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Royal College Peds 2021 > DERMATOLOGY > Flashcards

DERMATOLOGY Flashcards

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Royal College: Emergency Medicine flashcards
1
Q

What is the most common cause of erythema multiforme?

A

HSV infection

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2
Q

What are the clinical features of erythema multiforme?

  • most commonly appears in what age group?
  • what is the prognosis of EM?
  • treatment?
A
  1. Classic TARGET lesions with erythematous border
    - can also look like macules, papules, vesicles, bullae, URTICARIA
  2. Abrupt, symmetric eruption of rash usually on extensor upper extremities with SPARSE lesions on the face, trunk and legs
  3. Oral lesions only with SPARING of other mucous membranes (ie. genital, resp, etc.)
    * *Most commonly occurs between 10-40 yo
    - prognosis: lesions typicaly resolve without sequelae in approx 2 weeks; does NOT progress to SJS
    - treatment: supportive care with topical emollients, systemic antihistamines, NSAIDs to provide symptomatic relief
    - do NOT use steroids as could increase HSV replication and make EM more frequent/continuous
    - MAY give prophylactic oral acyclovir x 6 mo if recurrent episodes of HSV-associated EM
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3
Q

What are possible causes of SJS? (2)

A
  1. Infection: most common cause is MYCOPLASMA

2. Drugs: NSAIDs, sulfonamides, antibiotics, anticonvulsants

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4
Q

What are the clinical features of SJS?

-percentage of body surface area involvement

A
  1. Erythematous macules that rapidly develop central necrosis to form VESICLES, BULLAE and DESQUAMATION on face, trunk, extremities (widespread)
  2. TWO OR MORE MUCOSAL SURFACES involved: eyes, oral cavity, upper airway or esophagus, GI tract or anogenital mucosa
  3. Lots of pain from mucosal ulceration but skin tenderness is minimal to absent
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5
Q

What are main differences between erythema multiforme and SJS? (2)

A
  1. Location of rash:
    - EM: usually on extensor surfaces of upper extremities, occasionally on legs; rarely on face and trunk
    - SJS: more widespread involving face, trunk and extremities
  2. Mucosal membrane involvement:
    - EM: usually only involves mouth
    - SJS: involves TWO OR MORE mucosal surfaces (eyes, oral vacity, upper airway, esophagus, GI tract or anogenital mucosa)
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6
Q

What are the main differences between SJS and TEN? (2)

A
  1. BSA involvement of skin necrolysis:
    - SJS < 10% BSA
    - TEN > 30% BSA
  2. Pain of skin lesions:
    - SJS: only mucosal membrane pain from ulceration, minimal to NO skin tenderness
    - TEN: lots of pain from skin lesions
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7
Q

What are possible complications of SJS?

A
  1. Corneal ulceration
  2. Anterior uveitis
  3. Bronchitis
  4. Pneumonitis
  5. Myocarditis
  6. Hepatitis
  7. ATN
  8. Bacterial superinfection and sepsis
  9. High insensible fluid loss
  10. Urogenital strictures in long term
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8
Q

What are possible lab abnormalities seen in SJS?

A
  1. Leukocytosis
  2. Elevated ESR
  3. Increased liver enzymes
  4. Decreased serum albumin
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9
Q

What is the management of SJS?

A

SUPPORTIVE overall!

  1. Stop possible offending drugs asap
  2. Ophtho consult to assess for corneal scarring
  3. PAIN management for oral lesions (morphine, mouth wash, etc.)
  4. Monitor vaginal lesions to prevent vaginal stricture/fusion
  5. IV fluids if insensible fluid losses from bullous eruption or desquamation
    * ***no evidence for use of steroids!
    * **Can consider IVIG in early disease
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10
Q

What are the clinical features of TEN? (4)

  • what is a classic sign on exam of TEN?
  • complications?
  • etiology?
  • treatment?
A
  • **>30% BSA involvement in necrolysis
    1. Widespread blister formation and morbilliform or confluent erythema ASSOCIATED WITH SKIN TENDERNESS!
    2. NO NO NO target lesions!!!!!!
    3. Sudden onset and generalization within 24-48 hrs
    4. Full thickness epidermal necrosis!
    5. Usually involves multiple mucous membranes (3 or more)
  • **usually have prodrome of fever, malaise, diffuse erythema
  • classic exam finding: NIKOLSKY SIGN (gentle pressure on the skin causes desquamation of the bullae)
  • complications: strictures, fluid loss, sepsis, conjunctival scarring
  • etiology: same as SJS (mycoplasma, sulfonamides, antibiotics, anticonvulsants, NSAIDs)
  • treatment: supportive. NO STEROIDS. Consider IVIG
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11
Q

What are the two fungi that cause tinea capitis?

