# Lecture 8: Common Dermatologic Conditions ## Unit 2.10: Musculoskeletal System/Dermatology --- ## Learning Objectives By the end of this lecture, students will be able to: 1. Describe the pathophysiology and management of acne vulgaris 2. Explain the clinical features and treatment of atopic dermatitis 3. Describe the types and management of psoriasis 4. Explain contact dermatitis and its differentiation 5. Describe seborrheic dermatitis and rosacea 6. Explain the principles of topical therapy in dermatology --- ## Lecture Outline ### I. Acne Vulgaris Acne vulgaris is one of the most common dermatologic conditions encountered in clinical practice, affecting 80-90% of adolescents and representing a major source of morbidity during a developmentally critical period. The peak incidence occurs between ages 14 and 19, coinciding with the pubertal surge in androgen production that drives sebaceous gland activity. Although acne is traditionally considered a disease of adolescence, it may persist well into adulthood in a significant proportion of patients, particularly women, in whom hormonal fluctuations continue to influence sebaceous gland function. The impact of acne extends far beyond the skin, causing significant psychosocial distress including diminished self-esteem, social withdrawal, anxiety, and depression, and in severe cases producing permanent scarring that can affect quality of life for decades. The pathogenesis of acne involves four interconnected factors that create a self-perpetuating cycle of follicular obstruction and inflammation. Sebum overproduction is the initiating event, driven by androgen stimulation of sebaceous glands during puberty, with dihydrotestosterone being the primary hormonal stimulus for increased sebaceous gland size and activity. Follicular hyperkeratinization occurs when the keratinocytes lining the follicular infundibulum proliferate abnormally and become cohesive rather than shedding normally, creating the microcomedone that is the precursor to all visible acne lesions. Cutibacterium acnes (formerly Propionibacterium acnes) is an anaerobic commensal bacterium that thrives in the lipid-rich, oxygen-poor environment of the obstructed follicle and triggers inflammation through activation of innate immune pathways including Toll-like receptor 2 signaling. The resulting inflammatory response produces the papules, pustules, and nodules characteristic of inflammatory acne, with the intensity of inflammation determining whether lesions resolve without sequelae or progress to scarring. Acne lesions are classified as non-inflammatory (comedonal) or inflammatory, with the severity and predominant lesion type guiding treatment selection. Open comedones, commonly known as blackheads, feature a dilated follicular pore containing a plug of keratinized debris whose dark color results from oxidation of melanin and lipids rather than trapped dirt. Closed comedones, or whiteheads, are small, flesh-colored papules with an intact overlying epithelium that traps sebum and keratin beneath the surface. Inflammatory papules are red, tender, raised lesions resulting from rupture of the comedone wall and release of follicular contents into the surrounding dermis, while pustules represent a further stage with accumulation of purulent material. Nodules and cysts are the most severe acne lesions, representing deep, painful inflammatory masses in the dermis and subcutaneous tissue that carry the highest risk of permanent scarring. Acne characteristically distributes on the face, chest, and back corresponding to areas of highest sebaceous gland density. Clinical classification of acne severity guides therapeutic decision-making and facilitates communication between providers. Mild acne is characterized by predominance of comedones with few inflammatory lesions and is typically managed with topical therapy alone. Moderate acne features a greater number of papules and pustules with more prominent inflammatory involvement, often requiring a combination of topical and oral agents. Severe acne involves widespread nodules and cysts with significant inflammation and a high risk of scarring, often warranting consideration of isotretinoin. Acne fulminans is a rare but dramatic variant presenting with ulcerative, hemorrhagic lesions accompanied by systemic symptoms including fever, arthralgias, myalgias, and laboratory abnormalities, requiring urgent systemic treatment including corticosteroids. Panel A: Acne pathogenesis showing sebaceous gland hyperactivity with excess sebum production, follicular hyperkeratinization forming microcomedone, Cutibacterium acnes colonization, and inflammatory cascade activation. Panel B: Acne lesion types including open comedone (blackhead with oxidized keratin plug), closed comedone (whitehead), inflammatory papule, pustule with purulent material, and deep nodule/cyst. Panel C: Acne severity grading from mild (comedones with few inflammatory lesions), moderate (papules and pustules), to severe (nodules, cysts, widespread involvement). Panel D: Distribution pattern showing face (forehead, cheeks, chin), chest, and back involvement corresponding to sebaceous gland density. --- ### II. Acne Treatment Topical retinoids form the foundation of acne therapy and should be included in virtually all treatment regimens due to their unique ability to address follicular hyperkeratinization, the fundamental pathogenic event in acne. Tretinoin is considered the gold standard topical retinoid, acting as a potent comedolytic agent that normalizes keratinization within the follicular epithelium and promotes turnover of existing comedones. Adapalene is a synthetic retinoid that is generally less irritating than tretinoin and is available over the counter, making it an excellent first-line option for many patients, particularly those with sensitive skin. Tazarotene is the most potent of the topical retinoids but also the most irritating, and is typically reserved for patients with more resistant disease. All topical retinoids work by normalizing the keratinization process within hair follicles, and