Dermatitis

Question 1

what is atopic dermatitis

Answer 1

aka eczema or atopic skin

• chronic inflammatory dermatiits that affects 17% of canadians
• patients experience disease flares alternative w/ periods of remission

Question 2

what age groups are primarily affects by atopic dermatitis

Answer 2

primarily a childhood condition,

80% of patients developing AD within first year of life and severity dec with age

Question 3

what is the allergic triad

Answer 3

asthma, allergic rhinoconjunctivities and atropic dermatitis

called allergic or atopic triad

Question 4

what is contact dermitits

Answer 4

• includes both allergic and irritant subtypes
• almost eveyrone expeirnces onec ase in their lifetime, most cases (80%) are irritant driven

Question 5

what age group is CD most common in

Answer 5

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

Question 6

what is stasis dermatitis

Answer 6

aka stasis eczema

• inflammation of skin of lower legs caused by chornic venous insufficiency
• approx 6% of patients over 65 report haivng SD

-

Question 7

what skin changes are related to CVI

Answer 7

*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

Question 8

who does stasis dermatits most commonly affect

Answer 8

most prevalent in middle aged or older adults

more common in women than men

Question 9

etiology of atopic dermatitis

Answer 9

• 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

Question 10

what factors can contribute for to epidermal barrier dysfunction

Answer 10

Pruritus, scratching, and inflammation

Question 11

what is that itch-scratch cycle

Answer 11

• caused by pruritus, scratching and inflammatoin
• get more dysfunction of epidermal barrier, allows allergens, irritants and microbes to enter skin more easily

Question 12

Question 13

how does ACD occur

Answer 13

• 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

Question 14

in ACD when does inflammatory reaction occur

Answer 14

48 to 72 hours after allergen exposure

Question 15

what are common causes of contact dermatitis

Answer 15

benzocaine, lanolin, latex, nickel, the Rhus genus (e.g., poison ivy, poison oak), and topical antihistamines.

Question 16

what is stasis dermatitis

Answer 16

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

Question 17

what causes the hyperpigmentation in SD

Answer 17

proteolytic enzymes produced by macrophages, other forms of inflamation and deposition of iron storage complexes (hemosiderin)

Question 18

characteristics of

acute atopic dermatitis

contact derm

stasis derm

Answer 18

• 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
• Stasis dermatitis
  
  • inflammation
  • erythema
  • edema
  • pigmentation,
  • ulceration

Question 19

characterisitcs of chronic

atropic derm, contact derm and stasis derm

Answer 19

• Atopic derm
  
  • thickening
  • linchenification
  • scratching
• Contact derm
  
  • thickening
  • xerosis
  • discolouration
• Stasis derm
  
  • scaling
  • linchification
  • edema
  • discolouration

Question 20

location of atropic derm, contract derm and stasis derm

Answer 20

• 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
• Stasis dermatitis
  
  • any part of lower leg but proximal to medial malleols in most cases

Question 21

what are the risk factors for atopic dermatitis

Answer 21

• 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

Question 22

risk factors for contact dermatitis

Answer 22

• 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

Question 23

what are the risk factors for stasis dermatitis

Answer 23

• 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

Question 24

what drugs can cuase periheral edema

Answer 24

* inc risk of stasis dermatitis

• antihypertensives
  
  • beta blockers
  • calcium channle blockers
  • clonidine
  • hydrazine
• Hormones
  
  • corticosteroids
  • estogren
  • progesterone
  • testosterone
• Other
  
  • acyclovir
  • traxodone
  • pramipexole
  • quinolone antibiotics

Question 25

scholar for dermatitis

Answer 25

• 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

Question 26

HAMS for dermatitis

Answer 26

• Health conditions: asthma, allergic rhinitis
• Allergies: medication related or environemental
• medications: Rx, non Rx, NHP, other recreational/illicit
• social history: occupation

Question 27

what are common conditions mistaken for contact derm that can be self treated

Answer 27

Seborrheic dermatitis
Tinea infections
Candidiasis

Question 28

what are common conditions mistaken for dermatitis that warrent referral

Answer 28

Psoriasis
Nummular dermatitis
Eczema herpeticum
Scabies

Question 29

what are rare condiitons mistaken for contact derm

Answer 29

Cutaneous T-cell lymphoma

Non-bullous ichthyosiform erythroderma

Phenylketonuria

HIV/AIDS-related skin changes

Graft-versus-host disease

*require referral

Question 30

what are the red flags for dermatitis

Answer 30

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

Question 31

what are the goals of therapy for treating dermatitis

Answer 31

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.

Question 32

what is the first line therapy for AD

Answer 32

moisturizers to treat the irritation and itch

-topical corticosteroids are considered the mainstay of treatment for AD

Question 33

what is the mainstay treatment for AD

what options are available OTC

Answer 33

• 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

Question 34

what to do for AD when a bacterial infection is suspected

Answer 34

• 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

Question 35

histamine and AD

Answer 35

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

Question 36

second gen antihistamines for treatment of AD

Answer 36

• little role in management
• can be sueful in patients with co-exhisting allergic rhinitis

*topica antihistamines are strong contract sensitizers and should be avoided

Question 37

soaps and cleansers for treatment for AD

Answer 37

• 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

Question 38

what is second line therapy for treatment of AD

Answer 38

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

Question 39

crisaborole ointment for treatment of AD

Answer 39

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

Question 40

what to do when topic therapeis are infeective or inappopriate for AD

Answer 40

phototherapy with UV light or system therapy with oral immunosuppressants

cyclosporine, methotrexate, azathioprine) or biologics (e.g., dupilumab)