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MyDermatology-Bolognia > Ch. 12/13-Atopic dermatitis/other eczematous processes > Flashcards

Ch. 12/13-Atopic dermatitis/other eczematous processes Flashcards

1
Q

Name 3 cutaneous disseminated viral infections that can occur in the setting of atopic dermatitis

A

Eczema herpeticum (HSV)
Eczema vaccinatum (Vaccinia)
*Eczema coxsackium (Coxsackie A16; A6; Enterovirus 71; hand-foot-mouth)

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2
Q

What is the atopic march

A

AD (often food allergy occurs around same time or after)–> Asthma–>allergic rhinitis

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3
Q

What is white dermatographism

A

Stroking the skin leads to whitening of skin due to vasoconstriction

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4
Q

What are 3 essential features for AD
(Previously Major criteria for Hanifin and Rafka)

A

Pruritus
Typical morphology in right location
Chronic/relapsing course
Fam hx atopy

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5
Q

Name 23 minor features of AD

A

White dermatographism
Mid-facial pallor
Delayed blanch response (to intradermal Ach)
Pityriasis alba

Hyperlinear palms /Itchytosis vulgaris
Keratosis pilaris
Perifollicular accentuation
Xerosis
Hertoghe sign

Allergic shiners
Recurrent conjunctivitis
Keratoconus
Anterior sub capsular cataract

Dennie Morgan lines
Anterior neck folds

Hand/foot dermatitis
Nipple eczema

Early onset
Susceptibility to skin infections
Worsened with wools/lipid solvent
Impacted by environment/emotions
Pruritus when sweating

Increased IgE
Food intolerance
Immediate Type 1 skin reactivity

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6
Q

What is needed to make a diagnosis of AD according to HAnifin and Raja

A

3 major + 3 minor

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7
Q

Name 3 infections that can worsten/flare eczema

A

Molluscum
Staph
Viral URTI
Hand/foot/mouth

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8
Q

What is prevalence of AD in kids and adults

A

10-20% kids
2-10% adults

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9
Q

What is early onset AD? Late onset? senile onset?

A

Early: first 2 years usually, sometimes before age 5
Late: Post puberty
Senil: After 60

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10
Q

What % of kids with AD outgrow it by age 12?

A

60%

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11
Q

3 major categories of AD pathogenesis

A

1- Barrier dysfunction
2- Immune dysregulaton
3- Alteration microbiome

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12
Q

What is strongest RF for early onset AD

A

Fam history-specifically parents-specifically AD > other atopic conditions

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13
Q

What is the strongest known genetic RF for AD

A

Fillagrin (FLG) loss of function mutation

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14
Q

What is the % of Europeans/Asians with mod-severe AD that carry mutation for FLG

A

20-50%

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15
Q

What is filagrin?

A

Keratin filament organizing protein

Found in stratum corneum

Breakdown products such as histidine contribute to epidermal hydration, acid mantle formation, lipid processing, and barrier function

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16
Q

Name 1 genetic mutations increase risk for AD that is not FLG?

A

SPINK5–> codes for LEKTI= lymphoepithelial Kazaa-type trypsin inhibitor (protease inhibitor, thus loss of function results in increase protease activity)

–> Excessive degradation DSG-1, degradation lipid processing enzymes, activates proinflammastory cytokines

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17
Q

What Th response is seen in acute AD? Chronic AD?

A

Acute: Th2
Chronic: Th1, Th 17, Th22

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18
Q

What are 2 cytokines drives Th2 response

A

Il-4

TSLP (thyme stromal lymphopoeitin)-produced by keratinocytes in response to viral infection, trauma, allergens, others. Highly expressed in lesions acute and chronic AD, not-non-lesional.

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19
Q

Describe how IL-4 and Il-13 are related

A

The heterodimeric receptor for IL-4 and IL-13 both share the IL4alpha receptor subunit, which activates STAT-6–> promoted th2 differentiation

Dupixent is a IL4alpha receptor blocker, thus blocks IL-13 and IL-4

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20
Q

What is IL-31

A

Th2 cytokine highly expressed in AD and pruritic skin conditions such as PN

Cutaneous exposure to staph rapidly induces Il-31 production, role for staph colonization and itch induction

It is expressed in keratinocytes, nerve fibres, dorsal root ganglion

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21
Q

What is the name of the IL-31 inhibitor

A

Nemolizumab

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22
Q

What % of AD patients are colonized with staph aureus? Why?

