Eczematous Eruption Flashcards

0
Q

Describe Lichen Simplex Chronicus

A

Patch-like, leather-like, higher, hardened skin markings, circumscribed plaque, exaggerated skin lines

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1
Q

What is another name for Lichen Simplex Chronicus?

A

“Neurodermatosis”

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2
Q

What causes Lichen Simplex Chronicus?

A

Chronic scratching- this is a learned behavior and is the end stage of itchy (pruritic) and eczematous disorders including topic dermatitis

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3
Q

Where is Lichen Simplex Chronicus most common?

A

Nape of Neck, back of feet and ankles (also external forearms, lower legs, scrotum, and vulva)

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4
Q

What does circumscribed plaque mean?

A

confined to a limited area

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5
Q

DDx for Lichen Simplex Chronicus?

not provided in slides

A

psoriasis, lichen planus, nummular dermatitis (p 104)

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6
Q

What is the treatment for Lichen Simplex Chronicus?

A
  1. Break the cycle of itching (it is a learned behavior)
  2. High potency glucocorticoids w/ occlusion to penetrate more/ or intralesional injection of glucocorticoids
  3. Oral Antihistamine (hydroxyzine or tricyclic antidepressants with antihistamanic activity ex. doxepine)
  4. Higher doses of antihistamine- but people don’t want sedation–although can help them stop the scratching!
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7
Q

Where should a high potency of glucocorticoids be used on skin?

A

thicker skin areas / thicker lesions

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8
Q

What does recalcitrant mean?

A

stubborn

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9
Q

Name 1 oral antihistamine and 1 tricyclic antidepressant w/ antihistaminic activity that is used to treat Lichen Simplex Chronicus

A
  1. Hydroxyzine

2. Doxepine

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10
Q

Define Pruritic

A

Itchy!

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11
Q

Name 4 descriptors of skin lesions

A
  1. distribution of eruption
  2. types of primary and secondary lesions
  3. shape of individual lesions
  4. arrangement
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12
Q

What should you be checking for during a skin exam?

A

Skin, Hair, Nails, Mucous Membrane of Mouth, Eyes, Nose, Nasopharynx, Anogenital

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13
Q

What is the diagnostic criteria for atopic dermatitis?

A

pruritus, typical morphology and distribution (lichenification, and nipple/eyelid/hand eczema)
onset in childhood
personal or family history of asthma, allergic rhinitis, atopic derm
xerosis

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14
Q

When does atopic derm present?

A

before 5 years old in 90% of patients

occurs in 10-20% of children

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15
Q

The mutation of the filaggrin gene is associated with which type eczematous eruption?

A

atopic dermatitis

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16
Q

Describe acute, subacute, chronic atopic derm.

A

acute: very itchy lesions, erythematous papules, excoriation, vesicles w/ serous exudate
subacute: erythematous, excoriated, SCALING
chronic: LICHENIFICATION, fibrotic papules, hyper/hypo pigmentation

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17
Q

Where does atopic derm appear on adults? children?

A

adults–flexural folds

children–extensor surfaces, face/scalp, SPARES diaper

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18
Q

What are the foods associated with risk factors for atopic derm? (a cause in 1/3-1/2 of children)

A

foods: egg, soy, shellfish, meat, peanuts, wheat, fish (90% of food-induced cases)
many allergies self-resolve within first 5 years
allergens may be trigger for IgE autoreactivity to epithelial autoantigens in young children

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19
Q

What are general risk factors for atopic derm?

A

mutation of filaggrin gene, term IDMs, obesity, environmental allergens, contact irritants, aeroallergens (dust, mold, pollen, dander), microbial agents (S. aureus, pityrosporum yeasts, candida organisms, trichophyton dermatophytes), stress

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20
Q

What are the lab findings of atopic derm?

A

high serum IgE, eosinophilia, S aureus, RAST=specific IgE to milk, egg, peanut, fish correlates over 95% of time to symptoms
negative skin tests have high negative predictive value, ruling out a specific antigen
positive skin tests-lower correlation with food allergies

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21
Q

What are environmental treatments for atopic derm?

