Other Eczematous Disease Flashcards

1
Q

What two age groups are most commonly affected by seborrheic dermatitis?

A

Infants and adults, rarely kids

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2
Q

Pathogenesis of seborrheic dermatitis

A

Altered sebum and Malassezia spp

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3
Q

Most common areas affected by seborrheic dermatitis?

A

Scalp, ears (external canal retroauricular fold), medial eyebrows, upper eyelids, nasolabial folds, central chest and major body folds

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4
Q

First-line agents of seborrheic dermaittis?

A

Topical antifungal creams and shampoos, selenium sulfide or zinc shampoo’s, mild topical CS for face and body folds, moderate strength topical CS for scalp and ears (fluocinonide)

-2nd line: topical tacrolimus ointment (stings)

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5
Q

Diseases associated with severe seborrheic dermatitis?

A

HIV infection and neurological disease

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6
Q

Risk factors for asteatotic eczema?

A

Winter weather, dry weather, and increased age

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7
Q

Posterior axillary line involvement can be seen in what eczematous diseases?

A

Can be seen in chronic GVHD or asteatotic eczema

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8
Q

What is an Id reaction?

A

Systemic eczematous reaction to a previously localized dermatitis. Can also be a rebound phenomenon from a rapid CS taper.

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9
Q

Areas favored by Id reaction?

A

Symmetric extensor surfaces of extremities, palms and soles

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10
Q

What are the two entities which most often trigger id reaction?

A

Allergic contact dermatitis and stasis dermatitis

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11
Q

Clinical of nummular dermatitis

A
  • Doesn’t need the atopic march, coin-shaped lesions 2-3 cm in diameter commonly on the arms in women, but all extremities can be involved.
  • Has erythematous border
  • Chronic relapsing course
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12
Q

What must be seen for the dx of HTLV-associated infective dermatitis?

A

+ HTLV-1 serology

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13
Q

What age group most affected by HTLV-associated infective dermatitis?

A

Neonates, infants, rare in adults

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14
Q

Clinical of dyshydrotic eczema?

A

Firm extremely pruritic vesicles of palms>soles and on lateral and medial aspects of the digits

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15
Q

What medication can trigger dyshidrotic eczema?

A

IVIG

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16
Q

Triggers for dyshydrotic eczema?

A

Stress, allergic or irritant contact derm, IVig

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17
Q

Tx of dyshydrotic eczema?

A

Potent topical CS, topical tacrolimus (first line), PUVA, and systemic CS

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18
Q

Clinical of juvenile plantar dermatosis?

A

Dry and scaly skin w/ mild inflammation and “glazed” appearance on bottom of feet. +/- painful fissures on feet.

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19
Q

What is juvenile plantar dermatosis caused by?

A

Hydration of the corneal layer 2/2 wearing impermeable shoe materials –> shearing from the friction of softened corneum–> usually only seen in children w/ atopic diathesis.

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20
Q

Treatments for juvenile plantar dermatosis

A

Synthetic socks, keeping feet dry

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21
Q

Most common cause of diaper dermatitis ?

A

Irritant contact (urine, stool, etc)

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22
Q

What type of milk is a/w less candida diaper dermatitis?

A

Breast fed –> cow’s mild fed kids have more urease producing bacteria –> more basic and then you get more candidiasis

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23
Q

3 most common causes of diaper dermatitis?

A

Irritant contact dermatitis, candidiasis, seborrheic dermatitis

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24
Q

Less common causes of diaper dermatitis?

A

Bacterial infections (bullous impetigo, streptococcal perianal dermatitis and intertrigo), psoriasis, allergic contact dermatitis, atopic dermatitis

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25
Q

Rare causes of diaper dermatitis?

A

Dermatitis enteropathica, early kawasaki, langerhans histiocytosis

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26
Q

What is one of the most common allergens for contact dermatitis in the genital area?

A

Wipes! (Kathon CG, methychloroisothiazolineone / methylisothiazolinone)

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27
Q

Way to differentiate candida in the groin from tinea cruis

A

Candida has satellite lesions and it involves the scrotum. Candida should also be thought of when you see spreading at the periphery

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28
Q

Most common species of candida in the diaper area?

A

C. Albicans or C. Tropicalis

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29
Q

Most common bulleous dermatosis of children?

