Medical School · Year 3 · Family Medicine · includes a quiz and discussion video
Seminar 10: Dermatology in Primary Care
Family Medicine Clerkship
Learning Objectives
By the end of this seminar, students will be able to:
- Describe dermatologic lesions using standard morphologic terminology for primary and secondary lesions
- Diagnose and manage common bacterial, viral, and fungal skin infections encountered in primary care
- Recognize and treat inflammatory skin conditions including eczematous and papulosquamous disorders
- Identify suspicious skin lesions requiring biopsy using the ABCDE criteria and clinical assessment
- Apply appropriate topical therapies with correct potency selection based on anatomic site and severity
- Perform systematic skin cancer screening and counsel patients on sun protection and self-examination
Seminar Outline
Section 1: Dermatologic Examination
The dermatologic examination begins with the identification of primary lesions, which are the initial pathologic changes arising in previously normal skin. Flat lesions are classified by size: a macule is a flat, circumscribed area of color change measuring less than one centimeter, while a patch exceeds one centimeter and remains flat. Raised solid lesions include papules (less than one centimeter), plaques (greater than one centimeter with a flat top), and nodules (greater than one centimeter with deeper extension into the dermis or subcutaneous tissue). Fluid-filled lesions include vesicles (less than one centimeter), bullae (greater than one centimeter), and pustules (containing purulent material). The wheal is a distinctive transient, edematous lesion characteristic of urticaria. Mastery of this vocabulary is essential for accurate documentation and communication with consulting dermatologists.
Secondary lesions represent changes that evolve from primary lesions, either through natural disease progression or patient manipulation. Scale consists of flaking epidermal cells seen in conditions such as psoriasis and tinea, while crust forms from dried serum, blood, or purulent exudate overlying an eroded surface. Erosions represent superficial losses of epidermis that heal without scarring, whereas ulcers extend deeper into the dermis or beyond and typically produce scars. Excoriations are linear erosions resulting from scratching and are commonly seen in pruritic conditions such as atopic dermatitis. Lichenification describes thickened, leathery skin with exaggerated skin lines that develops from chronic rubbing or scratching, often observed in chronic eczema.
The distribution pattern of skin lesions provides critical diagnostic information. A dermatomal distribution, following the path of a single nerve root, is virtually pathognomonic for herpes zoster. Lesions confined to sun-exposed areas suggest photosensitivity reactions or cutaneous malignancy. In children, flexural involvement of the antecubital and popliteal fossae points toward atopic dermatitis, while extensor surface involvement of the elbows and knees is characteristic of psoriasis. A symmetric distribution often suggests a systemic etiology, including drug eruptions and autoimmune conditions. Recognizing these patterns allows the clinician to narrow the differential diagnosis efficiently and direct the workup appropriately.
A thorough dermatologic history complements the physical examination and often clinches the diagnosis. The clinician should establish the duration and timeline of the eruption, determine whether it is improving, worsening, or unchanged, and identify associated symptoms such as pruritus, pain, or burning. Potential triggers including sun exposure, topical products, foods, and new medications must be explored. Prior treatments and their effectiveness should be documented, and the medical history should be reviewed for conditions that predispose to skin disease, such as atopic diathesis and immunosuppression. This systematic approach ensures that relevant information is gathered to guide diagnosis and management.
<image>Panel A: Diagram illustrating primary skin lesions including macule, patch, papule, plaque, nodule, vesicle, bulla, pustule, and wheal with cross-sectional views showing depth and fluid content. Panel B: Photographs demonstrating secondary skin lesions including scale, crust, erosion, ulcer, excoriation, and lichenification with clinical examples. Panel C: Body diagram mapping common distribution patterns including dermatomal, sun-exposed, flexural, and extensor surfaces with associated diagnoses. Panel D: Flowchart for systematic dermatologic history taking covering duration, evolution, symptoms, triggers, prior treatment, and medical history.</image>
Section 2: Bacterial Skin Infections
Impetigo is the most common superficial bacterial skin infection and is caused predominantly by Staphylococcus aureus, with Group A Streptococcus as a secondary pathogen. The non-bullous form, which accounts for the majority of cases, presents with honey-colored crusted lesions that typically cluster around the mouth and nose. The bullous variant, caused exclusively by toxin-producing S. aureus, manifests as flaccid blisters that rupture easily. Impetigo is highly contagious and spreads through direct contact, making it particularly common in children and in crowded living conditions. Treatment of localized disease involves topical mupirocin applied three times daily, while extensive or refractory cases require systemic antibiotics such as cephalexin or dicloxacillin.
Cellulitis represents a deeper, spreading infection of the dermis and subcutaneous tissue, most commonly caused by Streptococcus pyogenes and, to a lesser extent, Staphylococcus aureus. The classic presentation includes an expanding area of erythema, warmth, swelling, and tenderness, often accompanied by regional lymphadenopathy and occasionally fever. The absence of purulence is an important distinguishing feature from cutaneous abscess and helps guide antibiotic selection. First-line treatment for nonpurulent cellulitis consists of cephalexin or dicloxacillin for five to seven days, targeting streptococcal coverage. When purulence is present or MRSA risk factors exist, such as recent hospitalization, injection drug use, or prior MRSA infection, coverage should be broadened to include trimethoprim-sulfamethoxazole or doxycycline.