A
avoidance of irritants, allergens
increase humidity
do not bathe more than once daily--careful about soaps
avoid specific foods
dust might mitigation
stress reduction
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22
Q

Medicines for atopic derm treatment?

A

Hydration: soak with prompt application of barrier ointment/cream
moisturizers/occlusives: avoid fragrances
**ointments>creams>lotions>solutions
Corticosteroids: low potency in face/groin–reduce inflammation,itch
Topical calcineurin inhibitors: tacrolimus (Elidel) & pimecrolimus (protopic)
Tar preparations: shampoos, may cause irritation, dryness, photosensitivity rxns, folliculitis
Wet dressings: use with topical corticosteroids to reduce scratching + hydrate in severe cases
antibiotics: topical ointments for erythema, crusting (mupirocin or OTC), oral antibiotics (against S aureus) for extensive legions, prophylactic treatment, approaches w/ MRSA (bleach baths/phisohex/nasal mupirocin)
antipruritic: avoid topical (sensitization), sedating antihistamines
Methoxypsoralen w/ UVA
immunosuppressive therapy (cyclosporine)

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23
Q

What do tacrolimus and pimecrolimus do?

A

inhibit transcription of proinflammatory cytokines
use sunscreen
associated wit T cell lymphoma
burning may occur but may resolve with continued treatment
do not atrophy skin & can be used on face & eyelids

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24
Q

What are the characteristics of sebhorrheic dermatitis?

A
  • common, chronic
  • greasy scales overlying erythematous patches or plaques
  • coexists with psoriasis
  • scalp (dandruff), eyebrows, eyelids, nasolabial folds, glabella, external auditory canal, postauricular areas, central chest, axilla, groin, submammary folds, gluteal cleft
  • not always itchy
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25
Q

What age of life do you get sebhorreic derm?

A

first few weeks usually on face, scalp, groin, up until 6 months
recurs at puberty/adulthood
-seen in Parkinson’s, HIV infection, acutely ill patients, CVAs
-MAJORITY have NO UNDERLYING DISORDER!

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26
Q

Treatment for seborrheic derm

A

Scalp: shampoos w/ zinc pyrithione or selenium, leave on for 3-5min

  • low potency topical glucocorticoids w/ topical antifungal agent
  • high potency topical glucocorticoid sol’ns for severe scalp condition
27
Q

What does nummular (discoid) eczema look like?

A

circular or oval-like coin lesions
small edematous papules->crusted & scaly
Found on trunk or extensor surfaces of extremities (pretibial areas/back of hands)

28
Q

What is the age range for nummular eczema?

A

mostly men, middle age, sometimes children

29
Q

What is the treatment for nummular eczema?

A

similar to atopic dermatitis

30
Q

What does xerotic/asteatotic eczema–winter itch– present as?

A

mild inflammatory dermatitis

  • extremely dry skin esp during winter
  • overlaps with nummular
  • pruritus
  • fine cracks, scale, sometimes erythema–areas of dry skin
31
Q

What is the treatment for winter itch?

A

topical moisturizers
avoid cutaneous irritants
avoid over bathing and harsh soaps

32
Q

What are the DDx for xerotic/asteatotic eczema?

A

irritant contact derm, allergic contact derm, stasis dermatitis, cellulitis

33
Q

Where is keratosis found on the body? How is it presented?

A

Keratin around follicles with bumps on arms, legs, cheeks

autosomal dominant disorder

34
Q

What is the treatment for keratosis pilaris?

A

moisturizers, keratinolytics

35
Q

What is the DDx for nummular eczema?

A

asteatotic eczema, atopic derm, allergic & irritant contact derm, lichen simplex chronicus, pityriasis rosea, psoriasis, tinea corporis

36
Q

What is irritant contact dermatitis?

