✅DDx: Skin Cancer / Common dermatologic conditions

Question 1

Differential Diagnosis of Melanoma:

Answer 1

• In a patient who has multiple pigmented lesions, a lesion with an appearance that is substantially different from the others (eg, dark brown rather than light brown, nodule rather than flat) may represent melanoma (“ugly duckling sign”). The “ugly duckling sign” has a sensitivity of up to 90% for melanoma.
• Vertical growth of a melanoma often corresponds to a palpable nodularity, as in this patient, and increases metastatic risk. The Breslow depth (distance from the epidermal granular cell layer to the deepest visible melanoma cells) is the most important prognostic indicator in malignant melanoma.
• Benign pigmented lesions are usually asymptomatic; therefore, biopsy should be considered for moles that itch or bleed, particularly in the presence of other concerning features.

If melanoma is suspected, the patient should undergo excisional biopsy with initial margins of 1-3 mm of normal tissue.

Question 2

Melanoma

Answer 2

Classically a pigmented macule or plaque that is asymmetric and has irregular, notched, scalloped, or poorly defined borders. The lesion usually has shades of brown, tan, red, white, blue-black, or combinations thereof.

Hx: Backs of men and legs of women

ABCDE of Melanoma:

Asymmetry: a lesion that is not regularly round or oval.

Border irregularity: a lesion with notching, scalloping, or poorly defined margins.

Color variegation: a lesion with shades of brown, tan, red, white, or blue-black, or combinations thereof.

Diameter: a lesion >6 mm in diameter; although a high level of suspicion exists for a lesion >6 mm in diameter, early melanomas may be diagnosed at a smaller size.

*Evolution: a lesion that changes in size, shape, symptoms (itching, tenderness), surface (bleeding), or shade of color.

Superficial spreading melanoma presents as a variably pigmented plaque with an irregular border and expanding diameter ranging from a few millimeters to several centimeters. It can occur at any age and anywhere on the body, although it is most commonly seen on the back in men and on the legs in women. Most superficial spreading melanomas appear to arise de novo. Superficial spreading melanoma accounts for approximately 70% of melanoma cases.

Nodular melanoma presents as a dark blue or black “berry-like” lesion that expands vertically (penetrating skin). It most commonly arises from normal skin and is most often found in people age 60 years or older. Nodular melanoma accounts for approximately 15% of melanoma cases.

Dx: Excisional biopsy. Fully excising the lesion allows for both assessment of the degree of cytologic atypia and the depth of invasion (termed the Breslow depth), which is the most significant prognostic feature of melanomas and is used to guide therapy.

Lentigo maligna melanoma presents initially as a freckle-like, tan-brown patch. When confined to the epidermis, the lesion is called lentigo maligna type. The lesion may be present for many years before it expands and becomes more variegated in color. When it invades the dermis, it becomes melanoma. It most often arises in sun-damaged areas (face, upper trunk) in older people. Lentigo maligna melanoma accounts for approximately 10% of melanoma cases.

Acral lentiginous melanoma can present in a variety of ways, including as a longitudinal dark pigmented streak on a fingernail or toenail, dark pigmentation of a proximal nail fold, and dark pigmented patches on the palms or soles. This variant of melanoma is the most common type among Asian and dark-skinned people. Acral lentiginous melanomas account for only 5% of melanoma cases.

Question 3

Basal cell carcinomas (BCC)

Answer 3

Basal cell carcinoma is the most common type of skin cancer (75% of all skin cancers) and usually presents as a pearly papule or plaque with small telangiectasias on sun-exposed areas (head and neck). The most important risk factors for the development of BCCs are fair skin and sun exposure (the same risk factors as for AKs), the two often occur in the same area.

Possible features of BCC include:

• Persistent open sore that bleeds, oozes, or crusts
• Reddish patch or irritated area (superficial BCC)
• Pearly or translucent nodule with pink, red, or white color (nodular BCC)
• Elevated or rolled border with central ulceration
• Pale scar-like area with poorly defined borders

Nodular BCC (~60% of BCC)

A skin-toned to 🀄pink, pearly translucent, firm papule with telangiectasias. May have rolled borders and a central depression with ulceration. The most readily recognized clue to the diagnosis of a BCC is a changing skin lesion, including ulceration or erosion that spontaneously bleeds. Often found on the head or neck.

Px: Sun-exposed areas face, neck, trunk legs.

Superficial BCC (~30% of BCC)

A well-defined, erythematous, scaling plaque or occasional papules with a thin pearly border. Larger lesions often have hemorrhagic crusts and occur predominately on the trunk. A complete skin examination to find other similar plaques may help distinguish the solitary lesion of superficial BCC from psoriasis.

Morpheaform BCC (~5-10% of BCC)

A skin-colored, waxy, scar-like area that slowly enlarges. Usually develops on the head or neck of an older person. The name is based on its resemblance to morphea (scleroderma).

Tx:

Low-risk lesions on the trunk or extremities can be managed with electrodessication and curettage (ED&C). However, ED&C is not recommended for higher-risk lesions or for BCC on the face, where the resulting scarring and hypopigmentation are undesirable.

Nodular BCC on the trunk or extremities may be easily managed with standard surgical excision, typically with 3-5 mm margins.

Mohs micrographic surgery is employed more often for the face. Mohs surgery is characterized by sequential removal of thin skin layers with microscopic inspection to confirm that the margins have been cleared of malignant tissue. This technique currently has the highest cure rate for BCC and provides the least disruption to surrounding tissues, making it ideal for delicate or cosmetically sensitive areas (eg, perioral region, nose, lips, ears).

Question 4

Squamous cell carcinoma (SCC)

Answer 4

Squamous cell carcinoma is the second most common skin cancer and occurs primarily on sun-exposed areas.

SCC should be suspected in patients with a rough, scaly nodule or nonhealing, painless ulcer that develops in the setting of a scar or chronic inflammatory lesion. Sun exposure is the most common cause of SCC, but other risk factors include radiation exposure; immunosuppression; and chronic wounds, burns, or scars.

Hx: Risk factors include smoking and alcohol consumption; for lesions that occur on the ear, lips, chronic sun exposure is an additional risk factor. SCC is especially common in patients who have a history of organ transplant and are on chronic immunosuppressive therapy. SCC in immunosuppressed patients is typically more aggressive, with an increased risk of local recurrence and regional metastasis.

SCC arising within a 🔥burn wound is known as a Marjolin ulcer. In addition, SCC has been seen within the skin overlying a focus of osteomyelitis, radiotherapy scars, and venous ulcers. SCC arising within chronic wounds tends to be more aggressive, so early diagnosis with biopsy is important for preventing metastatic disease.

Hx: Presents as a firm, isolated, flesh-colored, pink or red ulcerated keratotic macule, papule, or nodule commonly found on the scalp, neck, pinna, or lip (most common type of malignancy on the lips and oral cavity). Generally consist of red plaques or nodules that may be covered with scale, crust, and erosions. The lesions often become keratinized (with a thickened, rough surface) or ulcerate with crusting and bleeding.

Keratoacanthomas are red, volcano-like nodules with a prominent central keratin plug. They are considered to be a subtype of well-differentiated squamous cell carcinoma. They grow rapidly and may reach a size of several centimeters within a few weeks. Classic keratoacanthomas eventually stabilize in size and may spontaneously regress without treatment.

Bowen Disease: A solitary, sharply demarcated, pink to fiery red scaly plaque that resembles superficial BCC, psoriasis, or eczema. May have a keratotic surface. Most commonly occurs on sun-exposed areas.

The diagnosis of SCC should be confirmed with skin biopsy (punch, shave, or excisional) that includes the deep reticular dermis to assess the depth of invasion. Small or low-risk lesions are usually managed with surgical excision or local destruction (eg, cryotherapy, electrodessication); lesions that are high risk or located in cosmetically sensitive areas should be referred for Mohs micrographic surgery.