Cutaneous abscesses are localized collections of pus within the dermis and deeper tissues, frequently caused by methicillin-resistant Staphylococcus aureus in community settings. The hallmark finding is a fluctuant, painful, erythematous nodule that may have surrounding cellulitis. The primary treatment is incision and drainage, which involves making an adequate incision over the point of maximal fluctuance, breaking up loculations, irrigating the cavity, and packing with gauze if the cavity is deep. For small, well-drained abscesses in immunocompetent patients, antibiotics are not necessary. However, antibiotics should be added when there is surrounding cellulitis, the abscess is large, the patient is immunocompromised, or systemic signs of infection are present.
Folliculitis is an infection of the hair follicles that presents as pustules centered around individual follicular ostia. The most common causative organism is Staphylococcus aureus, but Pseudomonas aeruginosa produces a distinctive form known as hot tub folliculitis that develops after exposure to inadequately chlorinated water. Pityrosporum folliculitis, caused by Malassezia yeast, typically presents as pruritic papules and pustules on the trunk and is often confused with acne vulgaris. Most cases of bacterial folliculitis are self-limited and resolve with good hygiene and warm compresses, though more extensive or recurrent cases may require topical mupirocin or systemic antibiotics such as dicloxacillin or cephalexin.
<image>Panel A: Clinical photographs of non-bullous impetigo showing honey-crusted perioral lesions and bullous impetigo with intact and ruptured vesicles. Panel B: Photograph of lower extremity cellulitis demonstrating well-demarcated erythema, warmth, and swelling with demarcation lines drawn for monitoring progression. Panel C: Incision and drainage procedure for cutaneous abscess showing fluctuant nodule, linear incision, exploration of loculations, and packing technique. Panel D: Comparison of folliculitis types including staphylococcal folliculitis with perifollicular pustules, hot tub folliculitis distribution pattern, and Pityrosporum folliculitis on the trunk.</image>
Section 3: Viral Skin Infections
Herpes simplex virus infections are among the most prevalent viral skin conditions encountered in primary care. HSV-1 classically causes orolabial disease presenting as cold sores, while HSV-2 is the predominant cause of genital herpes, though either type can infect either location. The characteristic lesion consists of grouped vesicles on an erythematous base that evolve through stages of vesiculation, ulceration, crusting, and healing over seven to fourteen days. Primary infections tend to be more severe than recurrences, with greater pain, more extensive lesions, and possible systemic symptoms. Treatment with antiviral agents such as acyclovir, valacyclovir, or famciclovir shortens the duration and severity of episodes, and daily suppressive therapy is recommended for patients experiencing frequent recurrences, generally defined as six or more episodes per year.
Herpes zoster results from reactivation of varicella-zoster virus that has remained latent in dorsal root ganglia following primary varicella infection. The hallmark presentation is a painful, unilateral vesicular eruption confined to a single dermatome, most commonly involving thoracic or cranial nerve distributions. Pain often precedes the rash by several days and may be the only initial symptom, leading to diagnostic confusion before vesicles appear. Antiviral therapy with valacyclovir, famciclovir, or acyclovir should be initiated within seventy-two hours of rash onset to reduce the duration of the acute episode and decrease the risk of postherpetic neuralgia. Prevention with the recombinant zoster vaccine Shingrix is recommended for all immunocompetent adults aged fifty years and older, regardless of prior varicella or zoster history, as it provides greater than ninety percent efficacy against herpes zoster.
Warts are benign epithelial proliferations caused by human papillomavirus infection and are classified by their morphology and location. Common warts (verruca vulgaris) present as rough, hyperkeratotic papules most frequently on the hands, while plantar warts occur on the soles of the feet and cause pain with weight bearing. Flat warts appear as smooth, slightly elevated papules on the face and dorsal arms, and condylomata acuminata are soft, fleshy growths in the anogenital region associated with HPV types 6 and 11. Treatment options include destructive modalities such as cryotherapy with liquid nitrogen and topical salicylic acid, as well as immunomodulatory approaches including topical imiquimod. Many warts resolve spontaneously over months to years, and the decision to treat depends on symptoms, cosmetic concerns, and patient preference.
Molluscum contagiosum is caused by a poxvirus and presents as firm, dome-shaped papules with a characteristic central umbilication. In children, the lesions typically appear on the trunk, extremities, and face and spread by autoinoculation. In adults, molluscum is often sexually transmitted and presents in the genital and inguinal regions. The infection is self-limited in immunocompetent individuals, usually resolving within six to twelve months, though it may persist longer in immunosuppressed patients. Treatment options for symptomatic or persistent lesions include curettage, cryotherapy, and topical cantharidin, and these are particularly appropriate when lesions are numerous, cosmetically distressing, or in areas prone to spread through autoinoculation.
