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End of Rotation: Pediatrics > Dermatology > Flashcards

Dermatology Flashcards

1
Q

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A

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2
Q

What is contact dermatitis?

A
  • Inflammatory skin reaction resulting from contact with an external agent
  • Rhus dermatitis is an allergic dermatitis caused by contact with poison ivy or oak
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3
Q

What are the signs of contact dermatitis?

A
  • Patients complain of itching and burning in the effected area
  • Sharply demarcated, erythematous vesicles and plaques at site of contact with agent
  • Chronic lesions may be linchenified
  • Satellite papules and excoriations are common
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4
Q

How do we diagnose contact dermatitis?

A
  • Clinical: consider location, relationship to external factors, particular configurations
  • Patch tests that result in similar reactions support the diagnosis
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5
Q

How do we treat contact dermatits?

A
  • Remove offending agent
  • Topical lubrication
  • Wet dressings soaked in Burrow’s solution (aluminum acetate in water)
  • Topical corticosteroids for chronic lesions
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6
Q

xx

A

Atopic dermatitis

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7
Q

What is atopic dermatitis?

A
  • Eczema is a broad term used to describe several inflammatory skin reactions; used synonymously with dermatitis.
  • By definition atopic dermatitis is a hypersensitivity response.

Etiology:

  • Type 1 (IgE) immediate hypersensitivity response
  • Atopic dermatitis is part of the atopic triad: allergic rhinitis, asthma, and eczema
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8
Q

What are the signs and symptoms of atopic dermatitis?

A
  • Patients complain of dry, pruritus, scaly skin. Scratching leads to lichenification
  • Pruritic, you can think of atopic dermatitis as “the itch that rashes”
  • Susceptible to secondary bacterial (S. aureus) and viral (herpes simplex virus) infections
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9
Q

How do we diagnose atopic dermatitis?

A
  • Clinical; supported by personal or family history of atopy

- Don’t’ culture skin in atopic dermatitis – 90% of atopic patients are carriers for S. aureus

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10
Q

How do we treat atopic dermatitis?

A
  • Topical corticosteroids are the mainstay of therapy
  • Oral antihistamines to help reduce itching
  • Lubricate dry skin
  • Oral antibiotics only if clinical signs of secondary infection
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11
Q

How does the presentation of atopic dermatitis change amongst the pediatric population?

A

Lesions vary with patient age:
- Infantile- red, exudative, crusty, and oozing lesions primarily affecting face (especially cheeks) and extensor surfaces. Nose and paranasal areas often spared, the diaper area is also spared

  • Juvenile/adult: dry, lichenified, pruritic plaques distributed over flexural areas (antecubital, popliteal, neck)
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12
Q

What is diaper dermatitis?

A
  • Irritant contact dermatitis: Prolonged dampness, interaction of urine (ammonia) and feces with the skin, reactions to medications/creams, type of diaper
  • Candida or bacterial secondary infection can occur with satellite lesions

Pathophysiology:
- Overhydrating, friction, maceration, allergy, etc.

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13
Q

What are the signs and symptoms of diaper dermatitis?

A
  • Red, scaly, fissured, eroded skin within the boarders of the diaper
  • Patchy or confluent
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14
Q

What is the treatment for diaper dermatitis?

A
  • Keep infant dry, change diapers often
  • Avoid harsh detergents, wipes with alcohol, and plastic pants
  • Ointment can reduce friction and protect skin from irritation
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15
Q

What is periorbital dermatitis?

A
  • Typically occurs in young women; often with a history or prior topical steroid use in the area exists
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16
Q

What are the signs and symptoms of periorbital dermatitis?

A
  • Papulopustules form on erythematous bases and may become confluent with plaques and scales, vermillion boarder is spared and satellite lesions are common
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17
Q

How do we treat periorbital dermatitis?

A
  • Use topical metronidazole or erythromycin or oral minocycline, doxycycline, or tetracycline
  • Untreated lesions will fluctuate over time, similar to rosacea
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18
Q

What are drug eruptions?

A
  • Abnormal immunologically mediated hypersensitivity responses
  • Relatively rare
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19
Q

What are the signs and symptoms of a drug eruption?

A
  • Mild rash to anaphylaxis
  • Fixed drug eruptions: recur at the same site after each administration of causative drug (sulfonamides are the most common)
  • Most are afebrile. May worsen before improving after discontinuation of the drug
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20
Q

How do we diagnose a drug eruption?