Question 5

Actinic keratosis (AK)

Answer 5

Common erythematous scaly macules that typically occur on sun-exposed areas of older persons with fair skin.

AKs are premalignant (squamous cell precursor) lesions that occur in sun-damaged areas. Approximately 1% to 5% will develop into squamous cell carcinomas over time.

Early lesions (1-3 mm) often are felt, not seen, and have a rough sandpaper texture. Color ranges from skin-colored to pink to red to brown. Occur on sun-damaged skin. Early superficial BCC may look like early actinic keratosis. With time, superficial BCC develops a rolled border and actinic keratoses get a thicker keratotic scale.

Tx: Multiple treatment options are available, including cryotherapy (3 ten- second freeze thaw cycles), topical imiquimod, topical 5-fluorouracil, and photodynamic therapy.

Question 6

Common nevi (moles)

Answer 6

Nevi can become elevated and may be irritated by clothing, causing inflammation and bleeding. Nevi can undergo progressive loss of color over time. By age 60 y, nevi may be flesh-colored, dome-shaped, soft papules. Even inflamed nevi do not have overlying telangiectasias.

Congenital melanocytic nevus (CMN) is a benign proliferation of melanocyte cells. CMNs present within the first few months of life and are usually solitary, hyperpigmentedlesions with an increased density of overlying dark, coarse hairs. Initially presenting with flat homogenous hyperpigmentation, CMNs can grow during infancy and appear as heterogeneously pigmented and raised.

The risk of transformation to melanoma increases (up to 5%) with increasing size of a CMN, and large lesions are often removed surgically to reduce risk. Small lesions may be removed for cosmetic reasons given their low risk of melanoma transformation.

Nevus simplex and nevus flammeus are flat, blanchable, and erythematous vascular birthmarks. Nevus simplex lesions are typically located on the eyelids, glabella, and nape of the neck and fade with time; nevus flammeus lesions (port-wine stains) do not regress with time and are usually unilaterally located on the face.

Question 7

Sebaceous hyperplasia

Answer 7

Results from enlargement of the sebaceous oil glands, producing single or multiple small umbilicated pink or yellowish papules on the face. The main distinguishing features are the pink or yellowish color, the absence of telangiectasias, and the absence of translucency (“pearliness”) that is seen in BCCs.

Benign, 2- to 4-mm papules with a characteristic yellow color and central umbilication. Occur in clusters on the face without telangiectasia or bleeding.

Question 8

Actinic purpuras

Answer 8

Well-demarcated, smooth, reddish-violet patches that occur in elderly patients with significantly sun-damaged skin; they are indicative of skin fragility. They invariably arise from trauma, although often the inciting event is so mild as to escape notice. They typically occur on the dorsal arms and pretibial lower legs; patients on anticoagulant agents often have prominent lesions. They may heal with postinflammatory hyperpigmentation, which can sometimes mimic lentigo maligna.

Question 9

Solar lentigines

Answer 9

Solar lentigines are brown macules and patches that occur in elderly fair-skinned persons in areas of substantial sun damage. They are benign but are indicative of a region that is at risk for developing skin cancer because they are a marker for sun exposure.

Question 10

Actinic cheilitis

Answer 10

A chronic erythema and scaling of the lower lip caused by extensive sun damage. It is a precancerous condition. Appears as a rash rather than a tumor; however, any bulky area should be biopsied to rule out SCC.

Tx: Often treated with cryotherapy, topical 5-fluorouracil, or laser ablation to reduce the risk of malignant transformation.

Question 11

Lichen planus

Answer 11

Clinical findings

• 5 “Ps”: pruritic, 💜 purple/pink, polygonal papules & plaques
• Lacy, white network of lines (Wickham striae)

Disease associations

• Hepatitis C
• Medications: ACE inhibitors, thiazide diuretics

Natural history

• Chronic symptoms
• Formation of lesions at sites of trauma (Köbner reaction)
• Spontaneous resolution within 2 years

Treatment

• Topical high-potency glucocorticoids (eg, betamethasone)
• Widespread lesions: systemic glucocorticoids, phototherapy

The skin lesions in LP are characterized by the “5 P’s”: pruritic, purple/pink, polygonal papules and plaques. The lesions often show white, lacy markings known as Wickham striae and can form along lines of minor trauma or scratching (Köbner phenomenon).

LP is usually idiopathic, although it is often seen in patients with hepatitis C. However, drug-induced LP (lichenoid drug reaction) has been associated with a number of medications, including ACE inhibitors, thiazide diuretics, beta blockers, and hydroxychloroquine. Drug-induced LP typically has a more diffuse presentation than idiopathic LP, which is frequently limited to the flexor surfaces of the wrists and ankles, oral mucosa, and genitalia.

Treatment of drug-induced LP includes topical high-potency glucocorticoids and discontinuation of the offending medication. Some patients may develop recurrent bouts despite drug discontinuation, and residual hyperpigmentation is common.

Question 12

lentigo maligna

Answer 12

a slow-growing type of melanoma most commonly seen on the face of older fair-skinned persons who have received a substantial amount of cumulative sun exposure with resultant evidence of sun damage. It has a prolonged radial growth phase and can be present for many years before developing an invasive component (vertical growth phase). Once it becomes invasive, the staging and prognosis are identical to those of other types of melanoma.

Question 13

Ddx: Skin Infections (Bacterial)

Answer 13

Cellulitis

Erysipelas

Folliculitis

Furuncles

Impetigo

Ecthymia

Question 14

Cellulitis

Answer 14

A rapidly spreading deep subcutaneous dermis-based infection most often caused by S. aureus or group A streptococci.

Hx: Risk factors for lower extremity cellulitis include eczema, tinea pedis, onychomycosis, skin trauma (including insect bites, drug injection), chronic leg ulcers, long-standing diabetes mellitus, and edema. Risk factors for MRSA infection include recent close contact with persons having a similar infection, recent antibiotic use, recent hospitalization, hemodialysis, injection drug use, diabetes, and previous MRSA colonization or infection.

Px: Characterized by a well-demarcated area of warmth, swelling, tenderness, and erythema. possibly accompanied by lymphatic streaking or fever and chills.

Tx: Cellulitis without Purulence: Probable β-hemolytic streptococci or MSSA; MRSA unlikely.

Oral : Dicloxacillin, Cephalexin, Clindamycin

Intravenous: Oxacillin, Nafcillin, Cefazolin, Clindamycin

Cellulitis with Purulence: Probable MRSA; risk factors for MRSAc; failure to respond to non-MRSA therapy:

Oral: Trimethoprim–sulfamethoxazole, Clindamycin, Doxycycline, Minocycline, Linezolid

Intravenous: Vancomycin, Linezolid, Daptomycin

$ Cephalexin

$ Dicloxacillin

$ Doxycycline

$ Trimethoprim–sulfamethoxazole

$$ Clindamycin

$$ Minocycline

$$$ Linezolid

Question 15

Erysipelas

Answer 15

A superficial skin infection involving the upper dermis and superficial lymphatics.

Px: It is usually erythematous in appearance (“St. Anthony’s fire”) with well-demarcated borders and is almost always caused by group A streptococci.

Tx: Treatment is usually a β-lactam antibiotic (eg, penicillin or amoxicillin).

Question 16

Folliculitis

Answer 16

A pustular skin infection in the hair follicle. Causes include S. aureus and, less frequently, group A streptococci.

Px: Typically affects the beard, pubic area, axillae, and thighs.

Tx: Folliculitis often is effectively treated with local application of heat and a topical antibiotic (mupirocin, chlorhexidine cleanser).

