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Pediatric EOR exam > Pediatric Dermatology > Flashcards

Pediatric Dermatology Flashcards

1
Q

What is the pathogenesis of acne vulgaris

A
  1. increased sebum production
  2. follicular hyperkeratinization
  3. proliferation of cutibacterium acnes ( C. acnes)
  4. inflammation
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2
Q

why does acne vulgaris tend to start during puberty?

A
  1. androgen stimulation of the pilosebaceous unit
  2. changes in keratinization at the follicular orifice
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3
Q

MC places for acne

A

face
back
upper chest

(places with greatest density of sebaceous follicles)

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4
Q

what medications can cause eruptions of acne vulgaris

A
  • systemic/topical corticosteroids
  • anabolic steroids
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5
Q

characteristic lesion types for acne vulgaris

A
  • open comedones (blackheads)
  • closed comedones (whiteheads, noninflammatory base)
  • erythematous inflammatory papules
  • pustules
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6
Q

How would drug induced acne differ from acne vulgaris

A

drug induced acne has monomorphic inflammatory papules and pustules rather than open and closed comedones (black/whiteheads)

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7
Q

Describe the classification for mild acne

A
  • <20 comedones
  • <15 papules/pustules or nodules/cysts
  • <30 total
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8
Q

describe the classification for moderate acne

A
  • 20-100 comedones
  • 15-50 papules/pustules or nodules/cysts
  • 30-125 total
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9
Q

Describe the classification for severe acne

A
  • > 100 comedones
  • > 50 papules/pustules or >5 nodules/cysts
  • > 125 total
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10
Q

If a patient presents with pruritic acne, what is the likely cause and how is this diagnosed

A
  • pityrosporum folliculitis
  • KOH prep
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11
Q

What is the treatment for pityrosporum folliculitis

A

ketoconazole

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12
Q

Treatment for noninflammatory comedonal acne

A

topical retinoids

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13
Q

what are examples of topical retinoids

A
  • tretinoin
  • tazarotene
  • adapalene gel
  • trifarotene
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14
Q

What are the side effects and CI of topical retinoids

A
  • SE: photosensitivity and dryness
  • CI: pregnancy!!

must have 2 negative pregnancy tests prior to starting an oral retinoid and must use 2 forms of birth control.

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15
Q

What is the treatment for mild papulopustular acne

A
  • topical antimicrobial (BPO + Abx)
  • PLUS retinoid
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16
Q

What is the treatment for moderate papulopustular acne

A
  • topical retinoid + oral ABX + BPO wash
  • hormonal therapy
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17
Q

what is the treatment for severe nodular acne

A
  • topical retinoid + oral ABX + BPO wash
  • hormonal therapy
  • can use isotretinoin (accutane) as MONOtherapy.
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18
Q

what is the indication for topical antibiotics? when would you use this as monotherapy

A

mild-moderate inflammatory (papulopustular) acne.

NEVER used as monotherapy! at least used with BPO

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19
Q

what topical antibiotics are used for mild-moderate inflammatory acne

A

topical clindamycin
topical erythromycin

clindamycin is used more because resistance is emerging for erythromycin

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20
Q

when do you use oral antibiotics and which antibiotics are used?

A

moderate papulopustular or severe nodular acne

  1. tetracyclines (tetra, doxy, mino)
  2. Macrolides (erythro, azithro)
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21
Q

What antibiotics should be used for moderate papulopustular or severe nodular acne in pregnant patients

A

Macrolides

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22
Q

when do you use isotretinoin

A

severe/resistant nodular/cystic acne

this IS monotherapy, do NOT use with antibiotics

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23
Q

what are the CI for isotretinoin

A

Pregnancy
tetracycline use.

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24
Q

what is the iPLEDGE requirements

A

For patients starting oral retinoids.