A

90%

Due to disrupted acid mantle, decreased antimicrobial peptides

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23
Q

Most common sites AD infantile

A

Cheeks, forehead, scalp, neck, extensors, trunk
Spares central face (but 90% have face involvement)
Often spares axillae/groin

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24
Q

What is frictional lichenoid eruption

A

Skin coloured flat topped papules often elbows > knees, often atopic boys in spring/summer

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25
Q

What is juvenile plantar dermatosis

A

glazed erythema, scale and fissuring of the feet

Often symmetric, forefoot on plantar surface

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26
Q

Most common age of onset infantile AD

A

2 months of life

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27
Q

Who gets papular eczema

A

African American or asian
Perifollicular flat topped papules

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28
Q

What are the main sites of AD in childhood? (2-12 years)

A

ACF, Popliteal fossa (flexures)
Wrists, ankles, hands, feet, eyelids, neck

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29
Q

What are the main sites of adult/adolescent AD

A

Flexures persist
Eyelids/hands may be only manifestation

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29
Q

What are the main sites of adult/adolescent AD

A

Flexures persist
Eyelids/hands may be only manifestation

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30
Q

What are the main sites of adult/adolescent AD

A

Flexures persist
Eyelids/hands may be only manifestation

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31
Q

Name 10 regional varaints of AD

A

Eyelid
Lip lickers dermatitis
Atopic cheilitis
Ear eczema (often retroauricular or below earlobe)
Head/neck (consider malessezia triggers)
Nipple eczema
Frictional lichenoid eruption
Nummular
Prurigo nodules
Hand dermatitis including dishydrotic
Juvenile plantar dermatosis

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32
Q

What % of AD patients have ichthyosis vulgaris? How does it present?

A

15%

Fine, whitish-brownish polygonal scaling that favours lower legs and spares flexures

KP also seen in 75%

*50% of people with IV have AD

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33
Q

How does KP present

A

Follicular hyperkeratotic papules with patchy erythema, often on arms, legs and cheeks

Grow out after puberty, especially the facial lesions

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34
Q

What is Keratosis Pilaris Rubra

A

Numerous grain like follicular papules on background confluent erythema, more widespread on face and ears >trunk

Tends to persist post puberty

Erythema >hyperpigmentation differentiates from erythromelanosis follicular facie et Colli

Lack of atrophy differentiates from keratosis pillars atrophicans

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35
Q

What is Hertoghe sign? Other than AD where else is it seen

A

Missing or thinning lateral 3rd eyebrows

AD most commonly, also hypothyroid

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36
Q

What is pityriasis alba

A

Subclinical eczematous dermatitis seen in patients with AD often.

Multiple ill defined hypo pigmented macules and patches, 0.5-2cm, fine scale, mostly on face like cheeks, sometimes shoulders and arms

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37
Q

Ddx Pitryriasis alba

A

Post inflammatory hypopigmentation from AD or other dermatides

Tinea versicolor-more sharply demarcated with smaller lesions coalescing into larger areas

vitiligo -depigmented, more sharply demarcated

Hypopigmented MF

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38
Q

How does eczema herpeticum present

A

Hemmorhogic punched out erosions

Vesicles rarely evident

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39
Q

Name 6 ocular complications in AD

A

Allergic rhinoconjuctivitis

Atopic Keratoconjuctivitis-adults

Vernal keratoconjuctivitis-kids in warm climates (arge, cobblestone-like papillae on the upper palpebral conjunctiva,)

Blepharitis

Keratoconus

Sub capsular cataracts-anterior related to AD

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40
Q

Name 5 path findings of Acute eczema

A

Spongiosis with exocytosis
Intraepidermal vesicles or bullae
Dermal edema
Perivascular lymphocytes that extend into epidermis
Variable number eosinophils

