Pediatrics EOR Study Guide
Dermatology (15%)
1) Acne Vulgaris
a. Inflammatory skin condition associated w/ papules & pustules involving the pilosebaceous units
b. Pathophys: 4 main factors – follicular hyperkeratinization, increased sebum production, Propionibacterium
acne overgrowth & inflammatory response
c. S/S: common in areas w/ increased sebaceous glands (face, back, chest, upper arms
i. Comedones – small, noninflammatory bumps from clogged pores
1. Open comedones = blackheads (INCOMPLETE blockage)
2. Closed comedones = whiteheads (COMPLETE blockage)
ii. Inflammatory – papules or pustules surrounded by inflammation
iii. Nodular/Cystic – often heals w/ scarring
d. Diagnosis:
i. Mild: comedones, small amounts of papules and/or pustules
ii. Moderate: comedones, larger amounts of papules and/or pustules
iii. Severe: nodular (> 5 mm) or cystic acne
e. Management:
i. Mild: topical azelaic acid/salicylic acid/benzoyl peroxide/retinoids, tretinoin or topical Abx (Clinda or
Erythromycin)
ii. Moderate: above + PO Minocycline or Doxycycline, can try Spironolactone
iii. Severe (refractory nodular acne): PO Isotretinoin
f. Isotretinoin:
i. MOA: affects all 4 pathophysiologic mechanisms of acne (see above)
ii. Most effective med for Acne Vulgaris
iii. Usually reserved for severe or refractory acne
iv. ADRs: dry skin & lips (MC), dry eyes, increased Tg & cholesterol
1. Highly teratogenic – must obtain at least 2 pregnancy tests prior to initiation of tx & monthly
while on tx, must commit to 2 forms of contraception (used at least 1 month prior to
initiation & 1 month after it is DC’d)
2. Arthralgias, myalgias, hepatitis, leukopenia, premature long bone closure
3. Photosensitivity, worsening of DM, HA, idiopathic intracranial HTN, fatigue & possible psych
effects
2) Androgenic Alopecia
a. Genetically predetermined progressive loss of the terminal hairs on the scalp in a characteristic pattern
b. MC type of hair loss in men & women – gradual onset & usually occurs after puberty
c. Pathophys:
i. Dihydrotestosterone (DHT) is the key androgen
ii. Activation of androgen receptor shortens the anagen (growth phase) in the normal hair growth cycle
iii. Pathologic specimens show decreased anagen to telogen ratio
d. S/S: varying degrees of hair thinning & nonscarring
i. Males: begins as bitemporal thinning of the frontal scalp, then involves the vertex
ii. Women: thinning of the hair between the frontal & vertex of the scalp w/o affecting frontal hairline
e. Diagnosis: usually clinical, can do dermoscopy (will show miniaturized hair & brown perihilar casts
f. Management:
i. Topical Minoxidil: best if recent onset & involving a small area
1. Requires a 4-6 month trial before improvement & must be used indefinitely
2. MOA: widens blood vessels, allowing more blood O2 & nutrients to promote the anagen
phase
3. ADRs: pruritis & local irritation w/ flaking
ii. PO Finasteride
1. MOA: 5-alpha reductase type 2 inhibitor – inhibits the conversion of testosterone to
dihydrotestosterone
2. ADRs: decreased libido, sexual/ejaculatory dysfunction, increased risk of high-grade
prostate cancer, Category X
iii. Hair transplant if pt has sufficient # of donor plugs
3) Atopic Dermatitis (Eczema)
a. Rash d/t defective skin barrier susceptible to drying, leading to pruritis & inflammation
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, b. Atopic Triad = eczema, allergic rhinitis & asthma
c. Most manifest in infancy & almost always by age 5
d. Triggers: heat, perspiration, allergens & contact irritants (s/a wool, nickel, food, synthetic fabrics)
e. S/S:
i. Pruritis = hallmark (required for diagnosis)
ii. Erythematous, ill-defined blisters, papules or plaques that later dry, crust over & scale
1. MC in flexor creases in older children & adults
iii. Infantile atopic dermatitis – usually affects the face & extensor part of the extremities (from crawling
and rubbing the skin)
iv. Nummular eczema – sharply defined discoid/coin-shaped lesions, esp. on the dorsum of the hands,
feet & extensor surfaces (knees & elbows)
f. Dx: clinical, increased IgE supports the diagnosis
g. Management:
i. Acute Mgmt: 1st line = topical Corticosteroids
1. Antihistamines for itching, wet dressings (s/a Burrow’s solution), Abx if secondary infection
develops (staph aureus)
2. Topical calcineurin inhibitors – alternatives to steroids (don’t cause skin atrophy)
3. Systemic: phototherapy, Cyclosporine, Azathioprine, Mycophenolate, Mofetil, MTX,
Dupilumab
ii. Chronic Mgmt:
1. Maintain skin hydration!!! Skin emollients BID & w/in 3 minutes of exiting a lukewarm
shower or tepid bath
2. PO antihistamines for pruritis (Cetirizine, Fexofenadine, Loratadine, Hydroxyzine,
Diphenhydramine)
3. Avoid triggers (heat, low humidity) or irritants
4) Burns
a. Burn Size: Rule of 9’s (not used for 1st degree burns)
i. Palm size = 1% OR �
ii. Minor burns - <10% in adults, <5% in young/old, <2% full thickness burn
1. Must be isolated injury
2. Must not involve face, hands, perineum or feet
3. Must not cross major joints or be circumferential
iii. Major burns: >25% in adults, >20% in young/old, >10% full thickness burn
1. Burns involving the face, hands, perineum or feet