A
  • results from direct skin contact w/ chemicals/allergens
  • most common causes soaps, wet work, detergents
  • chronic low grade derm most common type
  • range from m inimal skin erythema->edema, vesicles, ulcers
  • well demarcated; thin skin, eyelids/intertriginous spots, areas where skin irritant was occluded
37
Q

Treatment for ICD

A

avoidance of irritants, protective gloves, protective clothing
-topical corticosteroids

38
Q

Immunological adverse reaction types–name four:

A
type I (IgE mediated)--release antihistamines and leukotrienes, resulting in angiodema, urticaria, bronchospasm, anaphylaxis
type II (cytotoxic)--involve IgM, IgG; recognize bound drug to cell, then cell is destroyed causing hemolytic anemia or thrombocytopenia
type III (immune complex)--created by soluble complexes of drug w/ IgM or IgG, immune complexes deposit on blood vessel walls activating complement cascade causing serum sickness
type IV (t-cell mediated, delayed hypersensitivity)--topical administration activates T-cells resulting in contact derm
39
Q

What rxn type is Allergic contact derm?

A

TYPE IV–hypersensitivity (delayed)

40
Q

How is Allergic contact derm presented?

A

erythema, vesiculation, SEVERE pruritus

  • -most common cause poison ivy, oak, sumac
  • -linear or angular eruption (depends on plant contact)
  • -Urushiol (rhus) is sensitizing antigen that sticks to skin, clothing, etc
  • -area hot and swollen
  • -Nickel LEADING CAUSE (earrings,necklaces, snaps)
  • -Rubber gloves, elastic waistbands, tennis shoes w/out socks
41
Q

Lab findings of allergic contact derm-

A

gram stain and culture RULE OUT impetigo or secondary infection

  • -if itching is generalized, consider scabies
  • -patch testing after allergic contact derm has cleared
42
Q

Describe latex allergy

A

complex combo of sugars, lipids, nucleic acids, proteins

  • common in spina bifida, genitourinary anomalies, VP shunt
  • common in children with atopy
  • aerosolized latex powder may present as asthma
43
Q

describe latex allergy presentation-

A

contact derm 24-48 hours after exposure

  • localized urticaria and pruritis
  • systemic rxns –anaphylaxis
44
Q

testing for latex allergy-

A

patch testing
skin prick test
immunoassay tests (variable results due to many components in rubber)

45
Q

List 4 other main causes of allergic contact derm-

A
  1. hair dye/temp tats: p-phenylenediamine (PPD) in these products–do patch test
  2. textiles: dyes/permanent press/wash and wear chemicals, typically on trunk, lateral sides of trunk, SPARES VAULT OF AXILLAE
  3. preservatives: cosmetics, moisturizers, topical meds
  4. fragrances: 4000 fragrance molecules available, even unscented
46
Q

Medications that cause allergic contact derm-

A

corticosteroids: use patch testing to assess
neomycin+aminoglycosides, such as gentamicin/tobramycin: more common w/ chronic
benzocaine: substitute lidocaine (xylocain), doesn’t cross-react
photoallergy: accentuated by UV light, may develop when chemical present on skin w/ sufficient UVA exposure

47
Q

How does dishydrosis/dishydrotic eczema present?

A
  • pruritic vesicular eruption on fingers, palms, soles
  • teenagers/adults
  • acute, recurrent, chronic
  • vesicular eruption: pompholyx (bubble)
  • pruritus of hands/feet
  • sudden onset of vesicles (maybe in waves)
  • burning pain before vesicles
  • vesicles first on lateral aspects then palms or soles
  • palms/soles may be red or wet with perspiration
  • vesicles can persist 3-4 weeks
  • frequency varies from 1mo – 1 yr
48
Q

Associated conditions with dishydrosis?

A

Hyperhidrosis (40%), atopic derm (50%), contact derm (70%)–nickel, balsam, cobalt; sensitivity to ingested metals; dermatophyte infection; bacterial infection, emotional stress, environmental factors, distant fungal infection (tinea) can cause palmar pompholyx as an ID RXN, genetics, UVA light

49
Q

Dishydrosis treatment

A

cold compresses, high dose topical corticosteriods, calcineurin inhibitors, oral corticosteroids, systemic immunosuppressive agents (azathioprine, methotrexate, mycophenolate mofetil, cyclosorine or etanercept), botulism toxin A intradermal injections, psoralen and subsequent exposure to long-wavelength UV light, low nickel/cobalt diets or systemic chelator

50
Q

How does stasis derm & stasis uleration present?