  • 2 birth control forms
  • 2 negative pregnancy tests
  • CMP, Lipids and pregnancy testing monthly
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25
Q

when should you consider stopping oral retinoids or adding a lipid lowering drug

A
  • > 700mg/dl lipids
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26
Q

MC form of alopecia

A

androgenic alopecia

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27
Q

what is the pathophysiology of androgenic alopecia

A

DHT causes terminal follicles to transfer into vellus like hair follicles

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28
Q

when does androgenic allopecia tend to occur in women vs men

A

Men - after puberty as early as 20’s and fully expressed by 40

women - MC after 50

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29
Q

what would you see on a biopsy of androgenic alopecia

A

telogen phase follicles and atrophic follicles

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30
Q

what would a trichogram show for androgenic alopecia

A

increase in telogen hairs

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31
Q

what lab studies should be conducted in a patient with suspected androgenic alopecia

A
  • free and total testosterone
  • DHEAS
  • Prolactin
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32
Q

What is the treatment for androgenic alopecia

A
  • topical minoxidil/rogaine BID
  • oral finasteride (MEN only)
  • oral Spironolactone for females
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33
Q

atopic dermatitis is mediated by…..

A

IgE

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34
Q

Where is atopic dermatitis MC found on the body

A

Face, scalp, torsos, extensors (MC in the flexures)

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35
Q

what is the atopic triad

A
  • atopic dermatitis (eczema)
  • allergic rhinitis (hay fever)
  • asthma
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36
Q

what characterizes atopic dermatitis

A

dry skin and pruritus. Consequent rubbing leads to the itch/scratch cycle.

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37
Q

what is the itch/scratch cycle

A

itching causes increased inflammation and lichenification which leads to further itching.

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38
Q

what results as a consequence of atopic dermatitis due to decreased barrier function

A
  • impaired filagrin production
  • reduced ceramide levels
  • increased trans-epidermal water loss
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39
Q

acute inflammation in atopic dermatitis is associated with a predominance of which IL

A

IL 4 and IL 13

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40
Q

acute vs subacute vs chronic atopic dermatitis

A
  • acute: erythema, vesicles, bullae, weeping, and crusting
  • subacute: scaly plaques, papules, round erosions, crusts
  • chronic eczema: lichenification, scaling, hyper and hypopigmentation
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41
Q

Darker skinned individuals are more commonly known to experience what subtype of atopic dermatitis

A

follicular

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42
Q

what is the hallmark symptom of atopic dermatitis

A

intense pruritus

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43
Q

treatment for atopic dermatitis

A
  • avoid triggers and use gentle facewash/moisturizers
  • Clearance with low strength steroids
  • antihistamines for pruritis
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44
Q

what is the preferred low potency topical steroid for localized atopic dermatitis

A

desonide

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45
Q

what are the medium potency topical steroids that can be used for atopic dermatitis

A

triamcinolone
mometasone
fluocinolone

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46
Q

what is irritant contact dermatitis

A

acute inflammatory reaction that occurs after a single exposure to an offending agent. it is confined to area of exposure and therefore is SHARPLY marginated and NEVER spreads.

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47
Q

what is allergic contact dermatitis

A

inflammatory reaction that is caused by an allergen that elicits a type 4 hypersensitivity reaction. tends to involve the surrounding skin and may spread beyond infected sites

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48
Q

what is the difference in the presentation of acute vs chronic contact dermatitis

A
  • acute: erythema, vesicles, and bullae
  • chronic: scaling. lichenification, fissures, and cracks
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49
Q

What is the treatment for contact dermatitis

A
  • avoid triggers
  • topical steroids (max 2 weeks on, 2 weeks off then repeat)
  • oral steroids
  • PUVA therapy can be used.
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50
Q

what is the etiology of diaper dermatitis

A
  • cutaneous candidiasis
  • ICD
  • miliaria
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51
Q

what is the presentation of typical diaper dermatitis

A

shiny erythema with dull margins

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52
Q

what is the presentation of a diaper dermatitis caused by maliaria

A

multiple papulopustular lesions/pruritus

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53
Q

what is the management for diaper dermatitis

A
  • proper diaper hygiene (frequent changes, disposable, tight fitting)
  • keep area dry and allow air flow
  • barrier creams (zinc oxide/petroleum jelly)
  • candidiasis = nystatin, clotrimazole, econazole
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54
Q

what is perioral dermatitis

A

erythematous papulopustular eruption involving the nasolabial folds, upper and lower cutaneous lip, and chin