A
  • Eosinophilia is a clue but is not diagnostic
  • Skin test is available for penicillin. It is not indicated for the patients with a history of penicillin-associated anaphylaxis, urticarial, or serum sickness
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21
Q

What is the treatment for a drug eruption?

A
  • Discontinue likely offending agent
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22
Q

What are the most common causes of drug eruptions?

A
  • Potentially any drug can cause a drug reaction

- Most common causes of drug reactions: penicillin, sulfonamide

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23
Q

xx

A

Drug eruption

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24
Q

What is lichen planus?

A
  • This is an acute or chronic inflammatory dermatitis that occurs in adults.
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25
Q

What causes lichen planus?

A

?

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26
Q

What are the signs and symptoms of lichen planus?

A
  • Designated as the 4 P’s: purple, polygonal, pruritic and papule
  • Lesions are flat topped, shiny, violaceous papules with fine white lines on the surface (Wickham striae). They typically are grouped and most commonly occur on the flexor aspect of the wrists, lumbar area, eyelids, shins, and scalp. Koebner phenomenon is seen.
  • Lesions may affect hair (scarring alopecia) or nails (destruction of nail fold and nail bed with longitudinal splintering
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27
Q

How do we diagnose lichen planus?

A
  • Biopsy and immunofluorescence confirm diagnosis
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28
Q

What is the treatment for lichen planus?

A
  • Topical steroids with occlusive dressings are used
  • Intralesional steroids or topical tretinoin is used for severe localized lesions
  • Cyclosporine mouthwash is used for oral lesions
  • Systemic therapy (cyclosporine, corticosteroids, or retinoids) may be needed in severe, painful cases
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29
Q

What is pityriasis rosea?

A
  • Common, self-limited eruption of single herald patch followed by a generalized secondary widespread symmetrical papular eruption
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30
Q

What causes pityriasis rosea?

A
  • Unknown but us thought to be viral
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31
Q

What are the signs and symptoms of pityriasis rosea?

A
  • There may be a mild upper respiratory tract infection-like prodrome before onset of rash
  • Herald plaque- 2 to 10 cm solitary, oval, erythematous, with collarette of scale. It typically precedes rash by a week or so
  • After a few days to a few weeks, followed in 80% by generalized eruption of multiple smaller, pink, oval, scaly patches over trunk and upper extremities in a “Christmas tree” distribution (oriented parallel to ribs).
  • Pruritus
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32
Q

How is pityriasis rosea diagnosed?

A
  • Clinical
  • Rapid plasma reagin (RPR) to differentiate from syphilis if suspected, KOH to differentiate from fungal infection.
  • The herald patch may be mistaken for tinea corpis
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33
Q

What is the treatment for pityriasis rosea?

A
  • Self-limited, resolves in 3-8 weeks

- Symptomatic: the goal is to control pruritus (baths, calamine, topical corticosteroids, oral antihistamines)

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34
Q

xx

A

pityriasis rosea

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35
Q

xx

A

Steven-Johnson Syndrome

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36
Q

What is steven-johnson syndrome?

A
  • Extreme variant of erythema multiforme (EM) with systemic toxicity and involvement of the mucous membranes.
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37
Q

What causes steven johnson syndrome?

A
  • Often viruses (herpes) or drugs
  • Drugs: sulfonamides and anticonvulsants
  • Mycoplasma pneumonia, herpes simplex virus
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38
Q

What are the signs and symptoms of steven-johnson syndrome?

A
  • Prodromal phase (1-14 days): fever, headache, malaise
  • Severe mucous membranes involvement (oral, vaginal conjunctival). Oral erosions on the palate and gingivae.
  • Extensive target like lesions and mucosal erosions covering < 10% of body surface area. Annular, with pink halo surrounding a pale halo and erythematous center. Palms and soles are involved.
  • Nikolsky sign: separation of normal epidermis at the basal layer caused by sliding finger pressure (“rubbed off” line)
  • Ocular involvement (purulent uveitis/exudative conjunctivitis) may result in scaring or corneal ulcers
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39
Q

How is steven-johnson syndrome diagnosed?

A
  • Clinical criteria: cutaneous lesion plus at least two mucosal surfaces involved
  • Skin biopsy is diagnostic (would show perivascular mononuclear cell infiltrate)
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40
Q

How is steven-johnson syndrome treated?