A

Bulleous impetigo, and autoimmune: linear IgA

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30
Q

What toxins cause bullous impetigo?

A

S. aureus produces exfoliatoxins A and B (ETA and ETB) this cleaves desmoglein-1–> sub corneal inter granular acntholysis w/ neutrophil iseen in blister cavity on histology. This is the same mechanism as staph scalded skin but is localized

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31
Q

Treatment for bullous impetigo?

A

Topical mupirocin, retapamulin or fusidic acid. If widespread IV antibiotics

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32
Q

Epi of perianal strep?

A

Children>>>adults

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33
Q

What do you call seb derm that is on the chest

A

Petaloid

34
Q

what is the gold standard tx for infantile seborrheic dermatitis?

A

Topical ketoconazole

35
Q

What is disseminated eczema/autosensitization?

A

It can be a rebound phenomenon from rapid CS taper or a reaction to a previously localized dermatitis.

36
Q

Most common locations for autosensitization reactions?

A

Symmetric extensor surfaces of extremities, palms, and soles.

37
Q

What are the two most common causes of id reaction or autosensitization?

A

Allergic contact dermatitis and/or venous stasis dermatitis.

38
Q

Presentation of HTLV-1 associated dermatitis?

A

Presents with exudative and crusty eczematous dermatitis of scalp, ears, eyelid margins, paranasal skin, axillae, and groin.

39
Q

What test is required for HTLV-1 associated dermatitis?

A

HTLV-1 serology

40
Q

What are endemic areas for HTLV-1?

A

Africa, NE South America, Caribbean basin, southern Japan, and Iran

41
Q

What are some potential triggers for dyshidrotic eczema?

A

Stress, allergic or irritant contact dermatitis, administration of IVIg, a/w atopic dermatitis and hyperhidrosis

42
Q

Why does candida secondary infection happen with diaper dermatitis?

A

You get a more basic pH environment (urine and ureases from fecal bacteria) which then leads to candidiasis.

43
Q

Babies fed what are at higher risk of getting candidiasis?

A

Cow-milk fed. Babies fed cow’s milk have more urease-producing bacteria –> more basic environment.

44
Q

What areas are spared in irritant diaper dermatitis?

A

The genitocrural folds.

45
Q

Presentation of diaper area candidiasis?

A

Intense erythema, satellite pustules/lesions, fabors folds, genitals.

46
Q

Seborrheic dermatitis presentation in the diaper area?

A

Well-demarcated salmon-colored to red moist or scaly patches and plaques

Favors folds involvement of other sites.

47
Q

Clinical presentation of asteatotic dermatitis?

A

Dry skin with cracking (looks like cracked river bed), erythema, and scale

-Can have oozing and crust

48
Q

Symptoms and distribution of asteatotic eczema?

A

Usually is itchy and favors the lower legs

49
Q

Histology of steatotic dermatitis?

A

Xerosis (compact corneum) and spongiosis

50
Q

Treatment for asteatotic eczema?

A

Emollients are key to tx and prevent flairs (apply immediately after bathing)

  • Avoid aggravating factors
  • Topical CS and TCI
51
Q

Morphology/presentation of nummular eczema?

A

Round or coin-shaped pink plaques, of on extremities

  • Very pruritic
  • Can look acute (eczematous) or chronic (lichenified)
52
Q

Treatment of nummular dermatitis?

A

Mid to high potency TS (ointments preferable to creams), TCI’s and phototherapy

53
Q

What is progesterone dermititis?

A

Cyclic flares of dermatitis during the luteal phase of the menstrual cycle

Starts 1 week prior to menses –> resolves a few days after menses

54
Q

If you have a women who is noting flares of eczematous dz a week prior to her period and it resolves after her period what test would you do to confirm dx?

A

Intradermal injection of progesterone –> induces skin reaction

55
Q

What are the treatments for progesterone dermatitis?

A

OCP’s, tamoxifen to inhibit ovulation

56
Q

What is a major ddx item for progesterone dermatitis and how do you tell these apart?

A

Estrogen dermatitis

-These can be compared b/c estrogen dermatitis gets wore just prior to menses, intradermal estrone test can identify

57
Q

What is the pathophysiology of statsis dermatitis?