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55
Q

what is the etiology of perioral dermatitis

A

topical steroids

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56
Q

what is the treatment for perioral dermatitis

A
  • discontinue the steroids (taper!!)
  • apply topical flagyl or erythromycin

advise pt that it may flare prior to subsiding

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57
Q

what are the 3 degrees of burns

A

1st - only epidermis
2nd - epidermis and dermis
3rd - full thickness

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58
Q

what burns are most common in which age groups

A

young - scalding burns
older - open flame

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59
Q

what classifies a minor burn

A
  • <10% BSA for 1st and 2nd degree
  • <2% for 3rd degree
60
Q

what is the treatment for 1st, 2nd and 3rd degree burns

A

-1st degree: cold compress and analgesics
-2nd degree: silvadene and analgesics
-3rd degree: referral to burn center

61
Q

what is the treatment of electrical burn

A

-watch for entrance or exit wounds
-EKG
-CK
-UA (myoglobinuria)
-BMP (rhabdomyolysis)

62
Q

what is considered an immediate drug reaction

A

occurs less than 1 hour of last dose with urticaria, angioedema, and anaphylaxis

63
Q

what is considered a delayed drug reaction

A

occurs >1hr but usually before 6hrs, occasionally weeks/months after initiation of drug use.

erythematous eruptions, fixed eruptions, or systemic reactions

64
Q

which viruses cause eruptions with the administration of PCN

A
  • EBV
  • CMV
65
Q

what is the MC of all drug reactions

A

exanthematous drug reaction

66
Q

what characterizes an exanthematous drug reaction

A

bright red, maculopapular rash that is symmetric. starts on the trunk and spreads to extremities.

can be itchy, scale and desquamate

67
Q

what is the tx of an exanthematous drug reaction

A
  • identify and DC offending agent
  • topical steroids and antihistamines for relief of symptoms
68
Q

what is a fixed drug eruption

A

drug reaction characterized by a solitary erythematous patch/plaque that will recur at the same site if re-exposure of offending agent occurs

69
Q

what is the clinical presentation of a fixed drug eruption

A
  • pruritus
  • burning pain
  • sharp marginated macule
  • dusky red color
70
Q

Tx for fixed drug eruption

A
  • remove offending agent
  • non eroded = topical steroid
  • eroded = topical antimicrobial
71
Q

what is drug induced hypersensitivity syndrome

A

skin eruptions with systemic symptoms and internal organ involvement

72
Q

what is the etiology of drug induced hypersensitivity syndrome

A
  • Antiepileptic drugs (phenytoin, carbamazepine, phenobarb)
  • sulfonamides (antimicrobials, dapsone, sulfasalazine)
73
Q

What are the clinical findings for drug induced hypersensitivity syndrome

A
  • onset 2-6 wks after drug initiation or increase in drug dosage
  • fever, malaise, facial edema, LAD and HSM
  • maculopapular eruption
    oropharyngeal mucosal lesions (cheilitis, erosions, pharyngitis, tonsilitis)
74
Q

what is the diagnostic criteria for drug induced hypersensitivity syndrome

A
  • cutaneous drug eruption
  • hematologic abnormalities
  • systemic involvement (LAD<2cm, elevated LFTs, elevated BUN/Cr)
75
Q

what is the treatment for drug induced hypersensitivity syndrome

A
  • stop/substitute ALL suspected medications
  • mild/mod reaction = topical steroids
  • mod/severe reaction = oral steroids w long taper
  • oral antihistamines for symptoms.
76
Q

what are pustular drug eruptions

A

acute febrile eruptions that are often associated with leukocytosis after drug administration

