Dermatitis Flashcards
1
Q
what is atopic dermatitis
A
aka eczema or atopic skin
- chronic inflammatory dermatiits that affects 17% of canadians
- patients experience disease flares alternative w/ periods of remission
2
Q
what age groups are primarily affects by atopic dermatitis
A
primarily a childhood condition,
80% of patients developing AD within first year of life and severity dec with age
3
Q
what is the allergic triad
A
asthma, allergic rhinoconjunctivities and atropic dermatitis
called allergic or atopic triad
4
Q
what is contact dermitits
A
- includes both allergic and irritant subtypes
- almost eveyrone expeirnces onec ase in their lifetime, most cases (80%) are irritant driven
5
Q
what age group is CD most common in
A
occurs in any age group
- the allergic version of contact dermititis may be less common in children due to limited allergen expsorue and opportunity for sensitization
6
Q
what is stasis dermatitis
A
aka stasis eczema
- inflammation of skin of lower legs caused by chornic venous insufficiency
- approx 6% of patients over 65 report haivng SD
-
7
Q
what skin changes are related to CVI
A
*CVI = chronic venous insufficiency
- skin hcanges related to CVI = edema, hyperpigmentation, atrophy or ulceration
*up to 20% of women and 17% of men reporting these changes
8
Q
who does stasis dermatits most commonly affect
A
most prevalent in middle aged or older adults
more common in women than men
9
Q
etiology of atopic dermatitis
A
- exact etiology is not known, ubt liekly multifactorial
- hysfunction of epidermal barrier allows for allergens, irritants and microbes to enter skin more easily
- allergens stimulate Th2 cells to produce interlukins, including IL-4, -5 and -13 which increase immunoglobulin E synthesis.
but role of IgE in pathogenesis of AD is not currently well known
10
Q
what factors can contribute for to epidermal barrier dysfunction
A
Pruritus, scratching, and inflammation
11
Q
what is that itch-scratch cycle
A
- caused by pruritus, scratching and inflammatoin
- get more dysfunction of epidermal barrier, allows allergens, irritants and microbes to enter skin more easily
12
Q
A
13
Q
how does ACD occur
A
- T cell mediated delayed hypersensitivity type reaction (need to be prev exposed)
- hapetens penetrate stratum corneum, form hapten-protein complexes and are processed by antigen presenting cells then presented to T calls to form memory cells
- antigen presenting cells stim natural killer cells to produce IL4 -> activates B cells
- B cells produce IgM and stimulate activation of complment immune system with subsequent exposure
- CD8 cells are primary effector cells in ACD causing apoptosis of keratinocytes
- accompanied by rapid vleavage of intercellular adhesion molecules -> get edema and the formation of vesicles
14
Q
in ACD when does inflammatory reaction occur
A
48 to 72 hours after allergen exposure
15
Q
what are common causes of contact dermatitis
A
benzocaine, lanolin, latex, nickel, the Rhus genus (e.g., poison ivy, poison oak), and topical antihistamines.
16
Q
what is stasis dermatitis
A
result of CVI
- normally movement of contraction of skeletal muscles cause venous blood to return to heart with help of competent venous valves
- if you impaire venous valves get limit blood return resulting in backward venous flow, venous hypertension and venous stasis
17
Q
what causes the hyperpigmentation in SD
A
proteolytic enzymes produced by macrophages, other forms of inflamation and deposition of iron storage complexes (hemosiderin)
18
Q
characteristics of
acute atopic dermatitis
contact derm
stasis derm
A
- Atopic
- pruritus
- xerosis
- erythema, edema
- blistering, oozing and crusting
- scratching
- Contract
- allergic
- intensely pruritic
- pain with scratching or infection
- signs ranging from transient erythema to severe swelling with bullae and/or ulceration
- irritant:
- more painful than pruritic
- signs range from mild erythema to crusting pustules, bullae, hemorrhage and erosions
- allergic
- Stasis dermatitis
- inflammation
- erythema
- edema
- pigmentation,
- ulceration
19
Q
characterisitcs of chronic
atropic derm, contact derm and stasis derm
A
- Atopic derm
- thickening
- linchenification
- scratching
- Contact derm
- thickening
- xerosis
- discolouration
- Stasis derm
- scaling
- linchification
- edema
- discolouration
20
Q
location of atropic derm, contract derm and stasis derm
A
- Atopic
- varies w/ age but face and flexural areas often affected
- infants and younger children: face and extensor areas
- older children: flexural areas
- Adults: face and hands
- Contact
- areas in contact with allergent or irritant
- in some cases can be generalized
- areas in contact with allergent or irritant
- Stasis dermatitis
- any part of lower leg but proximal to medial malleols in most cases
21
Q
what are the risk factors for atopic dermatitis
A
- family history or AD, asthma or allergic rhinitis -> risk 2-3x greater for children with one parent affects be atopic condition and 3-5x greater for children with two parents affected
- more common in developed cuntries, perhpas due to higher levels of pollution
- being female
higher socioeconomic status
- exposure to cold dry climates
22
Q
risk factors for contact dermatitis
A
- patients with AD or ipmaired cell mediated immunity bc increases susceptibilty to allergen and irritants