their common side effects include dryness, irritation, and photosensitivity, which can be mitigated through gradual introduction and concurrent use of moisturizers. Additional topical agents complement retinoids by targeting different aspects of acne pathogenesis. Benzoyl peroxide is a bactericidal agent that generates free radicals to kill C. acnes without inducing antimicrobial resistance, a critical advantage over antibiotics, and it is frequently combined with retinoids or topical antibiotics for synergistic effect. Topical antibiotics, primarily clindamycin and erythromycin, reduce the C. acnes population and exert anti-inflammatory effects, though they should always be used in combination with benzoyl peroxide to prevent the emergence of antibiotic-resistant organisms. Azelaic acid is a dicarboxylic acid with comedolytic, antimicrobial, and anti-inflammatory properties that is particularly useful in patients with post-inflammatory hyperpigmentation due to its additional inhibition of tyrosinase. Salicylic acid is a beta-hydroxy acid with comedolytic activity that is available in many over-the-counter formulations and is well-tolerated, though generally less effective than retinoids for comedone clearance. Systemic therapy is indicated for moderate-to-severe acne or when topical therapy alone is insufficient to achieve adequate control. Oral antibiotics, most commonly doxycycline and minocycline from the tetracycline class, are used for moderate-to-severe inflammatory acne and work through both antimicrobial and anti-inflammatory mechanisms. Hormonal therapy is an effective option for women with acne, with oral contraceptive pills containing anti-androgenic progestins reducing sebum production, and spironolactone acting as an androgen receptor blocker that is particularly useful for adult female acne. Isotretinoin is reserved for severe, nodulocystic acne or acne that is resistant to other therapies and scarring acne, as it is the only medication that targets all four pathogenic factors of acne simultaneously. Isotretinoin (13-cis-retinoic acid) is the most effective single agent for acne treatment and is unique in its ability to produce long-lasting remission in the majority of patients. Its mechanism of action includes dramatic reduction in sebaceous gland size and sebum production, decreased C. acnes colonization due to the unfavorable follicular environment, normalization of follicular keratinization, and direct anti-inflammatory effects. A typical course of treatment lasts 4 to 6 months, with dosing targeted to achieve a cumulative dose that minimizes relapse rates. The iPLEDGE program is a mandatory risk management program in the United States designed to prevent fetal exposure to isotretinoin, which is a potent teratogen classified as category X, requiring two forms of contraception and monthly pregnancy testing in female patients of childbearing potential. Common side effects include mucocutaneous dryness affecting the lips, skin, and eyes, elevated serum lipids (particularly triglycerides), transaminitis, and myalgias, necessitating baseline and periodic monitoring of pregnancy tests, liver function tests, and lipid panels throughout treatment. Panel A: Acne treatment algorithm showing mild disease (topical retinoid plus benzoyl peroxide), moderate disease (add oral antibiotic), and severe/nodulocystic disease (isotretinoin consideration). Panel B: Topical retinoid mechanism demonstrating normalization of follicular keratinization, comedone reduction, and anti-inflammatory effects at the cellular level. Panel C: Isotretinoin effects showing sebaceous gland atrophy with reduced sebum production, decreased C. acnes colonization, and anti-inflammatory activity. Panel D: Isotretinoin monitoring requirements including iPLEDGE program for pregnancy prevention, baseline and monthly pregnancy tests, lipid panel, and liver function tests with common side effects listed. --- ### III. Atopic Dermatitis Atopic dermatitis is a chronic, relapsing inflammatory skin disease that represents one of the most common dermatologic conditions in children and a significant cause of morbidity across all age groups. The prevalence is 10-20% in children and 1-3% in adults, with onset typically occurring in early childhood and often improving with age, though a subset of patients experience persistent or adult-onset disease. Atopic dermatitis is a key component of the atopic triad, frequently occurring in association with asthma and allergic rhinitis, reflecting a shared genetic predisposition to Th2-mediated immune dysregulation. The clinical course is characterized by periods of exacerbation and remission, with flares triggered by environmental factors, infections, stress, and irritant exposure. The pathophysiology of atopic dermatitis involves a complex interplay between epidermal barrier dysfunction and immune dysregulation that creates a self-amplifying cycle of inflammation. Barrier dysfunction, most notably associated with loss-of-function mutations in the filaggrin gene, results in impaired stratum corneum integrity and increased transepidermal water loss, allowing penetration of allergens, irritants, and microorganisms that trigger immune activation. Immune dysregulation is characterized by a predominance of Th2 lymphocytes that produce the key cytokines interleukin-4 (IL-4), interleukin-13 (IL-13), and interleukin-31 (IL-31), with IL-4 and IL-13 further impairing barrier function by downregulating filaggrin expression and IL-31 being a major mediator of the intense pruritus that characterizes this disease. The itch-scratch cycle is a central feature of atopic dermatitis pathophysiology, in which pruritus drives scratching that causes further epidermal damage, inflammation, and release of pruritogenic mediators, perpetuating a vicious cycle of barrier disruption and immune activation. The clinical features of atopic dermatitis vary characteristically with age, though intense pruritus is the hallmark feature across all age groups. In infants, the eruption typically involves the face, scalp, and extensor