“Hot tub folliculitis” infection is generally caused by Pseudomonas aeruginosa
or Pseudomonas cepacia. The condition is usually self-limited, and therefore reassurance is all that is necessary. Antibiotic therapy is only indicated in recalcitrant
cases, or if patients are symptomatic.

Question 17

Furuncles (boils/skin abscess)

Answer 17

Tender, pus-containing nodules that commonly appear on the neck or in the axillae or groin but may occur at any skin site

Boil: infection of the hair follicle that extends into the dermis and subcutaneous tissues

Abscess: Pus collections in the dermis and deeper tissues

Hx: Nearly always are caused by S. aureus.

Dx: Cultures from purulent material can distinguish MRSA from methicillin-susceptible S. aureus (MSSA) and can guide treatment.

Tx: Warm compresses to facilitate drainage may be adequate therapy for small furuncles. Incision and drainage (I & D) is required for larger furuncles and all abscesses. Incision and drainage may be adequate therapy for skin abscesses, and systemic antibiotics are not routinely required. However, they may be indicated if the patient is febrile or immunocompromised, has diabetes, or is at risk for MRSA or if there is a surrounding cellulitis

Question 18

Impetigo

Answer 18

A superficial infection of the skin (epidermis) characterized by a group of yellowish, crusted pustules. caused by staphylococci (staph aureus) or streptococci.

Hx: Predisposing factors include poor hygiene, neglected minor trauma, and eczema.

Tx: Limited disease usually can be treated effectively with topical mupirocin or bacitracin; more extensive disease can be treated with a cephalosporin, penicillinase-resistant penicillin, or β-lactam-β-lactamase inhibitor.

Question 19

Ecthyma

Answer 19

An ulcerative form of impetigo usually caused by streptococci or staphylococci.

Px: The classic findings are superficial, saucer-shaped ulcers with overlying crusts, typically on the legs or feet.

Tx: Effective treatment consists of cleansing with an antibacterial wash followed by topical mupirocin plus oral cephalexin, dicloxacillin, or clindamycin. If MRSA is suspected or there is β-lactam allergy, one should consider other options.

Question 20

Ecthymia Gangrenosum

Answer 20

Ecthyma gangrenosum is an ulcerative infection involving the dermis usually caused by Pseudomonas aeruginosa.

Hx: It is usually seen in immunocompromised patients and may indicate pseudomonal sepsis.

Px: Classic findings are ulcers with a central gray-black eschar and erythematous halo, typically on the legs or feet.

Tx: Initial therapy usually involves an antipseudomonal penicillin plus an aminoglycoside.

Question 21

FUNGAL

Question 22

Risk factors for dermatophyte infection

Answer 22

Environmental exposures

• Warm, humid environments
• Direct contact with infected person, fomites, or public showers
• Contact with animals (eg, kittens)

Patient factors

• Concurrent dermatophyte infection (autoinoculation)
• Occlusive clothing
• Obesity
• Peripheral artery disease

Immune deficiency

• Diabetes mellitus
• HIV infection
• Systemic glucocorticoid therapy

Question 23

Tinea capitis

Answer 23

Caused by T. tonaurans

Tx: Systemic therapy is necessary for a cure,

Griseofulvin is considered the treatment of choice in the United States, and should be used for 4 to 8 weeks.

Terbinafine, itraconazole, fluconazole, and ketoconazole can also be used. If fluconazole were to be used, the treatment duration would only be for 3 to 4 weeks.

Topical ketoconazole shampoo or selenium sulfide lotion may kill spores on the hair.

Question 24

Tinea corporis (“ringworm”)

Answer 24

Risk factors

• Athletes who have skin-to-skin contact
• Humid environment
• Contact with infected animals (eg, rodents)

Presentation

• Scaly, erythematous, pruritic patch with centrifugal spread
• Subsequent central clearing with raised, annular border

Treatment

• First-line/localized: topical antifungals
• (eg, clotrimazole, terbinafine)
• Second-line/extensive: oral antifungals
• (eg, terbinafine, griseofulvin)

Tinea corporis is a cutaneous dermatophyte infectionmost commonly caused by Trichophyton rubrum. Patches of tinea corporis are typically annular but may become confluent to form a “flower petal” shape.

Patients with tinea corporis often have concurrent infection elsewhere on the body, hands (tinea manuum), groin (tinea cruris), or between the toes or sides of the feet (tinea pedis). Those with immunocompromising conditions (eg, HIV, diabetes mellitus) can have severe or widespread disease. Other risk factors include exposure to warm, moist areas (eg, public showers, swimming pools), contact with infected animals or people (eg, during sports participation), and wearing tight or occlusive clothing.

The diagnosis is confirmed using potassium hydroxide (KOH) preparation of skin scrapings. Most cases can be treated with topical antifungals (eg, terbinafine, clotrimazole); patients who fail topical therapy or have extensive disease may need systemic therapy (eg, oral terbinafine, fluconazole).

Question 25

Tinea cruris

Answer 25

Caused by *T mentagrophytes* Occurs in the groin

Question 26

Tinea versicolor (pityriasis versicolor)

Answer 26

Pathogenesis * Malassezia globosa skin flora grows in exposure to **hot & humid weather** Clinical features * Hypopigmented, hyperpigmented, or mildly erythematous lesions (face in children, trunk & upper extremities in adolescents & adults) * ± Fine scale * ± Pruritus Diagnosis * KOH preparation shows hyphae & yeast cells in a "spaghetti & meatballs" pattern Treatment * Topical ketoconazole, terbinafine, or selenium sulfide Tinea versicolor (pityriasis versicolor) is a superficial fungal skin infection caused by Malasseziaspecies (nondermatophytic, lipid-dependent yeasts; eg, M globosa, M furfur). It is characterized by salmon-colored, **hyper- or hypopigmented macule**s that are sometimes covered by fine scales, most commonly on the upper trunk and extremities. Hypopigmented areas are frequently noticed following sun exposure due to tanning of the surrounding skin. **Potassium hydroxide (KOH)** preparation of skin scrapings shows large, blunt hyphae and thick-walled budding yeast ("spaghetti and meatballs" appearance). Topical treatment with selenium sulfide or ketoconazole is recommended, but the pigmentation changes can take months to resolve following treatment.

Question 27

Acne

Answer 27

The true cause is multifactorial, but familial factors are involved. The key factors are follicular keratinization, angrogens, and **Propionibacterium acnes**. In acne, the kertatinization pattern in the pilosebaceous unit changes, and keratin becomes more dense, blocking the secretion of sebum. The keratin plugs are called “comedones.” **Hx:** actors contributing to acne vulgaris include increased sebum production, follicular hyperkeratinization, bacterial colonization (Propionibacterium acnes), and, in some cases, an inflammatory response. Contributory factors to acne include certain medications, emotional stress, and occlusion and pressure on the skin, such as by leaning the face on the hands **(acne mechanica)**. Acne is **not** caused by dirt, chocolate, greasy foods or the presence or absence of any foods in the diet. **Tx:** Initial management of comedonal acne without a significant inflammatory component includes: **Topical retinoids** with the addition of: * **Organic acid preparations (eg, salicylic, azelaic, or glycolic acid)** if initial therapy fails. * **Benzoyl peroxide,** a widely used antibacterial agent, is another option for patients with comedonal acne, although it is preferred for inflammatory acne. Some patients with comedonal acne will develop inflammatory features, and benzoyl peroxide can be added at that time. * **Topical antibiotics (eg, erythromycin, clindamycin)** is used in most patients with moderate or moderate-to-severe inflammatory acne require . * **Oral antibiotics (eg, tetracyclines)** are reserved for patients with severe or nodular acne and for moderate inflammatory acne unresponsive to topical antibiotics. Oral antibiotics are also considered in patients with widespread inflammatory acne (eg, back, upper arms) that makes topical therapy impractical. * **Oral isotretinoin** is indicated for **nodular acne, severe acne, or moderate recalcitrant acne.** 🕷 In addition, since both tetracycline and isotretinoin cause pseudotumor cerebri, the two medications should never be used together. **Drug-induced acne** (also called steroid-induced folliculitis or steroid acne) Drug-induced acne is typically associated with systemic 🌑 **glucocorticoids** but can also be caused by topical **glucocorticoids**, **glucocorticoid-sparing agents** (eg, a**zathioprine, cyclosporine**), and a variety of other drugs (eg, anticonvulsants, antituberculous drugs). In contrast to acne vulgaris (which displays lesions in various stages of development and typically occurs on the face in adolescents), drug-induced acne can be seen in any age group, is characterized by monomorphic papules without associated comedones, and commonly involves the **upper back, shoulders, and upper arms**. Some patients may have small pustules, but lesions are found in the same stage of development, and scarring cystic and nodular lesions are not seen. Drug-induced acne does not respond to typical acne treatment but improves rapidly on **discontinuation of the offending agent.**