A
  • Hospitalization for supportive care, IV hydration
  • Discontinue offending agent (if identified)
  • Mouthwashes, topical steroids and anesthetics, pain control as needed
  • Regrowth of skin for SJS and TEN takes 3 weeks and is delayed in pinpoint areas
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41
Q

xx

A

Toxic Epidermal Necrosis

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42
Q

What is Toxic Epidermal Necrosis?

A
  • Increased severe variant/progression of erythema multiforme with widespread involvement.
  • Widespread blister formation and morbilliform or confluent erythema with skin tenderness
  • Sudden onset and generalization within 24-48 hours
  • Can be life threatening
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43
Q

What are the signs and symptoms of Toxic Epidermal Necrosis?

A
  • TEN exhibits a higher fever and more severe epidermal separation and loss compared with SJS
  • Widespread, full-thickness necrosis of skin, covering > 30% body surface area
  • Abrupt onset of fever and influenza like symptoms
  • Pruritus, pain, tenderness and burning
  • Absence of target lesions
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44
Q

How do we diagnose Toxic Epidermal Necrosis?

A
  • Clinical; confirm biopsy
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45
Q

How is Toxic Epidermal Necrosis treated?

A
  • Removal and/or treatment of causative agent
  • Hospitalization for severe disease
  • Fluid and electrolyte replacement
  • Systemic corticosteroids
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46
Q

xx

A

Erythema Multiforme

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47
Q

What is Erythema Multiforme?

A
  • General name used to describe an immune complex-mediated hypersensitivity reaction to different causative agents
  • Previous history is a strong risk factor for subsequent cases
48
Q

What causes Erythema Multiforme?

A
  • Can be induced by drugs, viruses or can be idiopathic (50% of cases)
49
Q

What are the signs and symptoms of Erythema Multiforme?

A
  • Lesions begin as macules and become papular, and then vesicles and bullae form in the center of papules. Target or iris lesions are characteristic
  • Lesions cane be localized to the hands and feet or become generalized
  • Mucosal lesions (hallmark of EM major) are painful and erode
  • Patients complain of fever, weakness and malaise. Lungs and eyes may be affected.
50
Q

What is the treatment for Erythema Multiforme?

A
  • Avoid precipitating substances, and control herpes outbreaks with acyclovir
  • Severely ill patients are treated with systemic steroids 
51
Q

xx

A

Acne Vulgaris

52
Q

What is acne vulgaris?

A
  • Disorder of pilosebaceous glands

- Develops in areas with the greatest concentration of sebaceous glands

53
Q

What causes acne vulgaris?

A
  • Results from a combination of hormonal (androgens), bacterial (Propionibacterium acnes), and genetic factors
  • Plugged follicles, retained sebum, bacterial overgrowth, and release of fatty acids. Androgens stimulate sebum production.
54
Q

What are the signs and symptoms of acne vulgaris?

A
  • Comedone: plug of sebaceous and dead skin material stuck in the opening of a hair follicle; open follicle (blackhead- melanin deposits on a keratin plug) or almost closed (whitehead)
  • Pustules and papules
  • Painful nodules and cysts if severe
  • Seborrhea of face and scalp (greasy skin)
  • Depressed or hypertrophic scars may develop with healing
55
Q

How do we diagnose acne vulgaris?

A
  • Clinical; confirmed by presence of comedones
56
Q

How do we treat acne vulgaris?

A
  • Benzoyl peroxide wash
  • Topical antibiotics (clindamycin or erythromycin)
  • Intralesional corticosteroid injections (triamcinolone acetonide)
  • Oral isotretinoin (Accutane) for severe, recalcitrant, nodular acne. Accutane is a teratogenic and must be prescribed with oral contraceptives; it also has many side effects
57
Q

xx

A

Cellulitis

58
Q

What is cellulitis?

A
  • Cellulitis is an acute, spreading inflammation of the dermis and subcutaneous tissue
59
Q

What causes cellulitis?

A
  • H. influenza, Streptococcus sp., and Staphylococcus sp.
60
Q

What are the signs and symptoms of cellulitis?

A
  • The area involved is swollen, hot, red and tender

- The patient may have lymphadenopathy, fever, chills and malaise

61
Q

How is cellulits treated?