surfaces of the extremities, presenting as erythematous, oozing, crusted patches that may be mistaken for seborrheic dermatitis or other infantile dermatoses. In older children, the distribution shifts to a flexural pattern with involvement of the antecubital fossae, popliteal fossae, and neck, where chronic rubbing leads to the development of lichenified plaques with accentuated skin markings. In adults, atopic dermatitis commonly affects the hands, flexural areas, face, and neck, and chronic disease produces lichenification that may be the predominant finding rather than the acute erythematous lesions seen in younger patients. Several associated features are characteristic of atopic dermatitis and aid in clinical diagnosis. Xerosis, or diffuse dry skin, is nearly universal and reflects the underlying barrier dysfunction that is central to disease pathogenesis. Ichthyosis vulgaris is comorbid in a significant proportion of patients due to shared filaggrin mutations. Keratosis pilaris, commonly described as "chicken skin," presents as rough, follicular papules on the lateral upper arms and thighs. Dennie-Morgan folds are prominent infraorbital creases resulting from chronic periorbital edema and rubbing, while allergic shiners refer to the periorbital darkening caused by venous congestion related to chronic nasal and sinus inflammation seen in the atopic patient. Panel A: Age-related distribution showing infant pattern (face, scalp, extensor surfaces), childhood pattern (flexural involvement of antecubital and popliteal fossae), and adult pattern (hands, face, neck, flexures). Panel B: Dennie-Morgan folds (infraorbital creases) and allergic shiners (periorbital darkening) as characteristic facial findings in atopic patients. Panel C: Lichenification from chronic scratching showing thickened skin with accentuated skin markings, hyperpigmentation, and comparison to normal skin texture. Panel D: Pathophysiology diagram showing filaggrin mutation leading to barrier dysfunction, Th2 immune predominance with IL-4, IL-13, and IL-31 cytokines, and itch-scratch cycle perpetuating inflammation. --- ### IV. Atopic Dermatitis Treatment Foundational skin care measures are essential in all patients with atopic dermatitis and form the basis upon which all other therapeutic interventions are built. Moisturizers should be applied at least twice daily and ideally immediately after bathing to trap moisture in the skin, with ointments being preferred over creams due to their greater occlusive properties and absence of potentially irritating preservatives. Bathing should be performed in lukewarm rather than hot water with limited duration to avoid further drying and disruption of the epidermal barrier. Identification and avoidance of triggers, including irritants such as wool, harsh soaps, fragrances, and known allergens, is crucial for preventing flares. Gentle, fragrance-free cleansers should replace traditional soaps, which can strip the skin of natural lipids and exacerbate xerosis. Topical anti-inflammatory agents are the first-line pharmacologic therapy for active atopic dermatitis flares. Topical corticosteroids remain the cornerstone of treatment, with potency selection guided by the anatomic location and severity of disease: low-potency agents such as hydrocortisone for the face, eyelids, and intertriginous areas, and medium-to-high-potency agents for the trunk and extremities. Topical calcineurin inhibitors, including tacrolimus and pimecrolimus, are particularly valuable as steroid-sparing agents for sensitive areas such as the face and periorbital region where prolonged corticosteroid use risks atrophy and telangiectasia. Crisaborole is a topical phosphodiesterase 4 (PDE4) inhibitor approved for mild-to-moderate atopic dermatitis that provides an additional non-steroidal option. Ruxolitinib is a topical Janus kinase (JAK) inhibitor that represents a newer class of topical therapy targeting the JAK-STAT signaling pathway central to Th2 cytokine activity. Systemic therapy is reserved for moderate-to-severe atopic dermatitis that is inadequately controlled with optimized topical management. Dupilumab is a monoclonal antibody targeting the interleukin-4 receptor alpha subunit, thereby blocking signaling of both IL-4 and IL-13, and has transformed the treatment landscape for moderate-to-severe atopic dermatitis with demonstrated efficacy in both clearing skin disease and reducing pruritus. Tralokinumab is a monoclonal antibody that specifically neutralizes IL-13, providing an alternative biologic option for patients with moderate-to-severe disease. Oral JAK inhibitors, including upadacitinib and abrocitinib, are small molecule agents that target intracellular signaling downstream of multiple cytokine receptors and offer the convenience of oral administration with rapid onset of action. Cyclosporine may be used for short-term control of severe flares, while methotrexate is sometimes employed off-label as a steroid-sparing systemic agent for chronic severe disease. Complications of atopic dermatitis result from the combination of barrier dysfunction and immune dysregulation that characterizes this disease. Eczema herpeticum is a potentially life-threatening superinfection with herpes simplex virus presenting as widespread punched-out erosions, vesicles, and hemorrhagic crusts with associated fever and lymphadenopathy, requiring urgent treatment with systemic antiviral therapy such as intravenous acyclovir. Staphylococcus aureus colonization is extremely common in atopic dermatitis, affecting over 90% of patients due to decreased antimicrobial peptide production and altered skin microbiome, and may require decolonization strategies including dilute bleach baths and intranasal mupirocin when contributing to disease flares. Secondary bacterial impetigo manifests as honey-colored crusts superimposed on eczematous lesions and requires appropriate antibiotic therapy in addition to ongoing anti-inflammatory management. Panel A: Topical corticosteroid potency ladder from low potency (hydrocortisone for face and groin) through