<image>Panel A: Clinical progression of herpes simplex infection showing grouped vesicles on an erythematous base evolving to ulceration and crusting, with comparison of orolabial and genital presentations. Panel B: Dermatomal distribution of herpes zoster vesicles in a thoracic dermatome with close-up of vesicular lesions, and diagram illustrating viral latency and reactivation from dorsal root ganglia. Panel C: Comparison of wart subtypes including common warts on hands, plantar warts with punctate thrombosed capillaries, flat warts on the face, and condylomata acuminata. Panel D: Molluscum contagiosum showing dome-shaped papules with central umbilication at various magnifications, including dermoscopic view demonstrating the characteristic white core.</image>
Section 4: Fungal Skin Infections
Dermatophyte infections, collectively known as tinea, are named according to the anatomic site involved and represent some of the most common fungal conditions in primary care. Tinea corporis presents as annular, erythematous, scaly plaques with central clearing on the body. Tinea pedis manifests in three patterns: interdigital maceration between the toes, a moccasin distribution of diffuse scaling on the soles and lateral feet, and a vesicular form with inflammatory blisters. Tinea cruris affects the inguinal folds as well-demarcated, erythematous, scaly patches that characteristically spare the scrotum, helping to distinguish it from candidal intertrigo. Tinea capitis presents with scalp scaling, alopecia, and occasionally a kerion, which is an inflammatory, boggy, purulent nodule representing an intense immune response to the fungal infection.
Diagnosis of dermatophyte infections can often be made clinically but may be confirmed through several laboratory methods. The potassium hydroxide preparation is the most useful bedside test, performed by scraping the active border of a lesion, placing the scale on a glass slide with KOH solution, and examining under microscopy for branching, septate hyphae. Fungal culture on Sabouraud agar is useful when the KOH preparation is negative but clinical suspicion remains high, though results may take two to four weeks. The Wood lamp examination, which uses ultraviolet light, causes certain species of Microsporum to fluoresce green and can aid in the diagnosis of tinea capitis, though most cases caused by Trichophyton species do not fluoresce. In many cases, clinical appearance alone is sufficient to initiate treatment, with confirmatory testing reserved for atypical presentations or treatment failures.
Treatment of dermatophyte infections varies by site and severity. Tinea corporis, cruris, and pedis respond well to topical antifungal agents such as clotrimazole, miconazole, or terbinafine applied twice daily for two to four weeks. Tinea capitis requires systemic antifungal therapy because topical agents cannot penetrate the hair follicle adequately; oral terbinafine for four to six weeks or griseofulvin for six to eight weeks are the standard regimens, with adjunctive antifungal shampoo to reduce fungal shedding. Onychomycosis, or fungal nail infection, also requires systemic therapy, with oral terbinafine for six weeks for fingernails and twelve weeks for toenails being the most effective option. Confirmation of onychomycosis with KOH, culture, or histopathology is recommended before initiating prolonged systemic therapy given the length of treatment and potential hepatotoxicity.
Candidiasis is caused by Candida species, most commonly Candida albicans, and manifests differently depending on the site of infection. Cutaneous candidiasis presents as beefy red erythema with satellite pustules in intertriginous areas such as the groin folds, axillae, and inframammary regions, distinguished from dermatophyte infection by the satellite lesions and involvement of moist, occluded skin. Oral candidiasis, or thrush, presents as white, curd-like plaques on the buccal mucosa, tongue, and palate that can be scraped off to reveal an erythematous base. Vulvovaginal candidiasis is characterized by pruritus, erythema, and thick white discharge resembling cottage cheese. Treatment for all forms involves antifungal agents, typically topical nystatin or azole creams for cutaneous and oral disease, and oral fluconazole or topical azole preparations for vulvovaginal infections.
<image>Panel A: Clinical photographs of tinea variants including tinea corporis with annular lesion and central clearing, tinea pedis in interdigital and moccasin patterns, tinea cruris with inguinal erythema sparing the scrotum, and tinea capitis with alopecia and scaling. Panel B: Microscopic images of KOH preparation demonstrating branching septate hyphae, and photograph of fungal culture growth on Sabouraud agar. Panel C: Flowchart for treatment selection based on infection site showing topical therapy for corporis, cruris, and pedis versus systemic therapy for capitis and onychomycosis with specific drug choices and durations. Panel D: Clinical presentations of candidiasis including intertriginous candidiasis with satellite pustules, oral thrush with white plaques, and vulvovaginal candidiasis with erythema and discharge.</image>
Section 5: Eczematous Dermatitis
Atopic dermatitis is a chronic, relapsing inflammatory skin condition strongly associated with the atopic triad of asthma and allergic rhinitis. The hallmark feature is intense pruritus accompanied by erythematous, dry, and often excoriated skin. The distribution is age-dependent: in infants, the face and extensor surfaces are preferentially involved, while in older children and adults, the disease localizes to the flexural surfaces including the antecubital and popliteal fossae, neck, and wrists. The pathophysiology involves a combination of epidermal barrier dysfunction, with deficiency of the structural protein filaggrin being a key genetic factor, and immune dysregulation favoring a type 2 inflammatory response. The chronic nature of the disease necessitates long-term management strategies centered on skin barrier restoration and inflammation control.