  • how do you contract this fungi?
  • treatment?
A
  1. Trichophyton
  2. Microsporum
    - contact with person, animal, or soil
    - treatment:
  3. Oral therapy is mandatory if kerion is present = terbinafine PO (lamisil) or itraconazole x 2-4 weeks
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12
Q

What kind of rashes can develop from methotrexate?

A
  1. Stevens Johnson
  2. Erythema multiforme
  3. Photosensitivity
  4. Hypo- or hyper-pigmentation
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13
Q

What is your differential diagnosis for midline neck mass? (3)
-what about neck mass in anterior triangle?

A
  1. Thyroglossal cyst
  2. Dermoid cyst
  3. Laryngocele
    - treatment: amoxi-clav if PO (oral anaerobes and skin bugs) or cefuroxime + clinda if IV

Neck masses in the anterior triangle:

  1. Cervical lymphadenitis
  2. Branchial cleft cyst
  3. Dermoid cyst
  4. Teratoma
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14
Q

What are clinical features of herpetic whitlow?

-treatment?

A

Usually seen in children who suck their thumb

  • vesicles look pus-filled but do NOT I&D because then you’re spreading the HSV everywhere
  • can get regional lymph ndoes
  • resolves in ~3 weeks
  • treatment: PO acyclovir
  • treat with PO acyclovir
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15
Q

A child with diffuse atopic dermatitis has been compliant with steroid treatment but is not improving. What is your next line agent?

A

Topical tacrolimus: calcineurin inhibitor

  • for kids > 2 yo who have failed topical steroids
  • if they fail to respond to topical tacrolimus: can try cyclosporine
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16
Q

How long is the treatment with Accutane (isotretinoin)?

  • recurrence risk?
  • side effects?
  • monitoring while on treatment?
A

-Treatment course is 5 months: 40% cure rate, 40% will require topical or oral maintenance, 20% will relapse and need repeat course

Side effects:

  1. Teratogenecity
  2. Increased triglycerides and cholesterol
  3. Dry mucous membranes
  4. Major depression with suicide risk BUT no case reports of actual suicide cases

Monitoring:

  1. Monthly pregnancy tests
  2. Counsel re: two forms of birth control
  3. Monthly lipid profile
  4. Monthly liver enzymes
17
Q

A patient presents with nail pitting. What is your differential diagnosis? (3)

A
  1. Psoriasis
  2. Alopecia areata
  3. Reactive arthritis
18
Q

How do you contract molluscum contagiosum?

  • affects which two populations the most?
  • description of rash
  • the child develops pustules around the lesion. What do you do?
  • management?
A

Contraction: contact with lesions or fomites

Two populations:

  1. school age children
  2. Immunosuppressed

Central umbilication, pearly papules, can be anywhere on the body

Pustules: don’t treat as this is an immunological reaction!

Treatment:

  1. Cantharidin
  2. Monitoring (resolves with time)
  3. Curettage
19
Q

What are the clinical features of incontinentia pigmenti?

-mode of inheritance?

A

Rare, X-linked (lethal in males, so females are ones you will), ectodermal disorder

  1. Derm:
    - erythematous, LINEAR streaks, plaques of vesicles, then become dry on limbs and trunk
    - follow lines of blaschkow
    - increased eosinophils in rash and serum
    - presents in neonatal period
  2. Ocular: neovascularization, strabismus, cataracts, optic atrophy
  3. CNS: seizures, spasticity, etc.
  4. Dental anomalies: late dentition, hypodontia, conical teeth
  5. Alopecia on top of head
  6. Nail dystrophy (ridging and pitting)
  7. Skeletal defects
20
Q

What is the treatment for scabies?

-what are contraindications to first line treatment?

A

5% permethrin x 8-14 hrs if > 6 yo, 6-8 hrs if < 6 yo

Contraindications: If < 2 mo or pregnant: use 6% sulfur in petroleum x 3 doses

21
Q

A patient presents with vesicles after sun exposure and hypopigmented flar scars with mild trauma. What is the most likely medication that causes this rash?

A

Pseudoporphyria: small hypopigmented depressed scars after mild trauma or after spontaneous vesicular lesions = caused by NSAIDs

22
Q

What organ is most commonly affected by hemangiomas?