A
  • Mild or early infections may be treated with oral penicillinase-resistant penicillin, such as dicloxacillin or cephalosporin. For patient who are allergic to penicillin, erythromycin is appropriate
  • In severe infections, first-generation cephalosporins are given intravenously. Patients started on parenteral therapy may be switched to oral therapy when the fever, chills, and malaise subside
  • It may be appropriate to mark the margins of involvement before treatment to follow progression or regression of the area
62
Q

xx

A

Lice

63
Q

What is pediulosis?

A
  • Lice are 1- to 3-mm flat creatures with three pairs of legs. Females lay 300 nits during a lifetime. Nits are opalescent, found on hair shafts, and hatch in about 1 week.
64
Q

What is the cause of Pediculosis?

A

Etiology:

  • Pediculus humanus corporis
  • Pediculus humanus capitis
  • Pthirus pubis

Epidemiology:

  • Poor hygiene
  • Head-to-head contact, sharing hair items
  • Sexual contact
65
Q

What are the signs and symptoms of Pediculosis?

A
  • Corporis – primary lesions is an intensely pruritic, small, red macule or papule with central hemorrhagic punctum on shoulders, trunk or buttocks; secondary lesions include excoriations, wheals and eczematous, secondarily infected plaques
66
Q

How do we diagnose Pediculosis?

A
  • Nits detectable on hair fibers

- Specimens can be viewed under the microscope to confirm the diagnosis

67
Q

How do we treat Pediculosis?

A
  • Permethrin rinse – once, then again at 1 week (alternatives – pyrethrin, lindane) – first line treatment
  • Prevention is key; avoid sharing contact items, such as hats, hairbrushes and so forth. All contacts should be examined
  • Hot water laundering
  • Special combs to remove nits
68
Q

xx

A

Scabies

69
Q

What causes Scabies?

A
  • Female mite Sarcoptes scabiei hominis

Epidemiology:

  • Physical contact with infected individual
  • Rarely transmitted by fomites, as isolated mites die within 2-3 days
  • School children are especially at higher risk
  • Rarely in children younger than 3 months
70
Q

What are the signs and symptoms of Scabies?

A
  • Pruritus at initial infestation
  • First sign: 1 to 2 mm red papules, some of which are excoriated, crusted or scaling
  • Threadlike burrows, these are classic for scabies, but may not be seen in infants
  • Multiple types of lesions
  • Typical presentation is generalized, intense nocturnal itching, and the classic sites are hairless areas with a thin stratum corneum (interdigital web spaces of fingers and toes, popliteal fossae, flexor surfaces of the wrists, and gluteal region)
71
Q

How do we diagnose Scabies?

A
  • Scraping for microscopic identification of mites, ova and feces. A drop of mineral oil before scraping facilitates yield
72
Q

What is the treatment for Scabies?

A
  • Lindane or Permethrin, neck down, scalp only if involved; leave on 8-12 hours; may be repeated after 1 week
  • Infants are particularly susceptible to the neurotoxicity of lindane; therefore avoid
  • Alternatives include permthrin or sulfur ointment
  • Antihistamines or topical steroids to help with the itching
  • All bedclothes and clothing of infected patients and household contacts should be washed
  • All close physical contacts should receive treatment as well
73
Q

xx

A

Alopecia

74
Q

What is Alopecia Areata?

A
  • Total hair loss in localized area
75
Q

What causes Alopecia Areata?

A
  • Immunologic mediated loss of hair. Infiltration of lymphocytes may be relapsing/remitting in some children
76
Q

What are the signs and symptoms of Alopecia Areata?

A
  • Loss of every hair within an area

- Exclamation point hairs

77
Q

What is the treatment for Alopecia Areata?

A
  • High rates of spontaneous resolution/regrowth within 12 months
  • In some cases, steroids (systemic, topical or local injection)
  • Minoxidil or other immune modulation
78
Q

xx

A

Verrucae

79
Q

What are the signs and symptoms of Verrucae?

A
  • Skin warts can be flat or superficial. Plantar warts are deeper. The surface is rough, resembling tiny heads of cauliflower
80
Q

What causes Verrucae?

A
  • Warts are caused by the human papilloma virus (HPV). There are greater than 100 known serotypes
81
Q

How are Verrucae diagnosed?