Contact dermatitis is divided into two mechanistically distinct categories that can appear clinically similar. Irritant contact dermatitis results from direct chemical or physical damage to the epidermis and is the more common type, exemplified by diaper dermatitis in infants and hand dermatitis from frequent handwashing or chemical exposure. Allergic contact dermatitis is a delayed type IV hypersensitivity reaction requiring prior sensitization, with common allergens including urushiol from poison ivy, nickel in jewelry, and fragrance and preservative chemicals in personal care products. The distribution of the eruption provides the key diagnostic clue, as lesions typically correspond to the area of contact with the offending agent. Treatment for both types involves identification and avoidance of the causative substance combined with topical corticosteroids for symptom relief and barrier repair.
The treatment of eczematous conditions follows a stepwise approach beginning with fundamental skin care practices. Liberal application of emollient moisturizers is the cornerstone of therapy, ideally applied immediately after bathing to trap moisture in the skin. Topical corticosteroids remain the mainstay of anti-inflammatory treatment for flares, with potency matched to the severity and anatomic location of the disease. Topical calcineurin inhibitors such as tacrolimus and pimecrolimus serve as steroid-sparing alternatives particularly useful for sensitive areas such as the face, eyelids, and genital region where chronic corticosteroid use risks atrophy and telangiectasia. Oral antihistamines provide symptomatic relief of pruritus, with sedating agents such as hydroxyzine being particularly useful at bedtime, and severe or refractory cases warrant referral to dermatology for consideration of phototherapy or systemic immunomodulatory agents including dupilumab.
Understanding topical corticosteroid potency is essential for safe and effective prescribing. The potency classification ranges from class one (super-high potency, such as clobetasol propionate 0.05 percent) to class seven (low potency, such as hydrocortisone 1 percent). Low-potency agents are appropriate for thin-skinned areas including the face, eyelids, axillae, and groin, as well as for use in children and for prolonged treatment courses. Medium-potency agents such as triamcinolone acetonide 0.1 percent are suitable for most body surfaces. High-potency agents such as fluocinonide 0.05 percent are reserved for thick plaques, palms, and soles where the stratum corneum limits penetration. Super-high-potency agents should be used for limited areas and short durations only, typically no more than two consecutive weeks, to minimize the risk of skin atrophy, striae, and systemic absorption.
<image>Panel A: Age-dependent distribution of atopic dermatitis showing facial and extensor involvement in infants, flexural involvement in children and adults, with clinical photographs of each pattern and histologic features of spongiotic dermatitis. Panel B: Comparison of irritant and allergic contact dermatitis with examples including diaper rash, hand dermatitis, poison ivy in a linear pattern, and nickel dermatitis beneath a belt buckle. Panel C: Stepwise treatment algorithm for eczema progressing from moisturizers through topical steroids, calcineurin inhibitors, antihistamines, and systemic agents with specific drug names and application instructions. Panel D: Topical corticosteroid potency ladder showing class one through seven with representative agents, appropriate anatomic sites for each potency level, and potential adverse effects of chronic use including atrophy and striae.</image>
Section 6: Papulosquamous Disorders
Psoriasis is a chronic, immune-mediated inflammatory disease that affects approximately two to three percent of the population and presents with well-demarcated, erythematous plaques covered by a thick, silvery-white scale. The classic plaque type is the most common variant and favors the scalp, elbows, knees, and intergluteal cleft. Other morphologic variants include guttate psoriasis, which presents with numerous small droplet-like papules often following streptococcal pharyngitis, inverse psoriasis affecting intertriginous areas without prominent scale, and pustular psoriasis characterized by sterile pustules. Nail involvement is common and manifests as pitting, onycholysis, oil-drop discoloration, and subungual hyperkeratosis. Approximately thirty percent of patients with psoriasis develop psoriatic arthritis, an inflammatory arthropathy that should be actively screened for with questions about joint pain, stiffness, and swelling.
Treatment of psoriasis is tailored to disease severity and patient preferences. Mild disease affecting less than three percent of body surface area is managed with topical corticosteroids, vitamin D analogues such as calcipotriene, and combinations of these agents. Moderate disease may require phototherapy with narrowband ultraviolet B, which is effective and well-tolerated, or combination topical regimens. Severe psoriasis or disease refractory to topical measures warrants systemic therapy, including traditional agents such as methotrexate and cyclosporine, as well as newer biologic agents targeting specific inflammatory cytokines. The biologic revolution has transformed the management of moderate-to-severe psoriasis, with TNF-alpha inhibitors, interleukin-17 inhibitors, and interleukin-23 inhibitors achieving high rates of skin clearance. Patients with moderate-to-severe disease should be referred to dermatology for initiation and monitoring of these specialized therapies.