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41
Q

Name 3 path findings subacute eczema

A

Hyperkeratosis
Parakeratosis
Acanthosis

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42
Q

Name 3 path findings in chronic eczema

A

Pronounced acanthosis
Hyperkeratosis and parakeratosis
Psoriasiform hyperplasia of rate ridges, regular or irregular
Dermal fibrosis
Mast cells
Hypergranulosis, or sometimes Hypogranulosis in nummular

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43
Q

Name 5 immune deficiency syndromes associated with eczema

A

Ataxia-telangiectasia

Wiskott-Aldrich

IPEX -immune dysregulation polyendocrinopathy, enteropathy, x-linked recessive

HyperIgE syndromes:
-DOCK8 syndrome (similar to HIES but viral infections)
-STAT3 deficiency
-PGM3

STAT

Omenn syndrome

DiGeorge

Ig deficiencies

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44
Q

What is the triad of hyper IgE syndrome/AD-HIES

A

Eczematous dermatitis (staph colonization related)
Neonatal pustular dermatosis
Lung disease
Cold abscesses
Skeletal abscesses and CT diseases

“Autosomal dominant Hyper IgE syndrome”

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45
Q

Name 7 general categories of protein contact dermatitis (IgE-mediated)

A

Fruit-banana, fig, kiwi, lemon, pineapple
Vegetables-carrots, cauliflower, celery
Spices/seeds- caraway, curry, dill, garlic, paprika, parsley
Nuts-almonds, hazelnuts, peanuts
Latex
Grains
Meat-fish, poultry, seafood, beef

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46
Q

What diagnosis to consider in someone with chronicn eczematous in adults

A

MF

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47
Q

Treatment ladder AD

A

Moisturizers
Topical steroids
Topical calcineurin inhibitors
Topical crisabarole
*Topical tofactinib not yet approved
nbUVB
MTX, CsA, MMF, AZA
Prednisone
Dupixent
Omalizumab (Anti IgE)-no benefit
Nemolizumab (Anti IL-31)-pruritus
Tofacitinib
Upadacitnib
Rituxumab
INF-gamma-mixed results

48
Q

Name 7 adjunctive therapies in AD

A

Wet wraps
Dilute sodium hypochlorite (bleach) baths

Treatment of associated bacterial, viral, or fungal infections

Oral antihistamines for antipruritic ‡ and sedative effects

Leukotriene antagonists

Sodium cromoglycate (topical or oral)

Probiotics(may have efficacy in primary prevention)

Vitamin D supplementation

49
Q

What is the maintenance strategy that can be used for AD that does not result in atrophy?

A

Twice weekly with mid potency TCS to active areas

50
Q

What TCI’s have been approved for AD

A

Tacrolimus (Protopic) 0.03% and 0.1%
Pimecrolimus (Elidel) 1%

51
Q

Approve ages for Protopic and elidel

A

Protopic 2+
Elidel 3-23 months

52
Q

What % strength is crisabarole

A

2% ointment

53
Q

What age is crisabarole approved for

A

2+

54
Q

How does crisabarole work

A

PDE-4 inhibitor-prevents degradation cAMP, increase CAMP, prevents production cytokines like IL-10 and IL-4

55
Q

NAme 3 types of phototherapy for AD

A

nbUVB
UVA1
UVA+UVB

56
Q

What does dupixent target

A

Il-4Ralpha subunit of heterodimeric IL-4 and IL-13 receptors –> blocks Th2 inflammation

57
Q

What % of patients achieved EASI 75 for dupixent at 16 weeks

A

50%

58
Q

Dosing for dupixent

A

600 mg initially and then 300 mg every other week

59
Q

Percentage of conjunctivitis in dupixent

A

10%

60
Q

Typical starting dose for CsA inAd

A

5 mg /kg then taper

61
Q

Typical dose for MTX

A

7.5–25 mg or 0.3–0.5 mg/kg

62
Q

Typical dose for MMF

A

1 to 3 g/day in adults and 30–50 mg/kg/day in children

63
Q

Typical dose for AZA

A

2 mg/kg if normal TPMT
0.5-1 mg/kg

64
Q

How to decolonize superinfected AD?