A
  • Microscopic study shows characteristic hyperplasia and hyperkeratinosis. Koilocytotic squamous cells are present
  • The presence of HPV is confirmed by immunofluorescence.
82
Q

How are Verrucae treated?

A
  • Spontaneous regression is typical over time
  • Salicylic acid plasters can be effective for common warts. Cryosurgery or electrodessication can be effective but risks scarring
  • Surgical resection is successful but recurrence is common
83
Q

What are the types of burns?

A
  • Burns generally are classified as first, second, third and fourth degree. The classification of burns into a fourth degree is controversial, and many only use a three-tiered classification schema.
84
Q

What are first degree burns?

A

First degree burns involve minor damage to the epidermis

85
Q

What are second degree burns?

A

Second degree burns are subdivided into superficial partial-thickness burns that extend to the papillary dermis and deep superficial burns that extend into the reticular dermis

86
Q

What are third degree burns?

A

Third degree, or full-thickness, burns involve and destroy the epidermis and the dermis including the dermal appendages

87
Q

What are fourth degree burns?

A

Fourth degree burns destroy the skin and subcutaneous tissue, with further involvement of fascia, muscle, bone and other structures

88
Q

What are the most common type o burns?

A
  • Scald burns are the most common type of burn
89
Q

Where do burns typically occur?

A
  • Upper extremities most commonly
90
Q

What are the clinical features of a first degree burn?

A
  • First degree burns are characterized by erythema, tenderness, and the absence of blister
91
Q

What are the clinical features of a second degree burn?

A
  • Second degree burns (partial thickness)
    • Superficial second degree burns have thin-walled, fluid filled blisters; are moist; blanche with pressure and are painful

• Deep second degree burns have thicker walled blisters, many of which are ruptured, exhibit a mixture of erythema and pallor, and are painful with the application of pressure

92
Q

What are the clinical features of a third degree burn?

A
  • Third degree burns (full-thickness)
    • Third degree burns give the skin a white, leathery, or charred appearance
    • The skin is characteristically dry and without the presence of sensation
93
Q

What are the clinical features of a fourth degree burn?

A
  • Fourth degree burns

• Fourth degree burns are characterized by significant charring and exposure of muscles, fascia, tendons and ligaments

94
Q

What are fifth degree burns?

A
  • Fifth degree burns exist for coding purposes and are those burns that result in amputation of loss of a body part
95
Q

When should we worry about a burn affecting the airway or causing an inhalation injury?

A
  • Any burn that occurs on the face, on the upper torso, or in an unconscious patient should raise the suspicion for upper airway involvement
96
Q

What is important to remember with electrical burns?

A
  • In cases where burns are caused by electrical energy, the findings on the skin do not correlated with the extent of the clinical injury
97
Q

How do we classify the surface area of a burn?

A 
-	Estimate the percentage of burn
•	Rule of 9’s (only accurate for adults, does not apply to children)
•	Head: 9% 
•	Back: 9% 
•	Chest, abdomen and pelvis: 18% 
•	Genitals: 1% 
•	Gluteals 2.5% each 
•	Arms 9% each (4.5% front and back each)
•	Legs 14% each (7% front and back each)
98
Q

How do we treat burns?

A
  • Maintain ABCs
    • Airway: facial or neck burns, singed nose hair, hoarseness, or soot around the mouth or nares may indicated inhalational injury Assess for airway patency
    • Breathing: Check arterial blood gases (ABGs) and check CO levels
    • Circulation: IV fluid resuscitation
  • Parkland formula for IV/IO access, administer one-half over first 8 hours and remainder over next 16
  • Superficial and partial thickness burns:
    • Rapid and effective analgesia
    • Cold compress
    • Antiseptic cleansing
    • Debride open blisters
    • Topical antibiotic (silver sulfadiazine)
    • Protect with bulky dressing
    • Reexamine in 24 hours and serially after healing and infection
  • Full thickness or extensive partial thickness
    • ABCs of trauma, especially airway
    • Fluid and electrolyte replacement (as above)
    • Sedation and analgesia is usually necessary
    • Clean and manage as above
99
Q

When is a burn suspicious for abuse?

A
  • Burns indicating abuse generally do not have a splash pattern, but more linear (e.g., placing a child in a hot bath
100
Q

xx

A

Urticaria

101
Q

What is Urticaria?