A

Liver

23
Q

What are complications of hemangiomas?

A
  1. Bleeding
  2. Airway obstruction
  3. Ulceration
  4. Kasabach Meritt resulting in high output cardiac failure
  5. Association with other defects (PHACES, midline hemangiomas may be associated with other midline defects)
24
Q

What are the treatment modalities for psoriasis?

A
  1. Topical corticosteroids 1st line
  2. Topical vitamin D analogues: calcipotriene
  3. Topical retinoids
  4. Topical tar
  5. Phototherapy
  6. PO cyclosporine
  7. PO Methotrexate
  8. PO biologics
25
Q

What are treatment options for pustular acne?

A

Moderate acne:

  1. Topical retinoids + benzoyl peroxide
  2. Topical retinoids, benzoyl peroxide, topical antibiotics

Severe:
1. Oral antibiotic + topical retinoid + benzoyl peroxide + topical antibiotics

26
Q

What are the clinical features of pityriasis rosea?

  • most common cause?
  • treatment?
A
  • most often caused by HHV-6 or HHV-7
  • see herald patch preceding the eruption, then systemic eruption follows 5-7 days later in Christmas tree (skin cleavage lines)
  • lasts up to 12 weeks
  • treatment: antihistamine or topical steroids
27
Q

How is poison ivy spread?

-is it spread from fluid from burst vesicles?

A

Fluid from ruptured

  • antigen retained on skin under fingernails and on clothes can initiate new plaques of dermatitis if you don’t wash with soap and water
  • can also be on live or dead leaves, can be on animal fur
28
Q

What is the characteristic rash of poison ivy?

A

LINEAR VESICLES with excoriation, itchy and spreads where scratches

29
Q

What age is the peak incidence of erythema toxicum?

-what type of cells do you see inside?

A

2nd day of life

  • should disappear by 2nd week of life
  • see eosinophils
30
Q

What type of cell do you see in neonatal pustular melanosis?

-how long does it last?

A

PMNs!

-last several months

31
Q

What is the most common infection associated with id reactions?

A

Tinea pedis

32
Q

What are risk factors for development of hemangiomas?

  • 3 types of hemangiomas?
  • natural progression?
  • treatment?
A
  1. Prem
  2. Low birth weight
  3. Multiple gestation
    - think SMALL babies = might be because of ?hypoxic injury leading to vascular proliferation but no one knows for sure
  • 3 types:
    1. Superficial: strawberry hemangioma = papular or plaque
    2. Deep: sits under the skin
    3. Mixed: components of both
  • natural progression: grows until 4-5 mo of age, then starts to plateau and regresses until 9-10 yo. 50% of kids have lasting skin changes

Treatment: 90% require no active management

  • 10% require treatment IF vision or airway threatening or risk of significant negative cosmetic outcome
  • use propranolol at standard therapy (avoid in asthma, diabetes, PHACES because of cardiac defects)
33
Q

What are the differences between capillary malformation and hemangioma?

A

Capillary malformation: present at birth, grow with the child and persist

Hemangioma: usually not present right at birth, rapid growth, then resolves

34
Q

What are the ABCDEs of moles?

A

Acquired Nevi: this tells you when to worry!
Asymmetry
Border: irregular
Color: multiple colors, asymmetrical colors
Diameter > 6 mm
Evolution/changing

35
Q

Which of the following hypopigmented lesions is scaly?

a. vitiligo
b. tinea versicolor
c. tuberous sclerosis
d. post-inflammatory hypopigmentation

  • clinical features of tinea versicolor?
  • treatment?
A

Tinea versicolor! Malassessia furfur infection = see a fine scale over the rash. Also, the malassessia LIKES sebum/sebaceous glands! Will thus see tinea versicolor in older children/adolescents in areas of sebaceous glands (think where you get acne)

  • need to rub the rash to elicit the scale
  • treatment: antifungal shampoo daily x 1-2 wks, then 1x q3 mo to prevent recurrence
  • vitiligo: no scale, SHARPLY demaRCATED
  • post-inflammatory: no scale, poorly marginated
36
Q

A patient has salmon colored think scaling plaques on the trunk in the shape of a Christmas tree. What is your diagnosis?
-management?

A

Pityriasis rosea = self limited condition thought to be caused by a virus.

  • herald patch = salmon colored patch surrounded by darker rim and fine scale
  • management: reassurance - rash will self-resolve in several weeks

Royal College Peds 2021 (55 decks)

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