2. Burns crossing major joints or circumferential burns
iv. Lund-Browder chart – most accurate method for estimating TBSA in both children & adults
b. Thermal Burns
i. First Degree: minor damage to epidermis
1. S/S: erythema, pain, TTP & dry appearance w/o blistering, capillary refill intact (blanches w/
pressure)
2. Usually heals in 7 days w/o scarring
ii. Second Degree: affects the epidermis & the dermis, characterized by blistering
1. Superficial partial thickness: affects the epidermis & superficial portion of the dermis
(papillary)
a. S/S: blistering, erythematous, pink, moist skin, very tender to touch with intact
capillary refill
b. Heals w/in 7-21 days, typically w/o scarring but may leave pigment changes
2. Deep partial thickness: affects the epidermis & deeper portion of the dermis (reticular)
a. S/S: red yellow or pale skin, blistering, not painful (except with pressure), absent
capillary refill, decreased 2 point discrimination
b. Heals in 3 weeks-2 months without scarring
iii. Third Degree: full thickness
1. S/S: waxy, white, leathery & dry skin, painless, absent capillary refill, lack of blistering & lack
of sensation
2. Usually does not spontaneously heal well (may need skin grafting)
iv. Fourth Degree: skin into underlying fat, muscle & bone
1. S/S: skin is black, charred & dry, painless, loss of capillary refill
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, 2. Usually requires tissue reconstruction & debridement
c. Initial Burn Care:
i. Cooling: room temperature tap water or cooled, saline-soaked gauze (NOT ice directly to skin), soap
& water to cleanse & dressing
1. Pain & tetanus status addressed
2. 24h f/u needed with all burns if pt is not admitted to assess burn status, assure dressing
change competence & adjust analgesia as needed
ii. First Degree: generally do not require dressings or topical antibiotics, but do require f/u to monitor
for progression
iii. Partial & Full Thickness: usually requires dressings & topical antibiotics
1. Antimicrobial ointments, silver-containing agents, bismuth-impregnated petroleum gauze,
Chlorhexidine & Mafenide
d. Antimicrobial Ointments:
i. Bacitracin zinc-Polymyxin B sulfate, Neomycin: single or combo agents, easier to apply & remove &
can be used on sensitive areas
1. Mupiroicin is effective against MRSA
2. ADRs: systemic absorption of Polymyxin B can cause nephrotoxicity or neurotoxicity (but
rare), Neomycin is associated w/allergic reactions
ii. Silver-Containing Agents: Silver Sulfadiazine (SSD – MC used burn dressing) & silver nitrate
1. ADRs: SSD cannot be used on the face (causes yellowing of skin), in women who are
pregnant, breastfeeding or in infants < 2 months old, Sulfa allergies, oculotoxic, may cause
pseudoeschar formation & impedes reepithelialization
iii. Bismuth-impregnated petroleum gauze: often preferred dressing for skin graft donor sites & for
covering fresh skin drafts, useful in children (only applied once)
iv. Mafenide acetate: carbonic anhydrase inhibitor, alternative to SSD
1. ADRs: pain when first applied, metabolic acidosis, allergic reactions & respiratory
complications
v. Chlorhexidine: long-lasting antimicrobial cleanser that does not interfere w/ reepithelialization
(compared to SSD)
e. Moderate to Severe Burns:
i. Diagnostic studies: CBC (Hct may be increased initially), eletrolytes (hyperkalemia = MC abnormality
seen early on), Creatinine Kinase, UA & myoglobin, to evaluate for rhabdomyolysis,
carboxyhemoglobin & serum lactate for CO & cyanide poisoning in smoke inhalation
ii. Fluid Resuscitation:
1. Parkland (Modified): 4 mL/kg/%TBSA
a. Counting only partial thickness & full thickness + normal 24h maintenance fluids
b. Add maintenance fluid w/ glucose for children < 5 y/o
c. ½ of fluid given over first 8 hours, remaining ½ given over next 16 hours
2. Isotonic crystalloid fluids – LR is the resuscitation & maintenance fluid of choice for the first
24h, some add 5% dextrose to children < 20 kg to prevent hypoglycemia
3. Monitoring fluid status: UO should be maintained at 1-2 mL/kg/hr in children < 30 kg and
0.5-1 mL/kg/hr if 30kg or greater, 0.5 mL/kg/hr in adults
a. HR is a better monitor of circulatory status than BP
5) Contact Dermatitis
a. Inflammation of the dermis & epidermis from direct contact b/w a substance & the surface of the skin
b. 2 Types:
i. Irritant (MC): causes include chemicals, alcohols or creams; may develop superimposed Candida
infection
ii. Allergen: nickel = MC worldwide, poison ivy/oak/sumac, other metals, chemicals, detergents,
cleaners, acids, prolonged water exposure
c. Pathophys:
i. Irritant: non-immunologic reaction (immediate)
ii. Allergen: type IV hypersensitivity reaction (T-cell mediated – delayed by days)
d. S/S:
i. Acute: erythematous papules or vesicles (may be linear or geometric), often assoc. with localized
pruritis, stinging or burning, may ooze, develop edema & progress to blisters or bullae
ii. Chronic: lichenification fissuring & scales
e. Dx: clinical, patch testing to ID potential allergens, histology (not usually needed but will show spongiosis)
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, f. Management:
i. ID & avoid irritants!!!!