- being caucasion bc looser packing of skin layers and fewer intracellular lipids (allows irritants to penetrate more easily)
- females due to inc exposure to domestic and occipational detergents and “wet work” rather than a biological difference
- expsoure on face or back of hands where skin is thinner
- occupation like machinist or hair dresser
- old age (for ACD) or younger age (ICD)
- exposure to cold, dry climates
23
Q
what are the risk factors for stasis dermatitis
A
- same as CVI
- being older age
- female
- BMI >30
- family history of venous disease or personal histroy of deep bein thrombosis
- having a standing occupation
- being in hot, humid environemnt
- heart failure and hypertension can aggrevate it
- chronic edema of lower extremitis due to certain meds can dontribute to developemnt
24
Q
what drugs can cuase periheral edema
A
* inc risk of stasis dermatitis
- antihypertensives
- beta blockers
- calcium channle blockers
- clonidine
- hydrazine
- Hormones
- corticosteroids
- estogren
- progesterone
- testosterone
- Other
- acyclovir
- traxodone
- pramipexole
- quinolone antibiotics
25
scholar for dermatitis
* Symptoms: pruritis, oozing, apin
* Characteristics: severity, duration progression over time
* History of skin changes: initial onset in childhood
* Onset/timing of skin changes: flares alternating with periods of remission, post allergen/irritant exposure
* Location of skin changes: flexural areas, areas in cotnact w/ allergens/irritants, lower legs
* Aggravating factors: harsh soaps, wool, sweating
* Remitting factors: therapies treid, regimens follows and subsequent responses
26
HAMS for dermatitis
* Health conditions: asthma, allergic rhinitis
* Allergies: medication related or environemental
* medications: Rx, non Rx, NHP, other recreational/illicit
* social history: occupation
27
what are common conditions mistaken for contact derm that can be self treated
Seborrheic dermatitis
Tinea infections
Candidiasis
28
what are common conditions mistaken for dermatitis that warrent referral
Psoriasis
Nummular dermatitis
Eczema herpeticum
Scabies
29
what are rare condiitons mistaken for contact derm
Cutaneous T-cell lymphoma
Non-bullous ichthyosiform erythroderma
Phenylketonuria
HIV/AIDS-related skin changes
Graft-versus-host disease
\*require referral
30
what are the red flags for dermatitis
Affects more than 30% body surface area (BSA)
Involves the palms of the hands and/or soles of the feet
May be infected
Involves edema that persists or worsens over time
Significantly interferes with sleep or daily activities, or
Fails to improve with 7 days of pharmacologic and non-pharmacologic treatment or resolve with 14 days of treatment
31
what are the goals of therapy for treating dermatitis
The goals of treating atopic, contact, and SD are to
1) provide adequate symptomatic relief while attempting to resolve skin lesions
2) restore the barrier function of the skin
3) reduce the risk of secondary infection
4) identify and eliminate triggers
5) implement strategies to prevent or minimize recurrence.
32
what is the first line therapy for AD
moisturizers to treat the irritation and itch
-topical corticosteroids are considered the mainstay of treatment for AD
33
what is the mainstay treatment for AD
what options are available OTC
- topical corticosteroids
- hydrocortisone 0.5-1% is available in Canada without an Rx
- clobetasone butyrate 0.05% also available without Rx
\* using topical corticosteroid and mositurizer is more effective than topical corticosteroid alone
34
what to do for AD when a bacterial infection is suspected
- topical therapy with an prescription antibiotics/corticosteroid combination
ex: fusidic acid 2%/hydrocortisone 1%
- but prphylaxis with topical antimicrobial containing products is not rec due to risk of resistance
35
histamine and AD
NOT THOUGHT to be primary cause of itch in AD
- minimal evidence to supprot use of oral antihistamines
- some sources suggest first generation for sedating efefcts in patients experiencing sleep disturbences secondary to itch
\*first gen linked to adverse effects so do not recommend
36
second gen antihistamines for treatment of AD
- little role in management
- can be sueful in patients with co-exhisting allergic rhinitis
\*topica antihistamines are strong contract sensitizers and should be avoided
37
soaps and cleansers for treatment for AD
- mild soap or soapless cleansers should be used to remove irritants from skin
- other bath products sometimes can be bath oils and colloidal oatmeal -\> may increase skin hydration and reduce itch, respectiviely
38
what is second line therapy for treatment of AD
topical calcineurin inhibitors
- used when TCS are ineffective or not tolerated
- TCI can be first line off label when AD involves sensitizing areas (face, skinfolds) or when long term uninterrupted therapy is requoed
- TCI are effective for treating AD flared and may be used as maintenance therapy to prevent recurrences
39
crisaborole ointment for treatment of AD
crisaborole ointment = topical phosphodiesterase-3 (PDE-3) inhibitor
- considered second line therapy but may be 1t line in patients averse to using TCS or TCI
- prophylactic use of crisaborole ointment in AD has not been evaluated
40
what to do when topic therapeis are infeective or inappopriate for AD
phototherapy with UV light or system therapy with oral immunosuppressants
cyclosporine, methotrexate, azathioprine) or biologics (e.g., dupilumab)