Seborrheic dermatitis is an extremely common chronic inflammatory condition attributed to an immune response to Malassezia yeast colonizing sebum-rich areas of the skin. It presents as erythema with greasy, yellowish scale on the scalp, where it is commonly known as dandruff, and on the face, particularly affecting the eyebrows, nasolabial folds, and external ears. The condition follows a waxing and waning course and is aggravated by stress, fatigue, and changes in weather. An association exists with neurologic conditions such as Parkinson disease and with immunosuppression, particularly HIV infection, where seborrheic dermatitis may be severe and treatment-resistant. First-line management includes antifungal shampoos containing ketoconazole, selenium sulfide, or zinc pyrithione, with low-potency topical corticosteroids or topical calcineurin inhibitors for facial involvement.
Pityriasis rosea is a self-limited papulosquamous eruption that predominantly affects young adults and is thought to have a viral etiology, possibly related to human herpesvirus 6 or 7. The condition characteristically begins with a single oval, erythematous, scaly herald patch on the trunk, followed one to two weeks later by the eruption of numerous smaller oval patches distributed along the skin cleavage lines in a pattern described as a Christmas tree distribution on the back. The lesions may be mildly pruritic but are otherwise asymptomatic, and the eruption resolves spontaneously over six to eight weeks without treatment. Management is supportive, with topical emollients and oral antihistamines for pruritus. Importantly, secondary syphilis can mimic the appearance of pityriasis rosea, so RPR or VDRL testing should be considered in sexually active patients, particularly when palms and soles are involved or when the eruption is atypical.
<image>Panel A: Clinical photographs of psoriasis variants including plaque psoriasis with silvery scale on the elbow, guttate psoriasis with scattered droplet papules, inverse psoriasis in the axilla, and nail psoriasis demonstrating pitting and onycholysis. Panel B: Treatment algorithm for psoriasis stratified by severity from mild topical therapy through phototherapy to systemic biologics, with specific drug classes and response rates. Panel C: Seborrheic dermatitis affecting the scalp with greasy yellow flaking, nasolabial folds with erythema and scale, and eyebrows with close-up of characteristic features. Panel D: Pityriasis rosea showing the herald patch with collarette of scale, followed by the Christmas tree distribution of secondary lesions on the trunk along Langer lines.</image>
Section 7: Skin Cancer Screening
The ABCDE criteria represent the cornerstone of clinical assessment for melanoma in pigmented lesions. Asymmetry refers to a lesion in which one half does not mirror the other. Border irregularity describes ragged, notched, or blurred margins rather than smooth, round contours. Color variation within a single lesion, including shades of brown, black, red, white, and blue, raises suspicion. Diameter greater than six millimeters, roughly the size of a pencil eraser, is a traditional threshold, though melanomas can present at smaller sizes. Evolution, the most important criterion, encompasses any change in size, shape, color, elevation, or the development of new symptoms such as bleeding or itching. The ugly duckling sign, in which a lesion looks different from the patient's other moles, is an additional useful heuristic for identifying suspicious lesions.
The three major types of skin cancer differ in their clinical presentation, biologic behavior, and management. Basal cell carcinoma, the most common skin cancer, typically presents as a pearly or waxy papule with telangiectasia and rolled borders, most often on sun-exposed areas of the head and neck. Squamous cell carcinoma appears as a scaly, erythematous plaque or nodule that may ulcerate and can metastasize, particularly when arising on the lips, ears, or in immunosuppressed patients. Melanoma is the most dangerous skin cancer, presenting as an irregular pigmented lesion that may arise de novo or within a preexisting nevus, and has significant metastatic potential if not detected early. Actinic keratoses are precancerous lesions presenting as rough, gritty, scaly patches on sun-damaged skin that carry a small but measurable risk of progressing to squamous cell carcinoma.
Multiple risk factors contribute to the development of skin cancer and should be assessed during patient encounters. Cumulative ultraviolet radiation exposure is the primary risk factor for basal cell and squamous cell carcinoma, while a history of intermittent intense sun exposure with blistering sunburns correlates more strongly with melanoma risk. Fair-skinned individuals with Fitzpatrick skin types I and II who burn easily and tan poorly are at substantially higher risk. A family history of melanoma, particularly in first-degree relatives, confers increased risk, as does the presence of more than fifty common nevi or any atypical or dysplastic nevi. Immunosuppression, particularly in organ transplant recipients, markedly increases the risk of squamous cell carcinoma. Indoor tanning bed use has been definitively linked to increased melanoma risk and is classified as a group one carcinogen.
Current screening recommendations for skin cancer reflect the tension between the potential benefits of early detection and the limited evidence base. The United States Preventive Services Task Force has issued an I statement indicating insufficient evidence to assess the balance of benefits and harms of visual skin examination in the general asymptomatic population. However, clinicians should perform skin examinations in patients with identifiable risk factors and maintain a high index of suspicion during routine examinations. Patient education on monthly self-examination, including the use of mirrors to inspect the back and scalp, is an important component of preventive care. Any lesion meeting ABCDE criteria, appearing as an ugly duckling, or causing clinical concern should undergo biopsy, ideally an excisional biopsy for suspected melanoma. Prompt dermatology referral is appropriate for lesions of uncertain diagnosis or when the clinician lacks confidence in performing the indicated biopsy.