ii. 1st line – topical corticosteroids (ointments)
iii. PO corticosteroids in severe or extensive reactions
iv. Topical calcineurin inhibitors (Tacrolimus or Pimecrolimus) = alternatives
v. Cool saline or astringent compresses, cool baths, skin emollients
vi. If oozing/weeping – drying agents (s/a aluminum acetate) can be used
vii. Burrow’s solution, antihistamines or calamine lotion for itching
6) Dermatitis (Diaper, Perioral)
a. Diaper Rash
i. A type of irritant contact dermatitis
ii. MC involves areas in contact with the diaper with sparing of the skin folds
1. If superimposed Candida infection occurs, it involves the skin folds
iii. D/t prolonged exposure to urine or feces OR harsh detergents from washable diapers
iv. S/S: Acute – erythematous papules, may develop maceration or superficial erosions
1. If severe, may be assoc. with extensive erythema, painful erosions and nodules
v. Management: general skin care = 1st line tx
1. Frequent diaper changes, barrier of petroleum or zinc oxide, use of disposable diapers,
periods of rest w/o a diaper, keeping affected area clean & dry
2. Low potency CS & antifungals may be used in severe cases or Candida suprainfection
b. Perioral Dermatitis
i. MC seen in young adult women (age 20-45)
ii. RF: h/o topical CS use, fluorinated toothpaste
iii. S/S: erythematous grouped papulopustules that may become confluent into plaques with scales
1. May have satellite lesions
2. Classically spares the vermillion border, uncommonly may affect the periorbital or paranasal
skin
iv. Management:
1. Eliminate topical CS & irritants (self-limited)
2. Topical Pimecrolimus, Metronidazole or Erythromycin = 1st line medical tx
3. Topical azelaic acid
4. PO Tetracyclines may be needed if extensive or refractory
7) Drug Eruptions
a. Medication induced changes in skin & mucous membranes (most are hypersensitivity reactions)
b. Most are self-limited if offending drug is discontinued
c. Triggers: antigen from foods, insect bites, drugs, environmental, exercise-induced, infections
d. Pathophys:
i. Type I: IgE mediated (s/a urticaria & angioedema), immediate
ii. Type II: cytotoxic, Ab-mediated (drugs in combo with cytotoxic Abs cause cell lysis)
iii. Type III: immune antibody-antigen complex (s/a drug-mediated vasculitis & serum sickness)
iv. Type IV: delayed (cell mediated) – s/a Erythema Multiforme
v. Non-immunologic: cutaneous drug reactions d/t genetic incapability to detoxify certain medications
(s/a anticonvulsants or sulfonamides)
e. Exanthematous Drug Eruption:
i. Morbilliform or maculopapular drug eruption characterized by macules or small papules after the
initiation of drug treatment
ii. MC occurs 5-14 days after initiation of the offending medication or w/in 1-2 days in previously
sensitized individuals
iii. Pathophys: Type IV (delayed) hypersensitivity reaction
iv. Commonly caused by PCN, sulfa drugs, NSAIDs & Allopurinol
v. S/S: general distribution of bright red macules & papules that coalesce to form plaques, primarily
involving the trunk & proximal extremities, +/- fever & pruritis
vi. Management:
1. STOP THE OFFENDING MED – most are self-limited once the drug is DC’d
2. Symptomatic tx – PO antihistamines (H1 blockers, 2nd gen or 1st gen)
3. Short course of PO corticosteroids reserved for severe cutaneous reactions
f. Angioedema
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