Question 28

Acute urticaria (hives)

Answer 28

Urticaria is due to mast cell activation in the superficial dermis, which increases release of multiple mediators (eg, histamine) that cause pruritus and localized swelling in the upper layers of the skin. Urticaria can be accompanied by angioedema, which is due to mast cell activation in the deeper dermal and subcutaneous tissues (eg, face, hands, and buttocks). Etiologies of acute urticaria include infections (viral, bacterial, and parasitic), nonsteroidal antiinflammatory drugs, and IgE-mediated (eg, **antibiotics, insect bites, latex, food**) or direct (eg, **narcotics, radiocontrast medium, muscle relaxers**) mast cell activation. However, **nearly 50% of patients have no known cause (idiopathic urticaria)**. Chronic urticaria can be due to physical stimuli (eg, cold temperature, skin pressure), serum sickness, or systemic disorders (eg, autoimmune disease, vasculitis, malignancy). Patients with acute urticaria usually develop well-circumscribed and raised erythematous plaques with central pallor. The lesions can be **oval, round, or serpiginous,** and up to several centimeters in diameter. Patients usually have intense **pruritus** that can persist at night. Individual lesions appear and enlarge over minutes to hours before disappearing within 24 hours. **Tx:** An **H1-blocking nonsedating antihistamine (e.g., cetirizine [Zyrtec])**, which will stop the likely allergic cause of her urticaria. A short course of **systemic glucocorticoids** may also be helpful for patients with widespread or highly symptomatic involvement. In persistent cases, an **H2**-blocking antihistamine is sometimes added, although the effectiveness of doing so has not been established. **Topical corticosteroids** can occasionally provide additional relief for symptomatic urticarial lesions **❗Concerning features:** wheezing; stridor; and lip, tongue, or eyelid swelling; dyspnea, difficulty clearing secretions, or hemodynamic instability **Tx:** Administration of **epinephrine** would be indicated.

Question 29

Atopic Dermatitis (eczema)

Answer 29

Atopic dermatitis (eczema) is a very common condition characterized by pruritus, erythema, and scaly lesions on the skin. Pathogenesis involves epidermal dysfunction due to improper synthesis of stratum corneum components. Allergens can enter the disrupted skin barrier and generate an inflammatory response. Excessive bathing, dry environments, stress, overheating, and irritating detergents can trigger flares. Eczematous lesions usually begin with pruritus alone and evolve to erythematous papules and scaly plaques. Severe lesions may have serous exudates and crusting. Infants typically have lesions in the distribution of the face, scalp, and **extensor surfaces** of the extremities. The lesions can also be seen in **flexural** **creases** in older children and adults. Treatment includes trigger avoidance, frequent application of thick bland emollients, and use of hypoallergenic cleansers for bathing and laundry. Moderate and severe eczema may require **topical anti**-**inflammatory** ointments (eg, **hydrocortisone**).

Question 30

Dermatofibromas

Answer 30

Dermatofibroma (DF) is due to fibroblast proliferation causing isolated or multiple lesions, most commonly on the lower extremities. The etiology is unknown, but some patients may develop lesions after trauma or insect bites. Typical lesions are nontender and appear as discrete, firm, hyperpigmented nodules that are usually \<1 cm in diameter. The lesions have a fibrous component that may cause dimpling in the center when the area is pinched **("dimple" or "buttonhole" sign).** Diagnosis of DF is made clinically based on the appearance of the lesion. Treatment (cryosurgery or shave excision) is usually not required unless the lesion is symptomatic, bleeds, or changes in color or size. Patients may also request treatment for cosmetic reasons or because of recurrent cuts when shaving the legs.

Question 31

Epidermoid inclusion cyst

Answer 31

The **most common** type of skin cyst is an epidermoid inclusion cyst. A discrete benign nodule lined with squamous epithelium that contains a semisolid core of keratin and lipid. An EIC occurs when the epidermis becomes lodged in the dermis due to trauma or comedones, or it can arise de novo. EICs can be seen anywhere on the body, but are most common on the face, neck, scalp, or trunk. The lesion can gradually increase in size and may intermittently produce a cheesy white discharge. Some patients may develop significant inflammation with rupture and involvement of surrounding tissue. An EIC will usually resolve spontaneously but can recur. Diagnosis is made clinically with examination showing a dome-shaped, firm, and freely movable cyst or nodule with a central **punctum (small, dilated, pore-like opening).** Excision is typically performed only for cosmetic reasons. Incision and drainage are occasionally needed for infected and fluctuant cysts that are painful and erythematous.

Question 32

Keratocanthoma

Answer 32

Red, volcano-like nodules with a prominent **central keratin plug.** They are considered to be a subtype of well-differentiated squamous cell carcinoma. They **grow rapidly** and may reach a size of several centimeters within a few weeks. Classic keratoacanthomas eventually stabilize in size and may spontaneously regress without treatment.

Question 33

Erythema multiforme (EM)

Answer 33

erythema multiforme (EM), which is an acute, often recurrent mucocutaneous eruption that usually follows an acute infection, most frequently recurrent **herpes simplex virus (HSV)** infection. It may also be idiopathic or drug related. Most patients are between 20 and 40 years of age. Lesions range in size from several millimeters to several centimeters and consist of erythematous plaques with **concentric rings** of color. The **dusky center** may become necrotic and can form a discrete blister or eschar. Few to hundreds of lesions develop within several days and are most commonly located on the extensor surfaces of the extremities, particularly the hands and feet. Lesions occur less frequently on the face, trunk, and thighs. Mucosal lesions are present in up to 70% of patients and involve the cutaneous and mucosal lips, gingival sulcus, and the sides of the tongue. Mucosal lesions consist of painful erosions or, less commonly, intact bullae. The conjunctival, nasal, and genital mucosal surfaces can also be affected. Patients may have low-grade fever during an EM outbreak. Lesions usually last 1 to 2 weeks before healing; however, hyperpigmentation may persist. Recurrences are common, particularly in HSV-associated infection. Treatment of EM is primarily symptomatic. Systemic corticosteroids may provide symptomatic improvement but may be associated with complications. Antiviral therapy does not shorten the EM outbreak in HSV-associated infection, but continuous prophylactic antiviral therapy may help prevent further episodes. Treatment for bacterial infection-associated EM is appropriate for management of the specific active infection; however, there are no studies that demonstrate that treatment impacts the duration of the EM lesions. Antibiotic therapy is based on identification of an infectious cause. If EM is thought to be due to a new drug, the drug should be discontinued.