A

Swelling promotes venous HTN which leads to capillary distention and leak. The fluids, plasma, proteins, and erythrocytes cause edema –> fibrosis, ulceration, inflammation, and microangiopathy

58
Q

Where does stasis dermatitis often start?

A

Often starts on the medial ankle or the distal third of leg

59
Q

What is occurring if the legs start to take the shape of an “inversted wine glass” in the setting of chronic stasis dermatitis?

A

Lipodermatosclerosis (stasis panniculitis)

-This is caused by the chronic inflammation leading to a tight cuff of adherent skin/subcutaneous tissue to the fascia

60
Q

What can be seen in the setting of chronic stasis dermatitis?

A

Atrophie blanche, ulceration

-These are from the venous changes, often occur on the supra malleolar region

(compare with livedoid vasculopathy)

61
Q

What is the histology of stasis dermatitis?

A

Lobular capillary hyperplasia +/- vessel cuffing; hemosiderin and fibrosis of dermis and subcutaneous fat septae

62
Q

Treatment of stasis dermatitis?

A

Treat venous HTN w/ compression and elevation. Treat the skin component w/ emollients and topical CS

63
Q

How long after the initial triggering condition does ID reaction occur?

A

Days to weeks after primary lesion

64
Q

What are the most common causes of contact urticaria?

A

In Finland: Cow dander> natural rubber latex> Flour/grain/feed

65
Q

What are the risk factors for contact urticaria?

A

AD, hand dermatitis, and allergy to fruits (Kiwi, avocado, banana, and melon)

66
Q

What is the pathogenesis of contact urticaria?

A

Mediated by allergen-specific IgE on mast cells which leads to the release of histamine

67
Q

Common food-based causes of contact urticaria?

A

Potato, celery, raw meat, fish, shellfish

68
Q

What is the most common cause of contact urticaria in healthcare workers?

A

Latex

69
Q

What patients are at higher risk of contact urticaria from latex?

A

Patients with spinal bifida and those with atopic dermaittis

70
Q

What type of reaction is more common for latex?

A

Type I is much more common than type IV

71
Q

What are things that can increase the risk of anaphylaxis from latex allergy?

A

Aerosolized glove powder or mucosal exposure

72
Q

What things cross-react with latex?

A

“BACK Passion”

Banana

Avocado

Chestnut

Kiwi

Passion fruit

73
Q

What is the difference between contact urticaria immunological and non-immunologic mediated?

A

The non-immunologic is caused by something directly driving the skin response (i.e. nettles)

74
Q

What are the most common causes of non-immunologic contact urticaria?

A

Urticaceae/stinging nettles and jellyfish

75
Q

Pathophysiology of non-immunlogic contact urticaria?

A

Triggers (nettles etc) trigger the release of histamine, acetylcholine and serotonin

76
Q

What types of things can cross-react with contact urticaria and a reaction to birch pollen?

A

Apples, pears, and cherries (and others)

77
Q

What test should be used for contact urticaria?

A

The open patch test

  • The open part means that you apply the substances directly to the forearms and wait ~30 min to see if there is a response if nothing can wait 30 min longer
  • This is better than prick, scratch, and intradermal testing as these cna lead to anaphylaxis
78
Q

What is the treatment of contact urticaria?

A

Antihistamines, avoid trigger, epi and supportive care if anaphylaxis

79
Q

What are the changes to the sebum noted in seborrheic dermatitis?

A

Increased triglycerides/cholesterol and decreased squalene and FFA

Cholesterol is usually the lowest part of sebum and triglycerides are usually the most abudant followed by squalene

80
Q

What is the histology of seborrheic dermatitis?

A

Psoriasiform acanthosis, spongiosis, “shoulder parakeratoissi<” superficial perivascular/perifollicular lymphocytic infiltrate

81
Q

What is the gold standard treatment for seborrheic dermatitis?

A

Topical azoles

  • Can also use ciclopirox, topical CS, TCI, zinc/selenium sulfide shampoos, coal tar shampoos, mineral oil for babies
82
Q

What areas are favored in the pediatric population for seborrheic dermatitis?

A

Scalp (cradle cap), body creases (posterior neck, scalp, face, postauricular, presternal, and intertriginous areas (grown, axillae, popliteal fossae too)