medium (triamcinolone for body) to high potency (clobetasol for thick plaques on palms/soles). Panel B: Dupilumab mechanism showing IL-4 receptor alpha blockade preventing IL-4 and IL-13 signaling, reducing Th2 inflammation and improving barrier function. Panel C: Eczema herpeticum recognition showing clustered vesicles and punched-out erosions, fever and lymphadenopathy, and urgency of antiviral treatment. Panel D: Treatment ladder for atopic dermatitis from emollients and trigger avoidance through topical anti-inflammatories to systemic therapy (dupilumab, JAK inhibitors) for moderate-severe disease. --- ### V. Psoriasis Psoriasis is a chronic, immune-mediated inflammatory skin disease affecting approximately 2-3% of the population worldwide, with significant associated systemic comorbidities that extend its impact well beyond the skin. The age of onset shows a bimodal distribution, with the first peak occurring between 15 and 30 years of age and a second smaller peak between 50 and 60 years, though the disease can develop at any age. There is a strong genetic component to psoriasis, with the HLA-Cw6 allele being the most consistently associated genetic marker, particularly for early-onset disease. Environmental triggers including streptococcal pharyngitis, stress, medications (lithium, beta-blockers, antimalarials), alcohol, and smoking can precipitate disease onset or exacerbate existing psoriasis in genetically predisposed individuals. The pathophysiology of psoriasis centers on dysregulated immune activation involving the IL-23/Th17 axis, which drives the characteristic epidermal hyperproliferation and inflammation. Th17 and Th1 lymphocytes in the skin produce key pro-inflammatory cytokines including IL-17, IL-23, and TNF-alpha that create a self-sustaining inflammatory cascade. These cytokines stimulate keratinocyte proliferation, accelerating epidermal turnover from the normal 28 days to just 3 to 5 days, which does not allow adequate time for keratinocyte maturation and results in the accumulation of immature, nucleated cells in the stratum corneum that manifest clinically as the characteristic silvery scale. The inflammation involves both the epidermis and dermis, with dilated and tortuous capillaries in the dermal papillae, infiltration of neutrophils into the epidermis forming Munro microabscesses, and dense T-cell infiltrates in the dermis. Several clinical subtypes of psoriasis are recognized, each with distinctive morphologic features and clinical associations. Plaque psoriasis, also known as psoriasis vulgaris, accounts for 80-90% of cases and presents with well-demarcated, erythematous plaques covered by adherent silvery-white scale. Guttate psoriasis presents with numerous small, drop-like papules and plaques distributed widely over the trunk and proximal extremities, classically following streptococcal pharyngitis in children and young adults. Inverse psoriasis affects intertriginous areas including the axillae, groin, inframammary folds, and gluteal cleft, where moisture and friction modify the typical appearance, producing shiny, erythematous plaques with minimal or absent scale. Pustular psoriasis is characterized by sterile pustules that may be localized (palmoplantar) or generalized (von Zumbusch type), with the generalized form representing a dermatologic emergency. Erythrodermic psoriasis involves greater than 90% of the body surface area with confluent erythema and is a medical emergency due to risks of hypothermia, fluid losses, and high-output cardiac failure. The clinical features of plaque psoriasis are sufficiently distinctive to allow diagnosis on clinical grounds in the majority of cases. Plaques are typically erythematous with well-defined borders and covered by thick, silvery, micaceous scale that can be easily detached in sheets. The classic distribution involves the elbows, knees, scalp, and sacrum, reflecting a predilection for sites of mechanical trauma consistent with the Koebner phenomenon. The Auspitz sign, demonstrating pinpoint bleeding when the overlying scale is carefully removed, results from the exposure of dilated capillaries in the elongated dermal papillae and is a useful bedside diagnostic maneuver. The Koebner phenomenon, or isomorphic response, describes the development of new psoriatic lesions at sites of cutaneous trauma and is a characteristic feature shared with only a few other dermatoses. Nail involvement occurs in up to 50% of patients and manifests as pitting (small depressions in the nail plate from psoriasis of the nail matrix), onycholysis (separation of the nail plate from the nail bed), and the oil drop sign (yellow-brown discoloration of the nail bed resembling a drop of oil beneath the nail plate). Panel A: Plaque psoriasis morphology showing well-demarcated erythematous plaque with silvery-white micaceous scale, demonstrating characteristic thickness and color. Panel B: Auspitz sign demonstration with pinpoint bleeding upon scale removal due to dilated capillaries in elongated dermal papillae reaching close to skin surface. Panel C: Psoriatic nail changes including pitting (small depressions), onycholysis (nail plate separation), oil drop sign (yellow-brown discoloration), and subungual hyperkeratosis. Panel D: Classic distribution pattern with involvement of elbows, knees, scalp, sacrum, and umbilicus showing symmetric plaques. --- ### VI. Psoriasis Treatment and Complications Topical therapy is the mainstay of treatment for mild-to-moderate psoriasis affecting limited body surface area. Topical corticosteroids are the first-line topical agents, with potency selected according to the anatomic site and plaque thickness, ranging from low-potency agents for the face and flexures to super-high-potency agents for thick plaques on the palms and soles. Vitamin D analogs, particularly calcipotriene (calcipotriol), normalize keratinocyte proliferation and differentiation and are frequently combined with topical corticosteroids in fixed-combination preparations that provide superior efficacy to either agent alone. Topical calcineurin