A
  • lower extremities, chronic edema
  • mild erythema
  • scaling
  • pruritus
  • crusting, exudate, inflammation
  • medial side of ankle, sometimes over distended vein
  • history of venous thrombosis, vein removal, varicose veins
51
Q

How does chronic stasis dermatitis present?

A
  • dermal fibrosis, brawny skin edema
  • increasing pigment leads to hemosiderin
  • stasis ulcer develops
52
Q

Treatment for stasis derm and stasis ulceration?

A
  • leg elevation, compression stocking (30-40mmHg more compression)
  • emollients &/or mid-potency topical glucocorticoids, avoidance of irritants
  • protect legs from injury & scratching
  • control of chronic edema–may need diuretics!!
  • AVOID CORTICOSTEROIDS ON LESION!–use them to control scratching around ulcer
  • ulcers require removal of unhealthy tissue from wound
53
Q

What are the causes of diaper (nappy) rash?

A

wetness, friction, urine, feces, microorganisms

  • fecal proteases and lipases (increased by high pH)
  • acidic skin important for normal microflora
  • 4-35% prevalence in first 2 yrs of life
54
Q

What are the common forms of diaper rash?

A

irritant, contact derm
seborrheic
candida
bacterial

55
Q

What are the rare forms of diaper rash?

A

granuloma gluteal infantum
psoriatic
Kawasaki’s disease
Acrodermatitis enteropathica (Zn deficiency)
Langerhans cell histiocytosis, syphilis, HIV

56
Q

What is Miliaria?

A

obstruction of eccrine sweat glands when stratum corneum becomes excessively hydrated and edematous
–four types: miliaria rubra, miliaria crystallini, miliaria profunda, miliaria pustulosa

57
Q

What is intertrigo?

A

Wet skin more fragile, has higher coefficient of friction->is damaged due to maceration (softening and breaking down of skin due to prolonged exposure) and chafing

58
Q

What is contact derm (in diaper rash) ?

A

when urine is mixed with feces, skin becomes more alkaline due to ammonia, fecal lipases, ureases, and proteases are activated. they irritate the skin and increase its permeability to other low molecular weight irritants

59
Q

What is candidal diaper dermatitis?

A
  • compromised skin infected by Candida albicans (from feces) – this is the case in 40-75% of diaper rashes lasting >3 days
  • amoxicillin & other antibiotics increase colonization of Candida
  • Thrush usually present
60
Q

What is bacterial diaper dermatitis?

A
  • high pH disrupts integrity of skin
  • fecal microorganisms contribute to 2nd infections
  • bullous impetigo or folliculitis (staphylococcus aureus–MOST common), cellulitis (streptococci–SECOND MOST common), Enterobacteriacea also common
  • polymicrobial growth in rash >50% of time
  • ~50% of isolates contain anaerobes
61
Q

What is seborrheic diaper dermatitis?

A

associated w/ other signs of seborrhea (cradle cap)

-hydration and sometimes steroid creams helpful

62
Q

What is atopic eczema (diaper rash)?

A

spares diaper area due to hydration from occlusion

63
Q

What is granuloma gluteal infantum (diaper rash)?

A
  • rare disorder

- inflammatory response to long-standing irritation, candidiasis, fluorinated corticosteroids

64
Q

Treatment for diaper rash-

A

airing of diaper area
frequent diaper changes
absorbent gels, cloth
barrier ointments
non-fluorinated, low-potency corticosteroid ointment or cream for less than 2 wks (1% hydrocortisone)
antifungals for candida (OTC clotrimazole, oral Rx)
antibacterials for bacterial (OTC vs muprocin)
-abuse