A

Course of cephalexin
5 days monthly intranasal mupirocin x 3 months
Bleach baths twice weekly with 0.5 cup 6% sodium hypochlorite

65
Q

5 most common allergens in AD

A

Milk
Wheat
Eggs-most often linked to AD exacerbations
Peanut
Soy

66
Q

Name 2 possible preventive measures for AD

A

probiotics (e.g. Lactobacilli ) or prebiotics to pregnant mothers and infants was associated with significantly decreased frequencies of AD at 1 to 4 years of age

For infants with a family history of atopy, exclusive breastfeeding during the first 3–4 months of life or feeding with a formula containing hydrolyzed milk products may potentially decrease the risk of AD development compared to feeding with a formula containing intact cow’s milk protein

daily use of a moisturizing cream, oil, emulsion, or ointment beginning within the first 3 weeks of life resulted in a 30–50% reduction in the likelihood of developing AD by 6–8 months of age

67
Q

What is the most common sites of seborrheic dermatitis

A

Nasolabial folds
Scalp
Ears
Eyebrows
Chest
Folds

68
Q

Name 3 systemic associations with seborrheic dermatitis

A

HIV
Parkinsons
Stroke
Mood disorders

69
Q

What age range for seb derm

A

Peak in first 3 months (up to 1 year)
Second peak 5th/6th decade

70
Q

What is the most common cause seb derm

A

Malessezia species
-Globosa and restricta

71
Q

What are the changes in skin surface lipid composition in patients with seb derm?

A

Increased cholesterol and triglycerides, decreased squalene and free fatty acids

72
Q

What is the relationship between P.Acnes and Seb derm

A

P.Acnes produce bacterial lipases which convert triglycerides into free fatty acids

Seborrheic derm patients have significant less P.Acnes thus leading to decreased FFA and increased TG’s

73
Q

How does infantile seb derm appear

A

1 week after birth, persists for months

Starts with mild greasy scales–> cradle cap

The axillae, inguinal creases, neck, and retroauricular folds acutely inflamed, oozing, sharply demarcated, and surrounded by satellite lesions.

74
Q

What is a psoriasiform id reaction

A

Disseminated eruption of scaly papules with psoriasiform appearance on trunk, proximal extremities, often with severe seb derm or super infected seb derm (candida, strep), ESPECIALLY DIAPER area

75
Q

What are the adult forms of seborrheic dermatitis

A

Pityriasis simplex capillitii (dandruff)

Scalp seborrheic dermatitis-inflammation, pruritus, dandruff.

Facial/body seborrheic dermatitis-face, chest

Annular/discoid seb derm-facial lesions

Sebopsoriasis

76
Q

Most common sites of scalp seb derm? How does it differ from psoriasis

A

Vertex/parietal

More diffuse than psoriasis but sometimes sharply demarcated at the forehead

77
Q

Where does seb derm affect the face

A

Forehead
medial portions of the eyebrows
upper eyelids
nasolabial folds
lateral aspects of the nose
Retroauricular, non purulent otitis externa
Occiput and neck

78
Q

Where does seb derm appear on the body

A

Central chest
Intertriginous

79
Q

NAme 4 path findings of seb derm

A

Spongiosis
Superficial perifollicular and perivascular lymphocytic infiltrate

Older lesions:
Irregular acanthosis
Focal parakeratosis

80
Q

NAme 4 path findings of seb derm

A

Spongiosis
Superficial perifollicular and perivascular lymphocytic infiltrate

Older lesions:
Irregular acanthosis
Focal parakeratosis

81
Q

Name 4 differences between AD and seb derm in an infant

A

AD:
-irritable
-sleepless
-itchy

Seb derm:
-content, non irritated
-earlier onset
-intertriginous predilcietion

82
Q

Name 8 things on ddx for infantile seb derm

A

AD
Candida-especially intertrigo
Irritant dermatitis-diaper dermatitis esp.
Psoriasis
Streptococcal intertrigo
Langerhans cell histiocytosis
Acrodermatitis enteropathica
Leiner disease (erythroderma, seb derm, diarrhea, FTT)