inhibitors such as tacrolimus are useful for psoriasis affecting the face and intertriginous areas where corticosteroid-related atrophy is a concern. Tazarotene is a topical retinoid with efficacy in plaque psoriasis, though its use is limited by skin irritation. Tar preparations represent older therapy with anti-inflammatory and antiproliferative properties that are now less commonly used due to messiness and odor but remain available for selected patients. Phototherapy is an effective treatment for moderate-to-widespread psoriasis and represents an important option between topical and systemic therapy. Narrowband ultraviolet B (NB-UVB) phototherapy is the first-line phototherapy modality, typically administered two to three times weekly with gradual dose escalation, producing clearance in the majority of patients with an excellent safety profile. PUVA (psoralen plus ultraviolet A) therapy involves oral or topical administration of a photosensitizing agent followed by UVA exposure and is more effective than NB-UVB for thick plaques but carries greater risks including increased skin cancer risk and photoaging, limiting its long-term use. Excimer laser therapy delivers targeted 308-nanometer UVB light to individual plaques without exposing uninvolved skin, making it useful for localized, treatment-resistant plaques. Systemic therapy is indicated for moderate-to-severe psoriasis not adequately controlled with topical treatment and phototherapy. Methotrexate is a conventional systemic disease-modifying antirheumatic drug (csDMARD) administered in weekly dosing that inhibits dihydrofolate reductase and has anti-inflammatory effects, though its use requires monitoring for hepatotoxicity and myelosuppression. Cyclosporine is a calcineurin inhibitor that provides rapid and effective suppression of psoriasis but is limited to short-term use due to nephrotoxicity and hypertension. Acitretin is a systemic retinoid that is particularly useful for pustular and erythrodermic psoriasis but is teratogenic with an extremely prolonged elimination half-life, requiring avoidance of pregnancy for three years after discontinuation. Apremilast is an oral PDE4 inhibitor that offers a favorable safety profile without the need for laboratory monitoring, though its efficacy is generally modest compared to biologic agents. Biologic therapies have revolutionized the treatment of moderate-to-severe psoriasis by targeting specific cytokines in the inflammatory cascade. TNF-alpha inhibitors including adalimumab, etanercept, and infliximab were the first biologics approved for psoriasis and remain widely used, though they have been largely supplanted by newer agents with greater efficacy. IL-17 inhibitors such as secukinumab and ixekizumab directly block the effector cytokine most central to psoriasis pathogenesis and achieve high rates of complete or near-complete skin clearance. IL-23 inhibitors including guselkumab and risankizumab target the upstream regulatory cytokine that drives Th17 differentiation and offer the advantage of infrequent dosing with sustained efficacy. Ustekinumab targets both IL-12 and IL-23 through their shared p40 subunit, providing effective treatment for both skin and joint manifestations of psoriasis. Psoriatic arthritis is a seronegative inflammatory arthritis that develops in approximately 30% of patients with psoriasis and can produce significant joint destruction if not recognized and treated appropriately. The articular manifestations include several distinct patterns: oligoarticular (fewer than five joints), polyarticular resembling rheumatoid arthritis, distal interphalangeal joint predominant, axial spondylitis, and the destructive arthritis mutilans. Dactylitis, the diffuse swelling of an entire digit producing the characteristic "sausage digit" appearance, is a hallmark feature that distinguishes psoriatic arthritis from other inflammatory arthropathies. Enthesitis, or inflammation at the sites where tendons and ligaments insert into bone, commonly affects the Achilles tendon insertion and plantar fascia and is another distinguishing feature. Many of the same biologic agents effective for skin psoriasis are also approved for psoriatic arthritis, particularly TNF-alpha inhibitors, IL-17 inhibitors, and IL-12/23 inhibitors. Panel A: Psoriasis treatment algorithm from topical therapy (steroids, vitamin D analogs) through phototherapy (narrowband UVB) to systemic therapy (methotrexate, biologics) based on disease severity and extent. Panel B: Biologic drug targets showing TNF-alpha inhibitors, IL-17 pathway (secukinumab, ixekizumab), IL-23 pathway (guselkumab, risankizumab), and IL-12/23 (ustekinumab) with their mechanisms. Panel C: Psoriatic arthritis patterns including oligoarticular, polyarticular (RA-like), DIP predominant, spondylitis, and arthritis mutilans with corresponding radiographic changes. Panel D: Psoriatic arthritis features showing dactylitis (sausage digit with diffuse swelling), enthesitis at Achilles tendon insertion, and nail-joint association. --- ### VII. Contact Dermatitis Contact dermatitis is an eczematous eruption resulting from direct skin exposure to an external agent and is classified into two fundamentally distinct types based on the underlying immunologic mechanism. Allergic contact dermatitis (ACD) is a type IV (delayed-type) hypersensitivity reaction mediated by sensitized T lymphocytes that requires prior exposure and sensitization before a clinical reaction can occur upon re-exposure. Irritant contact dermatitis (ICD) results from direct cytotoxic damage to keratinocytes by the offending substance and is more common than allergic contact dermatitis, accounting for approximately 80% of all contact dermatitis cases. Allergic contact dermatitis involves a T cell-mediated delayed hypersensitivity response that develops in two distinct phases. The sensitization phase occurs during initial exposure when the allergen penetrates the epidermis, is captured by Langerhans cells, and is transported to regional lymph nodes where allergen-specific T cells are primed, a process