Question 34

Herpes zoster ophthalmicus (shingles)

Answer 34

Ophthalmic zoster, if not treated promptly, can lead to blindness. Shingles, which is reactivation of varicella-zoster virus, can occur any time after the primary varicella infection. It often begins with a prodrome of intense pain, and in more than 90% of patients, it is associated with pruritus, tingling, tenderness, or hyperesthesia. The cutaneous eruption typically involves a single dermatome and rarely crosses the midline. In a recent, prospective multicenter study, eye redness and rash in the supratrochlear nerve distribution had a statistically significant association with clinically relevant eye disease. One hundred percent of patients who developed moderate to severe eye disease presented with a red eye. Hutchinson sign (zoster eruption on the tip of the nose) was not predictive of clinically relevant eye disease. Clinical diagnosis is based on both history and physical examination. Testing by direct fluorescent-antibody testing or by polymerase chain reaction can confirm the diagnosis; however, decisions regarding antiviral therapy are often based on the history and physical examination rather than reliance on laboratory testing.

Question 35

Lipoma

Answer 35

A lipoma is a group of fat cells encased in a thin fibrous capsule. These are typically softer and more pliable than cysts and can be single or multiple. Lipomas can be superficial or deep and usually do not need to be removed. However, if there is growth or **pain**, removal should be carried out.

Question 36

Pityriasis rosea

Answer 36

Clinical features * ± Viral prodrome * Annular, pink herald patch on trunk * Oval lesions in "Christmas tree" pattern * Pruritus Management * Reassurance (spontaneous resolution) * Treatment of pruritus (eg, antihistamines) Pityriasis rosea is a common skin condition that typically presents from early adolescence to young adulthood. The rash classically begins with a **herald patch**, an erythematous, annular lesion on the trunk. This patch may increase in size and develop scaling around the edge. Within a week, clusters of smaller, erythematous, oval lesions appear on the trunk. These scaly macules and papules are typically distributed obliquely **along the lines of tension** in **a "Christmas tree" pattern 🎄,** most noticeable on the back. The rash is often asymptomatic but may be associated with mild pruritus. A viral prodrome may precede pityriasis rosea, as seen in this patient with preceding fever, headache, and malaise. Pityriasis rosea is self-limited and spontaneously resolves within weeks to months. Management is reassurance alone, although symptomatic relief of pruritus (eg, antihistamines, topical corticosteroids) may be indicated. A self-limited papulosquamous eruption. The classic history includes a single herald patch (an oval, slightly raised plaque with scale) followed in the next 1 to 2 weeks with a more generalized eruption. It will spontaneously resolve in 6 to 12 weeks, and recurrences are uncommon. The treatment is symptomatic, and includes antihistamines or corticosteroids to relieve itch.

Question 37

Psoriasis

Answer 37

A chronic skin condition in young adults. In the early phase, the sharply demarcated erythematous plaques with slight scale **may resemble superficial BCC.** As the psoriatic area matures, a silvery-white scale develops that has characteristic pinpoint bleeding when removed, Plaques are symmetrically distributed and usually occur on scalp, **extensor surfaces** (elbows, knees and back). **Tx:** For localized skin rashes, topical corticosteroids are appropriate therapeutic agent. Topical pimecrolimus is effective for inverse psoriasis (located on the perianal and genital regions) or on the face and ear canals, but is generally not used for lesions on the trunk or extremities.

Question 38

Pyoderma gangrenosum

Answer 38

Pyoderma gangrenosum is an ulcerative skin condition typically associated with an underlying systemic condition, such as **inflammatory bowel disease, rheumatoid arthritis, spondyloarthritis, or a hematologic disease or malignancy** (most commonly acute myelogenous leukemia). Lesions often are multiple and tend to appear on the lower extremities. They begin as tender papules, pustules, or vesicles that spontaneously ulcerate and progress to painful ulcers with a purulent base and undermined, ragged, violaceous borders.

Question 39

Rosacea

Answer 39

Rosacea is a chronic erythematous rash that is most prominent on the convex areas of the face. The etiology is unknown, but the rash may be due to a chronic inflammatory reaction to cutaneous microorganisms, ultraviolet light damage, or vasomotor dysfunction. Symptoms (eg, flushing, skin sensitivity) are often precipitated by hot or spicy foods, alcohol, sun exposure, or high ambient temperatures. In stage I, there is persistent erythema, generally with telangiectasia formation. Stage II is characterized by the addition of papules and tiny pustules. In stage III, the erythema is deep and persistent, the telangiectases are dense, and there may be a solid appearing edema of the central part of the face due to sebaceous hyperplasia and lymphedema (rhinophyma and metophyma). **Tx:** Management may include topical or oral therapies. Topical **metronidazole**, clindamyacin, and sodium sulfacetamide can work, but oral antibiotics are more effective than topical treatments. Minocycline or doxycycline are very effective first-line therapies. Topical steroids are NOT generally effective. Treatment of rosacea General measures * Avoidance of sun exposure, hot/spicy foods, alcohol * Gentle cleansers & emollients Erythematotelangiectatic rosacea (flushing, erythema, telangiectasia) * Topical brimonidine * Laser/intense pulsed light therapy Papulopustular rosacea (small papules & pustules) * First line: topical metronidazole, azelaic acid, ivermectin * Second line: oral tetracyclines Phymatous rosacea (irregular thickening of skin) * Oral isotretinoin * Laser therapy/surgery Ocular rosacea (burning/foreign body sensations, blepharitis, keratitis, conjunctivitis, corneal ulcers) * Lid scrubs & ocular lubricants * Topical or systemic antibiotics (eg, metronidazole, macrolides)

Question 40

Seborrheic keratoses

Answer 40

Seborrheic keratoses are common benign, painless neoplasms that present as brown to black, well-demarcated papules with a waxy surface and a “stuck-on” appearance (Plate 28 :). Seborrheic keratoses are more common in older patients. Treatment is not indicated unless the growths are inflamed, irritated, or pruritic.

Question 41

Stevens-Johnson syndrome (SJS) and TEN

Answer 41

Stevens-Johnson syndrome (SJS) and TEN are severe, idiosyncratic reactions that lead to sloughing of the epidermis. The two syndromes are differentiated by the degree of epidermal detachment, with **SJS defined as involvement of ≤ 10% of body surface** area and **TEN involving at least 30% of body surface area**; intermediate degrees of body surface area involvement are considered to be overlap syndromes (SJS/TEN). Both typically begins with a prodrome that may include fatigue, malaise, fever, sore throat, or a burning sensation in the eyes 1 to 3 days before skin lesions appear. Skin findings may be characterized by flat, purpuric, targetoid lesions that coalesce into patches, or there may be diffuse, tender erythema without identifiable individual lesions. The involved epidermis blisters and sloughs, leaving behind denuded dermis, and a positive **Nikolsky sign** **(lateral pressure on nonblistered skin leads to denudation)** is usually present. Skin **pain** is prominent. Two or more mucosal surfaces, such as the eyes, nasopharynx, mouth, and genitals, are involved in more than 80% of cases. SJS/TEN is most commonly caused by medications; **antiepileptic agents, nonsteroidal anti-inflammatory drugs, antibiotics, pantoprazole, sertraline, tramadol, and allopurinol** are the most frequently implicated drugs. The reaction most commonly occurs **within 4 and 28 days** of exposure. The diagnosis is often made clinically, but a **biopsy** can be confirmatory. Treatment requires discontinuation of the suspected causative medication and is otherwise supportive.

Question 42

Verruca vulgaris (common wart)

Answer 42

Verruca vulgaris (common wart) is caused by infection with a **human papillomavirus**. Common warts generally appear as 5- to 10-mm, rough-surfaced, skin-colored papules. The diagnosis is based on the typical verrucous appearance of a papule or plaque noted on the hands or feet. **Tx:** Spontaneous involution occurs in most patients within 3 years; thus, not treating cutaneous warts often is a reasonable option. Topical **salicylic acid** is the first-line therapy. **Cryotherapy** is used for warts that do not respond to initial topical management; cryotherapy should be avoided with subungual and periungual warts.