83
Q

Ddx of adult seb derm on the scalp

A

Psoriasis-more silvery scale, thicker plaques, more discrete, less pruritic, less greasy

Atopic derm

Dermatomyositis

84
Q

What type of organism is malessezia

A

Dimorphic fungi
Seb derm is reaction to the yeast form

85
Q

What is sebopsoriasis

A

Overlap between seb derm and psoriasis
Think that maybe malessezia drives psoriasis

Yellowish, greasy scale in typical seborrhoeic dermatitis areas (scalp, nasolabial folds, eyebrows, behind the ears and over the sternum)
Deeper red, more defined margins and thicker scale than normally seen in seborrhoeic dermatitis
Less silvery scale than seen in classic psoriasis

86
Q

Name 10 ddx’s for intetrigo/intetriginal dermatoses

A

Inverse psoriasis-well defined
Irritant dermatitis-ill defined
Tinea cruris

Candida-satellite lesions, papules, pustules
Erythrasma-re brown
Allergic contact dermatitis

Granular parakeratosis
Hailey-Hailey, Dariers
Pemphigus vegetans
SDRIFE
Toxic erythema of chemotherapy
Cutaneous chrons
Extra mammary pagets
Langerhans cell histiocytosis

87
Q

Treatment for infantile seborrheic dermatitis

A

Emollients, bathing.
Mild shampoos
Ketoconazole 2%
Low potency topical steroids

88
Q

Treatment for adult seb derm

A

Topical azoles-shampoo or cream (body)
-e.g. ketonconazol

Ciclopirox olamine

Adjuncts:
Emollients
low potency topical steroids
TCI’s
Shampoos containing selenium sulfide, zinc pyrthione, tar shampoo

89
Q

Most common cause disseminated eczema (auto sensitization)

A

Allergic contact dermatitis in setting of stasis dermatitis (2/3 of patients)

Sometimes in just plain ACD, stasis dermatitis or severe tinea pedis

90
Q

How does disseminated eczema present

A

Appears later than the primary lesions by a few days to weeks

symmetric distribution pattern

predilection for analogous body sites (e.g. extensor aspects of the lower and upper extremities, palms and soles).

91
Q

How does true nummular eczema present

A

round (discoid) eczematous patches almost exclusively of the extremities, often the lower legs in men and the forearms and dorsal aspects of the hands in women. well demarcated and measure 1–3 cm, only occasionally being larger.

They may be acutely inflamed with vesicles and weeping, but are often lichenified and hyperkeratotic.

92
Q

What is the other name for oid-oid disease, and what is it?

A

Sulzberger-Garbe disease or exudative discoid and lichenoid chronic dermatitis

Very therapy resistant

93
Q

Name 2 variants of nummular dermatitis

A

Wet and dry variants

94
Q

Name 4 associations with nummular dermatitis

A

Xerosis
ID reaction to ACD, stasis dermatitis or tinea
AD

*Staph often present, may need to treat this

95
Q

What is infected dermatitis

A

Dermatitis associated with HTLV-1 virus, immune dysregulation leads to infection with staph and strep

96
Q

What is HTLV-1? What other conditions is it associated with?

A

Human T-cell lymphotropic virus Type I

Human T cell leukemia/lymphoma
Tropical spastic paresis
Increased susceptibility to parasitosis/strongy
Infective dermatitis

97
Q

How does infective dermatitis present

A

Crusted oozing dermatitis to scalp, ears, eyelids, neck, paranasal, axillae, groin

Generalized fine papular rash

Secondly infection most often seen

98
Q

What are the 4 major criteria for HTLV-1 associated infective dermatitis

A

Eczema of the head and neck region, including the scalp, ears, eyelid margins and paranasal skin, as well as the axillae and groin (at least 2 sites)

Chronic watery nasal discharge or crusting anterior nares

Chronic relapsing dermatitis that responds to antibiotics but recurs on withdrawal

Onset early childhood (after done breastfeeding and ab’s wean)

HTLV-1 SEROPOSITIVY (must occur)