77
Q

what is the presentation of pustular drug eruptions

A
  • sterile pustules on erythematous base starting in intertriginous folds and/or the face
  • fever
  • leukocytosis
78
Q

what is the prognosis of pustular drug eruptions

A

pustules resolve over 2 weeks followed by desquamation 2 weeks later

79
Q

what is erythema multiforme

A

acute hypersensitivity reaction affecting the skin and mucous membranes

80
Q

what is the MCC of erythema multiforme

A

HSV

81
Q

what is the clinical presentation of erythema multiforme

A
  • erythematous, papular or urticarial type lesions (may precede bullae by months)
  • followed by tense, firm topped bullae
  • mucosal lesions
  • constitutional symptoms (fever, weak, malaise, fatigue)
  • usually BILATERAL AND SYMMETRIC
82
Q

what are the characteristics of erythema multiforme minor

A
  • little/no mucosal involvement
  • has vesicles but no bullae
  • no systemic symptoms
  • confined to extremities and face
83
Q

what are the characteristics of erythema multiforme major

A
  • mucosal involvement
  • confluence of lesions
  • nikolsky sign
  • constitutional symptoms
84
Q

what is the MCC of MAJOR erythema multiforme

A

drug reaction

85
Q

what is the treatment of erythema multiforme minor

A
  • antihistamines
  • low dose topical steroids
  • valacyclovir if HSV
86
Q

what is the treatment for major erythema multiforme

A
  • remove offending agent
  • IV fluids
  • magic mouthwash
  • systemic steroids for severe
87
Q

what is the magic mouthwash formula

A

viscous lidocaine, benadryl, and maalox

88
Q

treatment for recurrent erythema multiforme

A

daily prophylactic antiviral therapy

89
Q

what is the MCC of impetigo

A

MSSA and MRSA

90
Q

where does impetigo typically occur

A
  • minor breaks in the skin
  • around the nose
  • atopic dermatitis
  • traumatic wounds
91
Q

what is bullous impetigo

A

exfoliative toxin A leads to loss of cell adhesion in the superficial epidermis

92
Q

who is bullous impetigo MC in?

A

newborns and older infants

93
Q

what is the clinical presentation of non-bullous impetigo

A
  • erosions with honey colored crust
  • regional LAD
  • often asymptomatic but can be painful and tender
94
Q

what is the clinical presentation of bullous impetigo

A
  • vesicles that progress quickly into bullae
  • no erythema
  • negative nikolsky sign
  • lasts 1-2 days then collapses to leave erosions with crusts
95
Q

How do you diagnose impetigo

A
  • non-bullous = clinical
  • bullous = gram stain and culture
96
Q

what is the treatment for impetigo

A
  • warm water soaks and topical mupirocin
  • keflex or erythromycin for widespread infection
  • MRSA = doxy (critical = vanc/linezolid)
97
Q

Where are common places to see lice outbreaks

A
  • schools
  • daycare centers
  • nursing homes
  • dorms
  • prisons
98
Q

what is the presentation of pediculosis capitis

A
  • lice and nits in hair
  • itching
  • maculae cerulae
  • occipital lymphadenopathy
99
Q

what is maculae cerulae

A

purpuric stains on the skin of the occipital scalp and nape of neck

100
Q

How do you diagnose pediculosis capitis (lice)

A
  • visualization
  • woods lamp
100
Q

What is the treatment for pediculosis capitis

A
  • permethrin (nix)
  • removal of nits
100
Q

what is the clinical presentation of pitryasis rosea

A

-single herald patch initially (oval flat/raised papule/plaque)
-christmas tree like pattern on trunk
-salmon colored patches

101
Q

Diagnosis of lichen planus

A

biopsy

101
Q

what is the presentation of lichen planus

A
  • flat topped papules
  • sharply defined
  • whickham striae
  • on flexor surfaces
101
Q

what is the treatment for lichen planus

A

topical triamcinolone under occlusion

102
Q

what is the MCC of pitryiasis rosea

A

HHV 6 and 7

102
Q

what is the management for pityriasis rosea

A
  • spontaneous remission in 6-12wks
  • oral antihistamines
  • topical steroids or oral prednisone taper

(basically symptom management until spontaneous remission)

103
Q
A
103
Q
A
104
Q
A
105
Q

what is scabies

A

hypersensitivity reaction to mites that burrow into and just below the stratum corneum of the epidermis.

causes HIGHLY pruritic eruption!!

106
Q

how long after infestation do symptoms begin in scabies?