requiring 10 to 14 days during which the patient is clinically asymptomatic. Upon re-exposure, the elicitation phase occurs within 24 to 72 hours as memory T cells recognize the allergen and initiate an inflammatory cascade producing the characteristic eczematous eruption. The most common contact allergens include nickel (found in jewelry, belt buckles, and zippers), urushiol from poison ivy, poison oak, and poison sumac, and fragrances found in personal care products and cosmetics. The distribution of the eruption correlates precisely with the area of allergen exposure, providing an important diagnostic clue, and patch testing is the gold standard diagnostic procedure for identifying the responsible allergen. Irritant contact dermatitis differs from allergic contact dermatitis in its mechanism, timing, and clinical context. The mechanism involves direct cytotoxic damage to keratinocytes by the irritant substance rather than an immune-mediated response, meaning that no prior sensitization is required and the reaction can occur on first exposure. Common irritants include soaps, detergents, organic solvents, acids, alkalis, and disinfectants that disrupt the epidermal barrier through chemical or physical mechanisms. Irritant contact dermatitis is a significant occupational health problem, particularly affecting healthcare workers who perform frequent handwashing and use alcohol-based hand sanitizers and latex or nitrile gloves, as well as cleaners, hairdressers, and construction workers exposed to caustic materials. Treatment of contact dermatitis begins with identification and strict avoidance of the causative agent, which is the single most important intervention for both allergic and irritant forms. Topical corticosteroids of medium to high potency are the mainstay of pharmacologic treatment for acute flares, applied twice daily to affected areas until the eruption resolves. Emollients and barrier repair creams help restore the damaged epidermal barrier and prevent recurrence, particularly in occupational irritant dermatitis. Systemic corticosteroids may be necessary for severe or widespread allergic contact dermatitis, particularly when involving the face, genitals, or large body surface areas, and are typically administered as a tapering course over two to three weeks to prevent rebound. Patch testing should be performed by a trained dermatologist for patients with recurrent allergic contact dermatitis to identify all relevant allergens and guide comprehensive avoidance strategies. Panel A: Poison ivy allergic contact dermatitis showing linear vesicular eruption in streaky pattern corresponding to plant contact, with surrounding erythema and edema. Panel B: Patch testing procedure with allergen chambers applied to back, 48-hour reading, and interpretation of positive reactions (erythema, vesicles) for common allergens. Panel C: Occupational contact dermatitis patterns including healthcare worker hand dermatitis from gloves and cleansers, hairdresser dermatitis from dyes, and construction worker cement burns. Panel D: Comparison of allergic contact dermatitis (Type IV hypersensitivity, requires prior sensitization, well-demarcated) versus irritant contact dermatitis (direct damage, no sensitization needed, often glazed appearance). --- ### VIII. Seborrheic Dermatitis Seborrheic dermatitis is a chronic, relapsing dermatitis that affects 3-5% of the general adult population and preferentially involves areas of the skin with high sebaceous gland density. The distribution characteristically includes the scalp, face, and central chest, corresponding to the seborrheic areas where Malassezia yeast species thrive in the lipid-rich environment created by sebaceous gland secretions. The association between Malassezia yeast and seborrheic dermatitis is supported by the therapeutic response to antifungal agents, though the relationship is complex and likely involves an abnormal inflammatory response to the organism rather than simple overgrowth or infection. Seborrheic dermatitis follows a waxing and waning course with flares frequently triggered by stress, fatigue, seasonal changes, and intercurrent illness. The clinical features of seborrheic dermatitis vary by anatomic location but share the common finding of erythema with greasy, yellowish scale. Scalp involvement ranges from mild dandruff presenting as fine, white, flaky scale to more severe disease with thick, adherent, greasy scale on an erythematous base accompanied by pruritus. Facial involvement characteristically affects the nasolabial folds, eyebrows, glabella, and hairline margins with salmon-pink erythema and greasy scale in a symmetric distribution. The ears are commonly affected, particularly the posterior auricular area and external auditory canal. Chest involvement produces a distinctive petaloid pattern of erythematous, scaly patches arranged along skin folds. In infants, seborrheic dermatitis manifests as cradle cap, presenting as thick, greasy, yellowish scale adherent to the scalp vertex that is typically self-limited and resolves within the first several months of life. Several medical conditions are associated with more severe or recalcitrant seborrheic dermatitis and should be considered in the appropriate clinical context. HIV/AIDS is strongly associated with severe and extensive seborrheic dermatitis, with prevalence as high as 35-80% in affected individuals, and the sudden onset of severe seborrheic dermatitis should prompt consideration of HIV testing. Parkinson disease is associated with increased prevalence and severity of seborrheic dermatitis, thought to be related to increased sebum production from autonomic dysfunction and facial immobility. Psychological stress is a well-recognized exacerbating factor that can trigger flares through neuroendocrine mechanisms affecting both sebaceous gland function and immune responses. Any form of immune suppression, whether from medications, malignancy, or primary immunodeficiency, can produce more severe and treatment-resistant seborrheic dermatitis. Treatment of seborrheic dermatitis targets