<image>Panel A: Side-by-side comparison of ABCDE criteria with photographs of benign nevi versus melanoma demonstrating asymmetry, border irregularity, color variation, large diameter, and evolution over time. Panel B: Clinical photographs of skin cancer types including basal cell carcinoma with pearly papule and telangiectasia, squamous cell carcinoma with scaly erythematous nodule, melanoma with irregular pigmented plaque, and actinic keratosis with rough scaly patch. Panel C: Infographic displaying modifiable and non-modifiable skin cancer risk factors including UV exposure patterns, skin type, family history, mole count, immunosuppression, and tanning bed use. Panel D: Screening and management algorithm showing USPSTF recommendations, high-risk patient identification, self-examination technique, biopsy decision pathway, and referral criteria.</image>
Section 8: Common Benign Lesions
Seborrheic keratoses are the most frequently encountered benign skin growths in older adults and are often a source of patient concern due to their sometimes alarming appearance. These lesions present with a characteristic stuck-on appearance, exhibiting a warty, verrucous surface with a well-defined border and colors ranging from tan to dark brown or black. They develop on any body surface except the palms and soles and increase in number with age. Seborrheic keratoses have no malignant potential and require no treatment, though they may be removed if they become symptomatic from friction or irritation, or if they are cosmetically bothersome. The sudden eruption of numerous seborrheic keratoses, known as the sign of Leser-Trelat, has been associated with internal malignancy, though the strength of this association is debated.
Cherry angiomas are benign vascular proliferations that are extremely common in adults, increasing in prevalence with advancing age. They present as bright red to deep purple, dome-shaped papules ranging from one to several millimeters in diameter, occurring predominantly on the trunk. The color results from the dense collection of dilated capillaries within the lesion. Cherry angiomas are entirely benign and require no treatment or monitoring. Patients who find them cosmetically unacceptable may elect removal through electrocautery, pulsed dye laser, or shave excision. Reassurance regarding their benign nature is often the most important intervention, as patients frequently present with anxiety about the lesions.
Skin tags, known medically as acrochordons, are soft, pedunculated, flesh-colored to brown papules that arise in areas of skin friction. The most common locations include the neck, axillae, and inguinal folds. They are extremely common in adults, with prevalence increasing with age, obesity, and during pregnancy due to hormonal influences. Skin tags are associated with insulin resistance and the metabolic syndrome, so their presence, particularly in large numbers, may prompt screening for diabetes and assessment of cardiovascular risk factors. Treatment is not medically necessary, but symptomatic or cosmetically bothersome tags can be removed by simple snip excision with scissors, cryotherapy, or electrocautery, usually without the need for local anesthesia for small lesions.
Lipomas are benign soft tissue tumors composed of mature adipocytes that present as soft, mobile, well-circumscribed subcutaneous nodules. They are the most common benign mesenchymal neoplasm, occurring in approximately one percent of the population, and can develop anywhere on the body, with the trunk and extremities being most common. Lipomas are typically painless, though angiolipomas, which contain vascular elements, may be tender. Clinical diagnosis is usually straightforward based on the characteristic softness, mobility, and rubbery consistency of the mass. Observation is appropriate for typical lipomas, with excision reserved for those that are symptomatic, rapidly growing, or cosmetically bothersome. Red flags that should prompt further evaluation with imaging and possible biopsy include rapid growth, fixation to underlying structures, size greater than five centimeters, deep location, and pain, as these features raise concern for liposarcoma.
<image>Panel A: Clinical photograph of multiple seborrheic keratoses on the trunk showing the characteristic stuck-on appearance with waxy, verrucous surface and varying shades of brown, with dermoscopic view demonstrating cerebriform pattern and milia-like cysts. Panel B: Close-up photograph of cherry angiomas on the trunk showing bright red dome-shaped papules of varying sizes, with dermoscopic view revealing lacunar red structures. Panel C: Skin tags on the neck and axilla showing soft, pedunculated, flesh-colored papules, with demonstration of snip excision technique using iris scissors. Panel D: Lipoma on the forearm showing a smooth, mobile, subcutaneous nodule with normal overlying skin, compared with ultrasound image demonstrating a well-encapsulated homogeneous hyperechoic mass.</image>
Section 9: Acne and Rosacea
Acne vulgaris is a multifactorial inflammatory disease of the pilosebaceous unit and is the most common skin condition managed in primary care, affecting up to eighty-five percent of adolescents and young adults. The pathogenesis involves four key mechanisms: hyperkeratinization of the follicular epithelium leading to comedone formation, excess sebum production stimulated by androgens, colonization and proliferation of Cutibacterium acnes within the obstructed follicle, and subsequent inflammation. Clinical morphology ranges from non-inflammatory comedones, both open (blackheads) and closed (whiteheads), to inflammatory papules, pustules, and deep nodules or cysts. Acne severity is graded as mild (predominantly comedonal), moderate (mixed comedonal and inflammatory), or severe (nodulocystic), which guides treatment selection. The psychosocial impact of acne is significant and often underestimated, with effects on self-esteem, body image, and social functioning, particularly in adolescents.