A

2-6 weeks after initial infestation

107
Q

what is the clinical presentation of scabies

A
  • worse at night esp right after getting in bed
  • scratching in exam room
  • burrow is a fine, thread like line with terminal tiny black speck
  • classically SPARES head and neck
108
Q

Diagnosis of scabies

A
  • clinical
  • dermoscopy to visualize mites within the terminal end of a burrow.
  • “scabies prep”
109
Q

true/false a negative scabies prep rules out scabies

A

false. mites can be difficult to isolate so false negatives are common

110
Q

crusted scabies is MC in which patient group

A

immunocompromised or institutionalized patients

111
Q

what is crusted scabies

A

thousands to millions of mites

112
Q

what is the treatment of crusted scabies

A
  • topical permethrin full body application
  • PLUS oral ivermectin (days 1,2,8,9,15 and sometimes 22 and 29)
113
Q

what is the treatment for regular scabies (10-20 mites)

A

permethrin

114
Q

what is the MC etiology of SJS/TEN

A

Drugs

115
Q

what is the presentation of SJS/TEN

A
  • constitutional symptoms
  • NVD, skin tenderness
  • positive nikolsky
  • full thickness epidermal detachment
  • mucosal involvement
116
Q

SJS vs TEN

A
  • SJS: <10% body surface
  • SJS/TEN: 10-30%
  • TEN: >30%
117
Q

what is the treatment for SJS/TEN

A
  • IV fluids and parenteral nutrition
  • IV pain meds
  • wound care (wet dressing w burrow solution)
  • IV steroids/IVIG early!
118
Q

what is the presentation of tinea capitis

A
  • grey patch with broken off hairs
  • black dot appearance
119
Q

what is a kerion

A
  • inflammatory mass in which remaining hairs are loose
  • boggy, purulent, inflamed nodules
120
Q

what is favus

A
  • perifollicular erythema and matting of hair
  • thick/yellow crusts
121
Q

how do you diagnose tinea capitis

A
  • woods lamp
  • direct microscopy
  • fungal culture
  • bacterial culture
122
Q

How do you treat tinea capitis

A
  • PO griseofulvin or terbinafine
  • ketoconazole shampoo
123
Q

what is the presentation of tinea cruris

A

large scales with well demarcated plaques and central clearing in the upper thigh and adjacent inguinal and pubic regions

124
Q

what is the treatment for tinea cruris

A

topical ketoconazole

125
Q

what is the presentation of tinea corporis

A

sharply demarcated plaques with central clearing and crusting

126
Q

what is the treatment for tinea corporis

A

topical antifungal

if large surface area use topical terbinafine

127
Q

Presentation of interdigital tinea pedis

A
  • dry scaling
  • maceration
  • between 4th and 5th toes
128
Q

presentation of moccasin tinea pedis

A
  • scaling with erythema
  • papules at margin
  • bilateral
129
Q

Presentation of inflammatory tinea pedis

A

vesicles or bullae with clear fluid

130
Q

presentation of ulcerative tinea pedis

A

extension of interdigital onto the plantar and lateral foot

131
Q

What is the treatment for tinea pedis

A

Topical antifungal

132
Q

what is the etiology of tinea versicolor

A

overgrowth of malassezia furfur

MC IN ADOLESCENTS

133
Q

what is the presentation of tinea versicolor

A
  • seen in oily skin
  • itching
  • macules, patches, and plaques
  • NOT contagious
134
Q

how do you diagnose tinea versicolor

A

KOH prep showing hyphae and budding yeast (looks like spaghetti and meatballs!!)

135
Q

what is the treatment for tinea versicolor

A
  • selenium sulfide or zinc pyrithione
  • topical ketoconazole
136
Q

what is the presentation of urticaria

A
  • pruritic, raised, well circumscribed areas of erythema and edema
  • dermatographism
137
Q

what is the treatment for urticaria

A
  • evaluate in ED
  • antihistamine + famotidine + steroid
  • chronic is PRN antihistamine
138
Q

what is the etiology of verrucae

A

HPV

139
Q

what are the MC areas to see verrucae

A
  • hands/fingers
  • knees
140
Q

what is verruca plana

A

flat, skin colored verruca MC on face

141
Q

how do you treat verruca

A
  • file and then use SA
  • cantharone
  • cryotherapy

Pediatric EOR exam (20 decks)

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