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Skin Midterm > Dermatitis > Flashcards

Dermatitis Flashcards

1
Q

what is dermatitis

A

polymorphic inflammatory reaction; involves the epidermis and dermis

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2
Q

what are the primary lesions of acute dermatitis

A
  • erythematous macules, papules, vesicles; pruritus

- may conjoin to form patches

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3
Q

what are secondary lesions of scute dermatitis

A

may occur related to infection and excoriation

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4
Q

what is chronic dermatitis

A

pruritus, xerosis, hyperkeratosis, lichenification, fissuring

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5
Q

what are the three different types of dermatitis

A
  1. seborrheic dermatitis (SD)
  2. atopic dermatitis (AD)
  3. contact dermatitis (irritant/allergic)
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6
Q

what is seborrheic dermatitis

A

redness and scaling of the skin

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7
Q

what is the infantile form of seborrheic dermatitis

A

cradle cap, typically with in the first 3 months of life

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8
Q

what are some risk factors assoicated with SD

A
  • immunosuppression: HIV/AIDs, premature birth
  • alcoholism
  • endocrine disorders associated with obesity
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9
Q

what is SD caused by

A

Malassezia species (yeast), which is the cause for inflammatory response

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10
Q

How does SD appear

A

pink to red erythematous patches and plaques with a grey/white or yellow/red, greasy scale

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11
Q

what does SD on scalp occur with

A

dandruff

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12
Q

what are some exacerbating factors of SD

A
  • low humidity
  • cold temp
  • stress
  • medications: lithium (mood), buspirone (anxiety)
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13
Q

what can improve symptoms of SD

A

UV lighting

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14
Q

where are some areas that SD is located on the human body

A

face, scalp, eats, upper trunk, intertriginous areas (areas with high concentration of sebaceous glands)

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15
Q

how should cradle cap be treated

A
  • body oil
  • vegetable oil
  • then leave ALONE
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16
Q

what are some pharmacological treatments you can use on an infant that has cradle cap

A
  • low potency topical steroids: hydrocortisone 1% cream or lotion
  • antifungals: ketoconazole 2% cream/lotion or 1-2% shampoo
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17
Q

which of the following is more potent hydrocortisone cream or ointment

A

ointment

18
Q

what is the common age for adults getting SD

A

35-45

19
Q

is SD more common in males or females

A

males

20
Q

If a patent has acute scalp SD how should they be treated?

A
  • OTC shampoo containing selenium sulfide, zinc pyrithione, coal tar, salicylic acid
  • rx: ketoconazole 2% shampoo, cream, lotion, or foam
  • rx: ciclopirox shampoo, cream, gel
21
Q

If a patient has acute SD on face, ears, and trunk how should this be treated

A
  • antifungals: mainstay of therapy
    ketoconazole 2% shampoo, cream, lotion or foam (mainstay)
    Ciclopirox shampoo, cream, gel (side effects may be more tolerable)
  • topical steroids
    low potency for short duration
  • topical calcineurin inhibitors ( rare to use)
    pimecrolimus 1% cream
    tacrolimus 0.1% ointment
22
Q

How should you maintain chronic prevention of SD

A
  • ketoconazole 2% shampoo/gel/foam (decrease frequency)

- low potency steroids (hydrocortisone 1-2.5%)

23
Q

what is the MOA of ketoconazole

A
  • inhibits fungal P450 system to alter cell wall permeability
  • inhibits androgen synthesis
24
Q

How should ketoconazole be administered

A
  • twice weekly x 4-8 weeks; at least 3 days between applications (shampoo)
  • twice daily x 4 weeks (cream; foam)
  • daily x 2 weeks (gel)
25
Q

what are some side effects associated with ketoconazole cream/gel

A

contact dermatitis, headache, burning/irritation, paresthesia (all are relatively uncommon)

26
Q

what are some side effects of ketoconazole shampoo

A

hair loss, scalp/skin irritation, abnormal hair texture, dry skin, itching (all are relatively uncommon)

27
Q

what are some side effects of ketoconazole foam

A

burning (10%), application site reaction (6%), contact sensitization, dryness, erythema

28
Q

what is atopic dermatitis

A

eczema

29
Q

In what patient population does atopic dermatitis occur in

A

patients in urban areas and in smaller families

30
Q

what is the onset of AD

A

~ 90% occur before age 5

31
Q

what is the pathophysiology of AD

A

defective epidermal barrier allows greater access of allergens to the skin

32
Q

What does type 1 IgE-mediated include

A
  • atopic dermatitis/eczema
  • allergic rhinitis
  • asthma
33
Q

what are some predisposing factors with AD

A
  • genetics
  • weather
    heat is likely to cause perspiration which may increase pruritus
    cold, dry weather can exacerbate xerosis and dermatitis
  • S. aureus may increase AD symptoms
  • emotional stress
  • exposure to aeroallergens
  • food (controversial)
34
Q

how does AD present as in acute AD

A
  • pruritus
  • erythematous papules or plaques
  • may also occur with excoriations and scales
  • may also ooze or have crusting
  • may be accompanied by secondary infections
35
Q

what is the appearance of chronic AD

A

erythematous plaques; may have lichenification

36
Q

what are other common signs/symptoms of AD

A
  • Dennie-morgan folds (lines or folds under lower eyelid)
  • allergic shiners ( darkening of eyelid or under eye)
  • hyperlinearity of palms/soles
37
Q

where can AD be located on the body

A

face, scalp, bends or flexures in the extremities (wrists, dorsa of hands/feet)

38
Q

How is AD diagnosed

A 
must have:
- pruritus 
- eczema: skin swelling 
may also have:
- early age of onset
- atophy (personal or family history of IgE reactivity)
39
Q

What are the non-pharm treatments of AD

A
  • avoid rubbing or scratching lesions - keep nails trimmed
  • ELIMINATNG risk factors and exposure to triggers
  • take lukewarm (not hot) baths
  • keep temp cool and household humid
  • phototherapy: may be used as adjunct
  • use of skin moisturizers
  • apply emollients: keep skin hydrated (mainstay of therapy and may reduce the need for steroids)
40
Q

what are the pharmacological treatment options for AD

A
  • topical corticosteroids
  • topical calcineurin inhibitors
  • crisaborole ointment
  • biologic agents

Skin Midterm (4 decks)

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