Treatment of acne follows a stepwise, severity-based approach. Mild comedonal acne is treated with a topical retinoid such as tretinoin, adapalene, or tazarotene, which normalizes follicular keratinization and prevents microcomedone formation. For mild inflammatory acne, benzoyl peroxide or a topical antibiotic such as clindamycin is added, with benzoyl peroxide being preferred because it reduces C. acnes without promoting antibiotic resistance. Moderate acne typically requires combination topical therapy, often a fixed-dose combination product containing a retinoid, benzoyl peroxide, and sometimes clindamycin, with oral antibiotics such as doxycycline or minocycline added for more widespread disease. Severe nodulocystic acne that fails conventional therapy is the primary indication for isotretinoin, which is the most effective treatment for severe acne but carries significant teratogenic risk, necessitating enrollment in the iPLEDGE risk management program with mandatory pregnancy testing and dual contraception for female patients of childbearing potential.
Rosacea is a chronic inflammatory condition of the central face that affects adults, predominantly those with lighter skin types, and is classified into four subtypes. Erythematotelangiectatic rosacea is characterized by persistent central facial erythema and telangiectasia with a tendency to flush easily. Papulopustular rosacea presents with inflammatory papules and pustules superimposed on background erythema, closely mimicking acne vulgaris but lacking comedones. Phymatous rosacea involves thickening and irregular enlargement of the skin, most notably rhinophyma of the nose. Ocular rosacea manifests as blepharitis, conjunctival injection, and foreign body sensation. Common triggers include sun exposure, alcohol, spicy foods, extreme temperatures, and emotional stress. Treatment begins with trigger avoidance and gentle skin care, with topical metronidazole, azelaic acid, or ivermectin for erythema and papulopustular disease, and oral doxycycline for moderate-to-severe papulopustular or ocular involvement.
Perioral dermatitis is an inflammatory facial dermatitis that presents as grouped erythematous papules and pustules distributed around the mouth, with characteristic sparing of the skin immediately adjacent to the vermilion border. It predominantly affects young women and is strongly associated with the use of topical corticosteroids on the face, which initially suppress the eruption but lead to rebound flaring upon discontinuation, creating a cycle of dependence. Other inciting factors include fluorinated toothpaste, cosmetics, and physical sunscreen agents. Treatment requires cessation of all topical corticosteroids, which may initially cause a flare that should be anticipated and discussed with the patient. Definitive therapy consists of topical metronidazole or erythromycin for mild cases and oral doxycycline for more extensive disease, with improvement typically seen over six to twelve weeks.
<image>Panel A: Clinical spectrum of acne vulgaris showing open comedones (blackheads), closed comedones (whiteheads), inflammatory papules and pustules, and severe nodulocystic lesions, with diagram of pilosebaceous unit pathogenesis showing hyperkeratinization, sebum excess, C. acnes proliferation, and inflammation. Panel B: Acne treatment ladder diagram progressing from topical retinoid monotherapy for mild disease through combination topicals, oral antibiotics for moderate disease, to isotretinoin for severe refractory acne, with specific drug names and iPLEDGE requirements. Panel C: Rosacea subtypes with clinical photographs showing erythematotelangiectatic with central facial flushing and telangiectasia, papulopustular with inflammatory papules, phymatous with rhinophyma, and ocular with blepharitis and conjunctival injection. Panel D: Perioral dermatitis showing grouped papules and pustules around the mouth with sparing of the vermilion border, alongside before-and-after photographs demonstrating resolution following corticosteroid cessation and metronidazole therapy.</image>
Section 10: When to Refer
Biopsy is indicated whenever a skin lesion raises clinical concern for malignancy, fails to respond to appropriate empiric therapy, or presents with atypical features that preclude confident clinical diagnosis. Any changing mole that meets ABCDE criteria or appears as an ugly duckling warrants prompt biopsy, preferably excisional for suspected melanoma to allow accurate Breslow thickness measurement. Non-healing ulcers or nodules persisting beyond four to six weeks, particularly on sun-exposed skin, should be biopsied to exclude squamous cell or basal cell carcinoma. Diagnostic uncertainty after a reasonable treatment trial is also an appropriate indication, as histopathologic examination provides definitive characterization. Finally, patients may request biopsy for their own peace of mind, and this is a valid reason to proceed when the clinical scenario is reasonable.
Dermatology referral is appropriate for a range of conditions that exceed the typical scope of primary care management. Suspected skin cancer should be referred for definitive biopsy, staging, and treatment planning. Severe cystic acne requiring isotretinoin necessitates referral to a provider experienced with this medication and the iPLEDGE program. Moderate-to-severe psoriasis requiring systemic therapy or biologics, generalized or refractory eczema, and autoimmune blistering diseases such as pemphigus and bullous pemphigoid all warrant specialist management. Conditions that have failed adequate primary care treatment after appropriate therapeutic trials should also be referred, as the dermatologist brings additional diagnostic tools including dermoscopy, specialized biopsy techniques, and a wealth of pattern recognition experience.