Question 43

BUGS

Question 44

Head lice

Answer 44

Erythematous popular rash and “nits” on the hair follicles. The itching from lice generally begin approximately 2 to 3 weeks after infestation. Tx: Treatment options include premethrin and lindane. The preferred treatment is permethrin 1%, permethrin 5% is a second option, and lindane 1% is a third option. If treatment failure occurs, a second-line medcation is 0.5% malathion lotion.

Question 45

Scabies

Answer 45

Pathogenesis * Sarcoptes scabiei mite infestation * Spread by direct person-to-person contact Clinical features * Extremely pruritic pathognomonic burrows & small, erythematous papules * Rash located on interdigital web spaces, flexor wrists, extensor elbows, axillae, umbilicus & genitalia Treatment * Topical 5% permethrin OR Oral ivermectin Scabies, caused by infestation with the mite Sarcoptes scabiei, is characterized by an intensely pruritic rash classically located in the axillae, periumbilical area, genitalia, and **interdigital web spaces of the hands and feet**. The rash consists of small, erythematous papules or vesicles as well as pathognomonic burrows, or \<1-cm lines on the skin, caused by the female mite burrowing into the epidermis to lay eggs. Burrows may not be visible or may be difficult to visualize due to excoriation. Scabies is spread by direct person-to-person contact, with an incubation period of 3-6 weeks. Diagnosis is usually clinical but may be confirmed with skin scraping and microscopy to identify mites or eggs. First-line treatment is **topical 5% permethrin** or oral **ivermectin**. Prevention of spread includes treating household contacts and decontaminating linens (eg, hot water washing of clothing and bedding).

Question 46

Chigger bites

Answer 46

Typically found in a linear pattern over wrists, ankles, and legs.

Question 47

Bedbugs

Answer 47

Typically infest unclothed areas—the neck, hands, and face.

Question 48

Fleas

Answer 48

Flea bites often occur in clusters, and are typically on the lower extremities.

Question 49

Ddx: Hep C-related Dermatologic conditions

Answer 49

Porphyria cutanea tarda (PCT)

Question 50

Lichen planus

Answer 50

Lichen planus is a mucocutaneous disorder of unclear etiology that also appears to have an association with hepatitis C, although it may also be found as an isolated disorder or in association with autoimmune disorders and some medications. The skin findings are a generalized rash that is characteristically polygonal, pruritic, papular, planar, purple, and with plaques (the six Ps).

Question 51

Porphyria cutanea tarda (PCT)

Answer 51

There is a very strong association of PCT with chronic hepatitis C infection, although why this relationship occurs is not known. PCT is the most common of the porphyrias worldwide. PCT is caused by a deficiency in uroporphyrinogen decarboxylase, an enzyme in the heme biosynthesis pathway. PCT may be acquired (type 1) and familial (type 2); 80% are of the acquired type, and the enzymatic defect is limited to the liver. Whereas this type develops most often in mid-adult life, type 2 develops in younger patients and represents a decrease in enzymatic activity in all tissues. Both types of PCT often require susceptibility factors such as alcohol, hepatitis C or HIV infection, iron overload (e.g., hemochromatosis), or estrogen use for clinical evidence of PCT to occur. Sunlight activates the large amounts of uroporphyrinogen that are deposited in the skin, leading to photosensitization and tissue damage. The result is a variety of cutaneous findings, which include blisters, erosions, hyperpigmentation, hypertrichosis, and sclerodermoid plaques. Involvement of the liver usually is seen with modest elevations of the hepatic transaminases. The diagnosis should be suspected in at-risk patients with consistent skin findings and with reddish-to-brown urine in natural light (and pink to red with fluorescence). Measurement of urinary porphyrins confirms the diagnosis. Treatment is by sunlight avoidance, phlebotomy, or hydroxychloroquine (which mobilizes accumulated porphyrins), and treatment of hepatitis C.

Question 52

Erythema nodosum

Answer 52

Erythema nodosum causes tender, reddish, palpable inflammatory nodules that typically occur on the anterior lower legs. It is a hypersensitivity immune reaction to infection or systemic inflammation and may be seen with hepatitis C. However, it is a nonspecific finding that may occur in a wide range of systemic diseases or with different medications. Erythema nodosum is the result of a hypersensitivity immune reaction that may be secondary to drugs, infection (such as fungal or streptococcal), or systemic inflammation due to sarcoidosis, tuberculosis, lymphoma, or inflammatory bowel disease. At least 50% of cases are idiopathic. The condition usually is acute and self-limited, and treatment is supportive following treatment of any associated cause.

Question 53

Cryoglobulinemia

Answer 53

Cryoglobulinemia, in which temperature-dependent circulating immune complexes are deposited in small- to medium-sized blood vessels, is also associated with hepatitis C infection. The most common clinical manifestations include cutaneous palpable purpura, which often involves the lower legs, may come in “crops,” and can leave areas of hyperpigmentation after resolution. Cryoglobulins may also involve the kidney (causing glomerulonephritis) and other organ systems (e.g., the central nervous system).

Question 54

Nummular eczema

Answer 54

Is a chronic, relapsing/remitting condition that presents with erythematous, pruritic, coin-shaped patches on the extremities. The lesions may initially have a scant exudate and are uncommon on the back and upper trunk. Round, well-demarcated, eczematous patches (1-10 cm) found on the extremities and trunk. Pruritus may be intense, which results in scratching. The scratch marks may be the best way to discriminate nummular eczema from superficial BCC. Onset is usually spontaneous with no inciting event.

Question 55

Molluscum contagiosum

Answer 55

The lesion is due to an infection with a **poxvirus** transmitted through **direct skin-to-skin contact**. Lesions are common in children in a daycare or nursery school setting and are in that case not likely to be sexually transmitted. However, in adults and in the pubic region, they are sexually transmitted. Although the lesions can be similar to those seen with basal cell cancers, the lack of telangiectasia is a diagnostic clue. **Tx:** Most lesions will resolve spontaneously within months of appearance, but they can be treated with cryotherapy, cautery, or curettage.

Question 56

Pemphigus vulgaris (PV)

Answer 56

Including painful, flaccid bullae, mucosal erosions, and separation of epidermis from dermis by light friction (Nikolsky sign). The roof of the bullous lesions is fragile and rapidly desquamates, leaving raw ulcers. PV is an autoimmune disorder caused by **antibodies directed against desmogleins 1 and 3, which are components of desmosomes normally involved in adherence between epidermal keratinocytes.** Light microscopy of a biopsy specimen from a lesion edge shows intraepithelial cleavage with detached keratinocytes (acantholysis). **Because the attachment of keratinocytes to the basement membrane is mediated by hemidesmosomes, a single cell layer remains along the basement membrane with an appearance described as a "row of tombstones."** Immunofluorescence microscopy reveals IgG and C3 deposits in a netlike or **"chicken wire"** pattern. Serology for **antibodies to desmoglein 1 and 3** can further support the diagnosis.

Question 57

Bullous pemphigoid

Answer 57

An autoimmune disorder characterized by severe pruritus and tense bullaeon an erythematous base. It is most common in patients age \>65 and has an increased incidence in those with malignancy or neurological disorders (eg, Parkinson disease, multiple sclerosis). The extent of involvement may range from just a few lesions to hundreds covering a large portion of the body, although mucous membrane involvement occurs only in a minority of patients. A pre-bullous prodrome is common and can present as urticarial or eczematous lesions. Bullous pemphigoid is caused by IgG autoantibodies against the **hemidesmosome** and **basement membrane zone.** Antibody binding activates complement and inflammatory mediators, and the resultant inflammation leads to blister formation. The diagnosis is made by skin biopsy; light microscopy shows subepidermal cleavage, and direct immunofluorescence microscopy shows linear **IgG and C3 deposits along the basement membrane.** First-line treatment for bullous pemphigoid is a **high-potency _topical_ glucocorticoid 🌚 (eg, clobetasol)**, which is effective even for extensive disease. Systemic glucocorticoids are not more effective and are associated with an increased incidence of treatment-related complications, but these can be used when topical agents are not practical.