the Malassezia yeast component and the inflammatory response in a stepwise approach. Antifungal shampoos containing ketoconazole, selenium sulfide, or zinc pyrithione are the first-line treatment for scalp involvement and should be used two to three times weekly initially, then reduced to once weekly for maintenance. Topical antifungal creams such as ketoconazole are applied to affected areas on the face and body, typically twice daily until the eruption clears. Low-potency topical corticosteroids may be used for short-term control of inflammation and pruritus, though prolonged use on the face should be avoided due to the risk of corticosteroid-induced side effects including atrophy and perioral dermatitis. Topical calcineurin inhibitors such as tacrolimus and pimecrolimus serve as effective steroid-sparing agents for facial seborrheic dermatitis requiring ongoing maintenance therapy. Panel A: Facial distribution of seborrheic dermatitis showing erythema and greasy scale at nasolabial folds, eyebrows, glabella, and hairline margins. Panel B: Scalp involvement ranging from mild dandruff (fine white scale) to severe seborrheic dermatitis with thick yellowish adherent scale and erythema. Panel C: Cradle cap in infants showing thick, greasy, yellowish scale on scalp vertex with typical benign course and treatment approach. Panel D: Malassezia yeast association with seborrheic areas, conditions causing exacerbation (HIV/AIDS, Parkinson disease), and antifungal treatment targeting the organism. --- ### IX. Rosacea Rosacea is a chronic inflammatory condition affecting the central face that is most common in fair-skinned individuals, typically presenting between 30 and 50 years of age. The condition follows a waxing and waning course with flares provoked by a variety of well-recognized triggers including sun exposure, heat, emotional stress, alcohol consumption, spicy foods, hot beverages, and exercise. The pathogenesis is incompletely understood but involves vascular hyperreactivity, innate immune dysregulation with abnormal cathelicidin processing, and neurovascular dysfunction. Though sometimes confused with acne vulgaris due to the presence of papules and pustules, rosacea is distinguished by the absence of comedones and the predominance of facial flushing, erythema, and telangiectasias. Rosacea is classified into four subtypes that may occur independently or in combination, reflecting the heterogeneous nature of this condition. Erythematotelangiectatic rosacea is characterized by episodes of flushing, persistent central facial erythema, and visible telangiectasias, with patients often describing a burning or stinging sensation exacerbated by triggers. Papulopustular rosacea presents with inflammatory papules and pustules superimposed on a background of central facial erythema, closely resembling acne but distinguished by the absence of comedones and the presence of telangiectasias. Phymatous rosacea involves progressive skin thickening due to sebaceous gland hypertrophy and fibrosis, most commonly affecting the nose where it produces rhinophyma, a bulbous, lobulated nasal enlargement with prominent pores. Ocular rosacea affects the eyes in up to 50% of patients with cutaneous disease and manifests as blepharitis, conjunctivitis, and in severe cases keratitis that can threaten vision, warranting ophthalmologic referral. Treatment of rosacea is tailored to the predominant subtype and severity of disease. Mild disease is managed with topical agents including metronidazole, azelaic acid, and ivermectin, the latter being particularly effective due to its dual anti-inflammatory and anti-parasitic (Demodex mite) activity. Moderate disease with significant papulopustular involvement benefits from the addition of oral doxycycline at anti-inflammatory (sub-antimicrobial) dosing, which suppresses inflammation without the concerns of antibiotic resistance associated with full antimicrobial doses. Severe or refractory disease may warrant treatment with low-dose isotretinoin, which reduces sebaceous gland activity and inflammation. Telangiectasias do not respond to pharmacologic therapy and require vascular laser treatment such as pulsed dye laser or intense pulsed light for cosmetic improvement. Rhinophyma is managed surgically through tissue reduction using electrosurgery, CO2 laser ablation, or surgical reshaping to restore normal nasal contour. The differential diagnosis of rosacea includes several conditions with overlapping facial presentations that must be carefully distinguished. Acne vulgaris is differentiated from rosacea by the presence of comedones (open and closed), which are absent in rosacea, and by its broader distribution including the chest and back. Seborrheic dermatitis is distinguished by the presence of greasy, yellowish scale and predilection for the nasolabial folds, scalp, and ears, though it may coexist with rosacea. The malar rash of systemic lupus erythematosus characteristically spares the nasolabial folds, in contrast to rosacea which frequently involves this area, and lupus is associated with systemic symptoms and positive autoimmune serologies. Contact dermatitis can be distinguished by a clear history of exposure to an identifiable irritant or allergen and a distribution corresponding to the exposure pattern. Panel A: Erythematotelangiectatic rosacea showing central facial erythema, visible telangiectasias on cheeks and nose, and flushing response to triggers. Panel B: Papulopustular rosacea with inflammatory papules and pustules on erythematous background, notably without comedones (distinguishing from acne). Panel C: Phymatous rosacea with rhinophyma showing bulbous nasal enlargement, thickened skin with prominent pores, and sebaceous gland hypertrophy. Panel D: Differential diagnosis comparison showing rosacea (central face, telangiectasias, no comedones), acne vulgaris (comedones present), seborrheic dermatitis (scale, nasolabial folds), and lupus malar rash (spares nasolabial folds). --- ### X. Principles of Topical Therapy Topical corticosteroids are classified into seven potency