Urgent or emergent referral is required for several dermatologic conditions that carry significant morbidity or mortality risk. Melanoma suspicion mandates urgent biopsy, ideally within one to two weeks, given the direct relationship between tumor thickness at diagnosis and prognosis. Rapidly spreading rashes with mucosal involvement, skin pain, or systemic symptoms raise concern for Stevens-Johnson syndrome, toxic epidermal necrolysis, or drug reaction with eosinophilia and systemic symptoms, all of which require immediate evaluation and may necessitate hospital admission. Cellulitis accompanied by systemic toxicity, rapid progression despite antibiotics, or periorbital involvement may require inpatient parenteral antibiotic therapy. Herpes zoster ophthalmicus, involving the ophthalmic division of the trigeminal nerve, requires urgent ophthalmology evaluation to assess for ocular involvement that could threaten vision.
Patient education is a fundamental component of dermatologic care in the primary care setting. Sun protection counseling should emphasize the use of broad-spectrum sunscreen with SPF thirty or higher applied generously and reapplied every two hours or after swimming or sweating, along with protective clothing, wide-brimmed hats, and avoidance of midday sun exposure between ten in the morning and two in the afternoon. Patients should be instructed in monthly self-examination of the skin, including the use of a full-length mirror and a hand mirror to inspect the back, scalp, and other difficult-to-see areas. Proper use of prescribed topical medications, including amount, frequency, and duration, should be reviewed explicitly, as adherence to topical regimens is notoriously poor. Return visit criteria should be clearly communicated, including signs of infection such as increasing redness, warmth, or purulent drainage, non-healing lesions, and any changing moles.
<image>Panel A: Decision algorithm for skin biopsy showing indications including suspicious pigmented lesions, non-healing ulcers, treatment-refractory conditions, and atypical presentations, with preferred biopsy type for each scenario. Panel B: Referral pathway diagram showing conditions appropriate for routine dermatology referral including severe acne, moderate-severe psoriasis, refractory eczema, and blistering diseases with expected wait times and interim management. Panel C: Urgent dermatologic conditions requiring emergent evaluation including suspected melanoma, Stevens-Johnson syndrome with mucosal erosions and skin pain, rapidly progressive cellulitis, and herpes zoster ophthalmicus with Hutchinson sign. Panel D: Patient education materials showing proper sunscreen application technique, monthly self-examination steps with mirror positioning, correct topical medication application using the fingertip unit measurement, and return-to-clinic warning signs.</image>
Summary
- Primary lesions are classified as flat (macule, patch), raised solid (papule, plaque, nodule), or fluid-filled (vesicle, bulla, pustule), and distribution patterns provide critical diagnostic clues
- Cellulitis presents with erythema, warmth, and swelling without purulence and is treated with cephalexin, with MRSA coverage added when purulence or risk factors are present
- Herpes zoster presents as dermatomal vesicles requiring antivirals within seventy-two hours, and the Shingrix vaccine is recommended for adults aged fifty and older
- Tinea is diagnosed with KOH preparation showing branching hyphae, treated topically for body infections and systemically for scalp and nail involvement
- Atopic dermatitis management centers on liberal moisturizer use with topical corticosteroids for flares, matching potency to anatomic site
- Topical corticosteroid potency should be low for face and skin folds, medium for body surfaces, and high potency reserved for thick plaques with limited duration
- Psoriasis presents with silvery scale on elbows, knees, and scalp, and moderate-to-severe disease should be referred for systemic or biologic therapy
- The ABCDE criteria for melanoma assessment are Asymmetry, Border irregularity, Color variation, Diameter greater than six millimeters, and Evolution of the lesion
- Acne treatment follows a stepwise approach from topical retinoid through combination topicals and oral antibiotics to isotretinoin for severe disease
- Any changing mole, non-healing lesion, or lesion suspicious for malignancy warrants biopsy, with urgent referral for suspected melanoma
Key Terms
| Term | Definition |
|---|---|
| Macule | Flat, circumscribed lesion less than one centimeter in diameter |
| Papule | Raised solid lesion less than one centimeter in diameter |
| Vesicle | Fluid-filled lesion less than one centimeter in diameter |
| Scale | Flaking epidermal cells on the skin surface |
| Dermatomal | Following the distribution of a single nerve root |
| KOH prep | Potassium hydroxide preparation used to visualize fungal hyphae under microscopy |
| Topical steroid | Anti-inflammatory corticosteroid medication applied directly to the skin surface |
| Actinic keratosis | Pre-cancerous rough scaly lesion resulting from chronic ultraviolet radiation exposure |
This content is subject to the MIT License. © 2024–2026 Hibbert School of Medicine.