Question 58

ALLOPECIA

Question 59

Alopecia areata

Answer 59

An autoimmune disorder characterized by circumscribed patches of hair loss. Hair shafts show narrowing close to the surface and may be broken off.

Question 60

Androgenetic alopecia

Answer 60

Causes uneven hair loss in a characteristic pattern. Men have thinning at the frontotemporal hairline and vertex; women predominantly have thinning at the vertex and sides with preservation of the hairline.

Question 61

Trichotillomania

Answer 61

A behavioral disorder characterized by compulsive pulling of hair. It presents with irregular patches of hair loss and broken fibers, and typically affects the front and sides of the scalp, eyebrows, and eyelashes.

Question 62

**Telogen effluvium (TE)**

Answer 62

One of the most common causes of hair loss in adults. Hair follicles pass through 3 phases: growth phase (**anagen**; 90% of follicles), transformative phase (**catagen**; \<1%), and rest/shedding phase (**telogen**; 10%). In TE, follicles undergo a widespread shift into the rest/shedding phase, with cessation of growth and subsequent shedding. It is often triggered by a **stressful event, such as weight loss, pregnancy, major illness or surgery, or psychiatric trauma.**

Question 63

Hidradenitis suppurativa (HS, also known as acne inversa)

Answer 63

A chronic inflammatory condition that involves recurrent occlusion of hair follicles in intertriginous regions (eg, groin, axilla). Hidradenitis suppurativa commonly develops in women age 20-40; risk factors include obesity, tobacco use, and family history. Hidradenitis suppurativa often initially presents as a solitary, painful nodule surrounding a follicle that can persist up to several months and eventually develops into a spontaneously draining abscess. This disease has a chronic, progressive course with recurrences that affect follicles within the same region. Patients have multiple lesions with subsequent inflammation and abscess drainage that eventually develop into sinus tract and scar formation (eg, fibrotic bands, acneiform scars, thickened plaques), as seen in this patient. The diagnosis is made clinically, and treatment is aimed at reducing frequency of lesions and preventing disease progression and complications (eg, contractures, **lymphatic obstruction**, fistula). Most commonly occurs in intertriginous areas (eg, axilla; inguinal, perineal areas) but can occur in any hair-bearing skin. HS is due to **chronic inflammatory occlusion of folliculopilosebaceous units**, which prevents keratinocytes from properly shedding from the follicular epithelium. Risk factors include family history of HS, smoking, obesity, diabetes, and mechanical stress on the skin (eg, friction, pressure).

Question 64

Senile purpura (solar or actinic purpura)

Answer 64

Is a noninflammatory disorder that is most common in the elderly but can also be seen in middle-aged patients with extensive sunlight exposure. It is caused by loss of elastic fibers in perivascular connective tissue. Minor abrasions that would merely stretch the skin in younger patients can rupture superficial blood vessels in the elderly. The subsequent extravasation of blood leads to ecchymosis over vulnerable areas, such as the dorsum of the hands and forearms. Patients can have residual brownish discoloration from hemosiderin deposition. The incidence and severity are also increased in patients taking anticoagulants, corticosteroids, or nonsteroidal anti-inflammatory drugs.

Question 65

🧤 DERM

Answer 65

Neonatal rashes **Erythema toxicum neonatorum** * Asymptomatic * Scattered, erythematous papules & pustules * No **Tx** Neonatal HSV Three types: * Vesicular clusters on skin, eyes & mucous membranes * CNS infection * Fulminant, disseminated, multiorgan disease * Acyclovir Staphylococcal scalded skin syndrome * Fever, irritability * Diffuse erythema → flaccid, flexural blistering * Positive Nikolsky sign Oxacillin, nafcillin, or vancomycin

Question 66

Erythema toxicum

Answer 66

Erythematous papules and pustules in a healthy neonate. ETN is common in full-term neonates in the first 2 weeks of life. The rash typically evolves from papules to pustules, may wax and wane, and can occur on any part of the body (although it spares the palms and soles). ETN is a clinical diagnosis, and diagnostic workup and **treatment are unnecessary.** Parents should be reassured that the rash resolves spontaneously without sequelae. Benign, self-limited condition of unknown etiology. It is found in about 50% of term newborns. The lesions are 2 to 3 cm erythematous macules; some have a central yellow-white pustule. "Toxicum" is a misnomer as the rash is benign and evanescent. The etiology is unknown, and ETN pustules have been shown to be sterile and to contain many eosinophils.

Question 67

Pityriasis rosea

Answer 67

is preceded by a “herald patch,” an annular, scaly, erythematous lesion. The lesions are salmon-colored and in a Christmas-tree formation, following the lines of the skin. The cause is unknown. Treatment may include antihistamines, topical antipruritic lotions and creams, low-dose topical corticosteroids, and phototherapy. The rash usually lasts up to 6 weeks and then resolves. It can be confused with nummular eczema and tinea versicolor. In the sexually active adolescent, syphilis should also be considered.

Question 68

Salmon patches

Answer 68

(aka nevus simplex or nevus flammeus) are flat vascular lesions that occur in the listed regions and appear more prominent during crying. The lesions on the face fade over the first few years of life. Lesions found over the nuchal and occipital areas often persist. No therapy is indicated.

Question 69

Pustular melanosis

Answer 69

is another benign, self-limited disease of unknown etiology of the newborn period. It is more common in blacks than in whites. These lesions are usually found at birth and consist of 1- to 2-mm pustules that result in a hyperpigmented lesion encircled by a collarette of scale upon rupture of the pustule. The pustular stage of these lesions occurs during the first few days of life, with the hyperpigmented stage lasting for weeks to months. No therapy is indicated.

Question 70

Sebaceous nevi

Answer 70

(nevus of Jadassohn) are small, sharply edged lesions that occur most commonly on the head and neck of infants. These lesions are yellow-orange in color and are slightly elevated. They usually are hairless. Malignant degeneration is possible, most commonly after adolescence.

Question 71

Milia

Answer 71

are fine, yellowish white, 1- to 2-mm firm raised lesions scattered over the face of the neonate. They are cysts that contain keratinized material. Commonly, these lesions resolve spontaneously without therapy.

Question 72

Seborrheic dermatitis

Answer 72

can begin anytime during life and frequently presents as cradle cap in the newborn period. This rash is commonly greasy, scaly, and erythematous and in smaller children involves the face, neck, axilla, and diaper area. In older children, the rash can be localized to the scalp and intertriginous areas. Pruritus can be marked.

Question 73

Ddx: Frostbite

Answer 73

Frostbite The condition in which tissue is frozen and destroyed. There is initial stinging, followed by aching, culminating in numb areas. Once rewarmed, the area becomes red, blotchy, and painful. Gangrene may develop. Frostnip Manifest by small, firm, white, cold patches of skin in exposed areas; treatment is rewarming the areas before they become numb. Trench Foot Occurs with prolonged exposure to cold and/or moisture. The foot will become cold, numb, pale, edematous, and clammy. A prolonged autonomic disturbance after this condition can persist for years. Hypothermia Can develop in any cold weather exposure. As the core temperature drops, the individual becomes lethargic, tired, uncoordinated, apathetic, mentally confused, irritable, and bradycardic. Chilblains Small, ulcerated lesions on exposed areas such as the ears and fingers. Lesions may last 1 to 2 weeks. Cold Panniculitis Destruction of fat cells caused by exposure to cold weather or a cold object; in this case, the child had “Popsicle panniculitis,” which is usually a benign condition that self-resolves.