99
Q

5 minor criteria of infective dermatitis

A

Hyperimmunoglobulinemia
Fine papular rash
Postive cultures: staph or strep, from lesions or nares
Anemia, ESR
Elevated CD4 and CD8 T cell counts, elevated CD4:CD8 ratio

100
Q

Name 8 findings of chronic venous hypertension

A

Hemosiderin deposits/purpura
Edema
Varicose veins
Petechiae overlying yellow-brown discoloration (stasis purpura)
Stasis dermatitis
Lipodermatosclerosis
Stasis ulcerations
Acroangiodermatitis/psuedo KS

Livedoid vasculopathy/atrophie blanche-porcelain white scars surrounded by punctate telangiectasis and ulcerations

101
Q

Describe the progression of stasis dermatitis

A

Pitting edema at medial shin and calf proximal to the ankle –> stasis purpura with hemosiderin deposition–> dry/itchy skin–> edema extends to the distal third of the calf and subfascial edema arises = psuedoerysipelas/acute lipodermatosclerosis–> chronic LDS (inverted wine bottle)–> ulcers and atrophic blanche

102
Q

Name 3 biopsy findings of venous HTN

A
  1. Dilated capillaries surrounded by cuffs of fibrin
  2. hemosiderin deposits
  3. hyperplastic (and at times thrombotic) venules
103
Q

What is one procedural treatment that can be used for dishydrotic eczema

A

Botox if hyperhidrosis

104
Q

What conditions can you see dishydrotic eczema in

A

AD
ID
ACD

105
Q

What is the name for larger bullae in dishydrotic eczema

A

Pompholyx

106
Q

What is Dyshidrosis lamellosa sicca

A

variant dishydrotic eczema with no bullae or vesicles but annular collates of white scale

107
Q

Name 4 treatments for dishydrotic eczema

A

TCS
TCIs
Phototherapy
Systemic steroids

108
Q

Treatment for plantar juvenile plantar dermatosis

A

impermeable socks and shoes
emollients
keratolytics
paraffin-type ointments
Dry socks

109
Q

Name 6 ddx for plantar foot dermatosis

A

Juvenile plantar dermatosis (young males)
Acquired plantar keratoderma
Tylosis
ACD
Tinea pedis
Psoriasis
Dishydrotic eczema and recurrent focal plantar and palmar peeling (likely mild form of the former)
Pustulosis palms and soles

Others:
PRP
Keratoderma blenorrhagicum
Crusted scabies

110
Q

What is the main cause of diaper dermatitis? What is the pathophysiology

A

Irritant contact dermatitis from the alkaline diaper environment due to
1)alkaline pH of urine
2) fecal bacteria (esp. cows milk fed babies) have urease enzymes

111
Q

How does diaper dermatitis secondary to irritation present

A

Spares the folds, favours convex surface areas

Glazed erythema, punched out erosions, scaling

Psuedoverrucous papules can develop

112
Q

Name the ddx for diaper dermatitis

A

SCAMP:
Seb derm
Candida, contact (allergic, irritant)
AD, acrodermatitis enteropathica
Milaria
Perianal strep and bullous impetigo, psoriasis

Others:
Extramammary pagets
LCH
Granuloma gluteal infantum

113
Q

How does candida present in diaper area

A

Bright red intense erythema, involvement of skin folds (+/- scrotum), and satellite papules and pustules at the periphery of dermatitis

Recent abx use, thrush

114
Q

How does candida present in diaper area

A

Bright red intense erythema, involvement of skin folds (+/- scrotum), and satellite papules and pustules at the periphery of dermatitis

Recent abx use, thrush

115
Q

How does seb derm present in diaper area

A

Well demarcated salmon-red coloured patches

Look for involvement other intertriginous zones

116
Q

How does perianal strep present

A

Brith red eyrhtme perianal and folds, no satellite lesions, foul odour

Family member with history sore throat

116
Q

How does perianal strep present

A

Brith red eyrhtme perianal and folds, no satellite lesions, foul odour

Family member with history sore throat

MyDermatology-Bolognia (31 decks)

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