need liver or kidney to be eliminated

Promising results but there is a chance it will not work for certain patients