classes that guide appropriate selection based on anatomic location and disease severity. Super-high potency (Class I) agents such as clobetasol are reserved for thick, resistant plaques on the palms and soles where the thick stratum corneum limits penetration. High-potency (Class II-III) agents such as fluocinonide are appropriate for lesions on the body and scalp where moderate absorption occurs through skin of intermediate thickness. Medium-potency (Class IV-V) agents such as triamcinolone acetonide represent the most commonly prescribed steroids for generalized eruptions on the trunk and extremities. Low-potency (Class VI-VII) agents such as hydrocortisone are appropriate for the face, groin, axillae, and use in children, where thin skin and increased absorption raise the risk of local and systemic adverse effects. Prolonged or inappropriate use of topical corticosteroids produces a well-recognized spectrum of cutaneous side effects that must be communicated to patients. Skin atrophy manifests as thinning of the epidermis and dermis with a tissue-paper quality and increased fragility. Striae (stretch marks) develop in areas of skin subjected to mechanical stress during corticosteroid use and are permanent once established. Telangiectasia, or visible dilated blood vessels, results from loss of connective tissue support around dermal capillaries. Perioral dermatitis is a distinctive papulopustular eruption around the mouth that paradoxically results from chronic facial application of topical corticosteroids, creating a cycle of worsening with continued use and flaring upon withdrawal. Hypothalamic-pituitary-adrenal (HPA) axis suppression can occur with extensive application of potent topical corticosteroids, particularly under occlusion or in infants and young children with a high body surface area to weight ratio. The vehicle in which a topical medication is formulated significantly influences both its efficacy and patient acceptability. Ointments are the most occlusive vehicle, enhancing drug penetration and providing maximum moisturization, making them ideal for dry, lichenified, or hyperkeratotic lesions, though their greasy texture limits cosmetic acceptability on visible areas. Creams are water-based emulsions that offer a cosmetically elegant option with moderate potency enhancement and are well-accepted by patients for use on the face, body, and intertriginous areas. Lotions are liquid preparations with low viscosity that spread easily over large or hairy areas, providing convenience for scalp and widespread body application. Solutions and foams are primarily used for scalp application where they can penetrate through hair without leaving visible residue. Gels are water-based or alcohol-based preparations with a drying effect that makes them particularly suitable for acne-prone skin and other conditions where excess moisture is undesirable. Several general principles govern the safe and effective use of topical corticosteroids in dermatologic practice. Appropriate potency must be matched to both the anatomic location and the severity of the condition being treated, with the general rule of using the lowest potency that achieves disease control. Duration limits should be observed, typically restricting use to two weeks or less on the face and groin and four weeks on the body, with reassessment at each interval. Tapering should be gradual rather than abrupt to prevent rebound flares, particularly with potent agents used for extended periods. Steroid-sparing strategies using calcineurin inhibitors, PDE4 inhibitors, or other non-steroidal agents should be employed whenever possible for maintenance therapy, particularly in areas prone to corticosteroid side effects. Patient education on proper application technique, including appropriate quantity (the fingertip unit as a guide), frequency, and duration, is essential for optimizing therapeutic outcomes while minimizing adverse effects. Panel A: Topical corticosteroid potency classification from Class I (super-high: clobetasol) through Class IV-V (medium: triamcinolone) to Class VI-VII (low: hydrocortisone) with appropriate anatomic applications. Panel B: Vehicle selection guide showing ointments (most occlusive, for dry skin), creams (cosmetically elegant, moderate potency), lotions (hairy areas), and gels/solutions (scalp, acne-prone skin). Panel C: Body site-appropriate steroid selection showing low potency for face, eyelids, and groin; medium for trunk and extremities; and high potency only for palms, soles, and thick plaques. Panel D: Corticosteroid side effects including skin atrophy, striae, telangiectasia, and perioral dermatitis with duration limits and steroid-sparing strategies. --- ## Summary - Acne: sebum, follicular hyperkeratinization, C. acnes, inflammation - Acne treatment: topical retinoids, benzoyl peroxide; isotretinoin for severe - Atopic dermatitis: barrier dysfunction, Th2 inflammation; moisturizers essential - AD treatment: topical steroids, calcineurin inhibitors; dupilumab for severe - Psoriasis: Th17-mediated; silvery plaques, Auspitz sign, nail changes - Psoriasis treatment: topical agents → phototherapy → systemics/biologics - Contact dermatitis: allergic (Type IV) vs irritant; patch testing for ACD - Seborrheic dermatitis: Malassezia-associated; antifungal shampoos - Rosacea: facial flushing, papulopustules, rhinophyma; no comedones - Topical steroids: match potency to location; limit duration on face --- ## Key Terms | Term | Definition | |------|------------| | Comedone | Plugged follicle (blackhead/whitehead) | | Atopic triad | Eczema, asthma, allergic rhinitis | | Lichenification | Thickened skin from chronic rubbing | | Auspitz sign | Pinpoint bleeding when psoriasis scale removed | | Koebner phenomenon | New lesions at sites of trauma | | Patch testing | Diagnostic test for allergic contact dermatitis | | Rhinophyma | Bulbous nose in rosacea | | Vehicle | Carrier for topical medication | --- *This content is subject to the [MIT License](https://opensource.org/licenses/MIT). © 2024–2026 Hibbert School of Medicine.*