Question 74

seborrheic dermatitis (SD)

Answer 74

Incidence of SD peaks in the first year of life and again in adulthood. SD is associated with colonization by Malassezia species and primarily affects areas with numerous sebaceous glands. In infants, these areas include the **scalp ("cradle cap"), eyelids, nasolabial folds, postauricular area, and umbilicus.** The diagnosis of SD is based on characteristic examination findings of erythematous patches and plaques with yellow, oily scales, and mild pruritus may be present. Treatment is not always necessary as spontaneous resolution is common. First-line treatment for children includes gentle **emollients** and non-medicated **shampoos**. Widespread or recalcitrant SD is managed with low-potency glucocorticoid creams or topical ketoconazole.

Question 75

Atopic dermatitis

Answer 75

A recurrent rash that can affect the cheeks, scalp, trunk, and extensor surfaces in infants. In contrast to SD, atopic dermatitis is associated with **severe pruritus,** and most patients will have a **family history of atopic disorders (eg, asthma, allergic rhinitis).** An immediate hypersensitivity reaction to common environmental irritants Inflammatory patches and weeping, crusted plaques on the neck, face, groin, and extensor surfaces characterize the infantile form. In older children, dermatitis of the flexural areas is common. Soaps and hot water are common irritants. Therapy is based on avoidance of irritants, adequate hydration of the skin, and use of topical steroids, as well as treatment of infected lesions.

Question 76

**Kasabach-Merritt phenomenon**

Answer 76

**Kasabach-Merritt phenomenon** is seen with large vascular anomalies (ie, Kaposiform hemangioendothelioma and tufted angioma). Platelet and RBC sequestration within the vascular tumor causes peripheral thrombocytopenia, coagulopathy, and microangiopathic hemolytic anemia. Treatment options include corticosteroids, α-interferon, and vincristine. Surgery frequently results in excessive bleeding. **Nevus simplex** is a common minor vascular malformation seen on the glabella, eyelids, and nape of the neck in newborns; such lesions on the face are also called “angel or stork kiss,” while lesions on the back of the neck are called “stork bite.” **Nevus flammeus**, or port wine stain, is a large sharply demarcated pink to purple vascular malformation that can occur anywhere. Port wine stain involving the VI distribution of the trigeminal nerve should raise the suspicion of **Sturge-Weber syndrome**. **PHACE(S) syndrome** includes posterior fossa malformations, large facial hemangiomas, arterial abnormalities, coarctation of the aorta, eye abnormalities, and sternal defects. Infantile fibrosarcoma is a malignant congenital tumor that can be easily mistaken for an infantile hemangioma; a high index of suspicion is required to investigate further if a “hemangioma” is not resolving as expected.

Question 77

Erythema marginatum

Answer 77

Is a manifestation of acute rheumatic fever characterized by numerous, widespread plaques with a sharp annular or serpiginous border and central clearing. It is transient, nonpruritic, and most common in children.

Question 78

Irritant Contact Dermatitis

Answer 78

ICD is a localized inflammatory reaction that can be triggered by a variety of chemicals, solvents, cleaning products, or acidic/alkaline solutions. ICD is nonimmunologically mediated but can resemble **allergic contact dermatitis** with pruritus, erythema, local swelling, and vesicles. Symptoms can develop acutely (within hours of exposure) but are often chronic, leading to excoriations, hyperkeratosis, and fissuring of involved skin. **Emollients** and use of protective barriers can often relieve symptoms. However, identification and **avoidance of the offending agent** are also essential, although this is frequently challenging, as many common household and occupational products can contribute to symptoms. The diagnosis of ICD (and allergic contact dermatitis) is usually based on clinical findings, but if initial measures do not clear the rash, skin biopsy may be required for confirmation.

Question 79

Dermatitis herpetiformis (DH)

Answer 79

Dermatitis herpetiformis (DH) causes intensely pruritic erythematous papules, vesicles, and bullae that occur symmetrically in grouped ("herpetiform") clusters on the extensor surfaces of the elbows, knees, back, and buttocks. DH represents an autoimmune dermal reaction due to dietary gluten and is commonly associated with **celiac disease** (the likely cause of this patient's diarrhea and weight loss), although it may precede the gastrointestinal manifestations. Skin biopsy in DH shows subepidermal microabscesses (blisters) at the tips of the dermal papillae; immunofluorescence studies show deposits of anti-epidermal transglutaminase IgA in the dermis. Initial treatment includes dapsone, which has anti-inflammatory and immunomodulatory properties and provides rapid relief of symptoms. Long-term management requires a gluten-free diet.

Question 80

Infantile hemangioma

Answer 80

Natural history * May present as patch of telangiectasias at birth * Proliferation: * Age 0-1 * Bright red, raised nodule * Involution: * Age 1-9 * Deeper red/violet, regression in size Management * Observation * Topical beta blocker (eg, propranolol) for ulcerated or cosmetically sensitive areas (eg, face) Complications * Ulceration/scarring * Vision impairment if near eye * Life-threatening if near airway Superficial infantile hemangioma, also known as a 🍓 **strawberry hemangioma,** is a benign capillary tumor formed from abnormally proliferating endothelial cells. This vascular birthmark appears during the first few weeks of life as a bright red, sharply demarcated, blanching nodule or plaque. The lesion typically undergoes rapid growth during the first year of life followed by spontaneous regression during childhood. Although most patients require no intervention**, 🎺beta blockers** (eg, propranolol) are recommended for complicated hemangiomas that are disfiguring, ulcerating, disabling (eg, strabismus from eyelid hemangioma), or life-threatening (eg, tracheal lesions). Propranolol **promotes involution by causing vasoconstriction and by inhibiting growth factors.**

Question 81

Chronic stasis dermatitis

Answer 81

chronic stasis dermatitis due to venous insufficiency. Venous stasis is common in patients who are older, obese, or have a history of venous thrombosis. Increased intraluminal pressure or loss of vessel wall tensile strength can lead to venous dilation and failure of the venous valves. The resulting backflow of blood exacerbates the venous hypertension, leading to further valvular incompetence and venous congestion. Elevated venous pressure and increased vascular permeability lead to extravasation of fluid, plasma proteins, and red blood cells. Clinical manifestations include scaling, weeping, superficial erosions, and pitting edema. Itching and achy pain are common but usually mild. Acute inflammation can manifest as erythema and warmth resembling cellulitis (although unlike cellulitis, it is typically bilateral and symmetric). Chronic findings include red/brown discoloration (due to deposition of hemosiderin), woody induration, and fibrosis. Microvascular disease, platelet aggregation, and increased expression of proteolytic enzymes can cause chronic irregular ulcers, most commonly at the medial malleolus. The diagnosis of stasis dermatitis is usually obvious based on clinical findings. Duplex ultrasonography is not routinely performed but can confirm venous hypertension and reflux and rule out venous thrombosis in patients with acute unilateral symptoms. Management includes compression stockings, leg elevation, exercise, and avoidance of prolonged standing.

Question 82

Torus palatinus (TP)

Answer 82

A benign bony growth (ie, exostosis) located at the midline suture of the hard palate. It is thought to be caused by both **genetic and environmental factors** and is more common in women and Asian individuals. TP can be congenital or develop later in life. Similar lesions at the lingual surface of the mandible are termed "tori mandibulari." TPs are usually \<2 cm in size but can gradually enlarge over time. They are typically asymptomatic and are frequently ignored by the patient but noted by clinicians (or family members) when examining the mouth for unrelated reasons. However, the thin epithelium overlying the bony growth may ulcerate with minor trauma of the oral cavity and heal slowly due to poor vascular supply. The diagnosis is usually obvious on clinical grounds. Surgery is indicated for patients in whom the mass becomes symptomatic, interferes with speech or eating, or causes problems with the fitting of dentures later in life.