A
  • Urticaria is a group of disorders that can have many causes, most commonly food or drug allergies, heat or cold and stress or infection
  • Hives or wheals are raised areas on the skin or mucous membranes caused by the release of histamines and other vasoconstrictive substances from mast cells and basophils in the skin.
  • The lesions most commonly are pruritic but may sting or burn
102
Q

What causes Urticaria?

A
  • Type 1 hypersensitivity reaction of immunoglobulin E (IgE) with mast cells causes the release of histamine, leading to vasodilation and an increase in vascular permeability and axonal response.
103
Q

What are the signs and symptoms of Urticaria?

A
  • Urticaria- well circumscribed, but can be coalescent, erythematous raised lesions (wheals or welts)
  • Raised pale and pink pruritic areas of annular or serpiginous pattern.
  • Rash often migratory, waxing and waning
  • The lesions are typically pruritic and erythematous, often showing a central clearing. Systemic symptoms develop if it is associated with anaphylaxis.
104
Q

How do we diagnose Urticaria?

A
  • Clinical; no tests needed
105
Q

How do we treat Urticaria?

A
  • Avoiding the precipitating cause
  • Usually self limited
  • Antihistamines to relieve pruritus
  • Epinephrine or steroids for severe cases
106
Q

xx

A

Tinea

107
Q

What is Tinea?

A
  • Group of noninvasive fungi that can infect keratinized tissue of epidermis, nails and hair
  • Clinical presentation depends on anatomical site of infection and is named accordingly
108
Q

What causes tinea?

A

Etiology:
- Trichophyton, Microsporum, Epidermophyton

Epidemiology:
- Exacerbated by warm, humid climates

109
Q

What are the signs and symptoms of tinea?

A
  • Generally dermatophytosis presents as an erythematous, annular patch with distinct borders and a central clearing. A fine scale usually covers the patch
  • Symptoms include itching, stinging and/or burning. Maceration or peeling fissures are common between digits.
  • A kerion (indurated, boggy, inflammatory plaque studded with pustules can be seen in any of these but is most common with tinea capitis
  • Tinea corporis (“ring worm”): body. Lesions are annular with peripheral scale and central clearing
  • Tinea versicolor: superficial, asymptomatic. Has hyphae and yeast forms in a “spaghetti and meatball” distribution on KOH preparation.
110
Q

How do we diagnose tinea?

A
  • Clinical presentation and history
  • KOH preparation reveals multiple, septated hyphae
  • Wood’s lamp reveals bright green fluorescence of hair shaft in tinea capitis
  • Fungal culture of affected area may demonstrate dermatophyte
111
Q

How do we treat tinea?

A
  • Prevention: wearing well-ventilated shoes and clothing
  • Topical antifungal agents (imidazoles and terbinafine)
  • Systemic antifungal agents if unresponsive to topical or if involvement of nails or hair (griseofulvin, systemic azoles, terbinafine). Griseofulvin can cause elevation of liver enzymes.
  • Mild-potency topical corticosteroids if inflammation and pruritus are severe
112
Q

xx

A

Impetigo

113
Q

What is impetigo?

A
  • Contagious, superficial, bacterial infection transmitted by direct contact

Pathophysiology:
- Only epidermis is affected

  • The bacteria colonize unbroken skin and, with abrasions or bites, inoculate the intradermal space, where lesions develop
114
Q

What causes impetigo?

A
  • Nonbullous impetigo (70%)- Streptococcus Pyoderma

- Impetigo can also be caused by Staphylococci (bullous impetigo) – most commonly infects neonates

115
Q

What are the signs and symptoms of impetigo?

A
  • Mild burning or pruritus
  • Initial lesion is a transient erythematous papule or thin-roofed vesicle that ruptures easily and forms a characteristic thick, crusted, golden “honey” yellow lesions
  • Lesions can progress for weeks if untreated
116
Q

How do we diagnose impetigo?

A
  • Clinical; can confirm with Gram stain and culture showing gram-positive cocci in clusters (S. aureus) or chains (GAS)
117
Q

How do we treat impetigo?

A
  • Remove crusts by soaking in warm water
  • Antibacterial washes (benzoyl peroxide)
  • Topical antibiotics if disease is limited (Bactroban) - Mupirocin
  • Oral antibiotics (cephalexin or macrolide) if more severe

End of Rotation: Pediatrics (12 decks)

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