Comprehensive Guide to Major Dermatologic Diagnoses
A systematic approach to common dermatologic conditions is essential for effective diagnosis and treatment in primary care settings, focusing on reducing morbidity and improving quality of life for patients with skin disorders. 1
1. Inflammatory Dermatoses
Psoriasis
Etiology:
- Immune-mediated inflammatory disease with genetic predisposition
- T-cell mediated inflammation with overproduction of inflammatory cytokines (TNF-α, IL-17, IL-23)
- Environmental triggers (stress, trauma, medications, infections)
Appearance:
- Well-demarcated, erythematous plaques with silvery scales
- Common locations: extensor surfaces (elbows, knees), scalp, intergluteal cleft
- Nail changes: pitting, onycholysis, oil spots, subungual hyperkeratosis
Natural Course:
- Chronic relapsing-remitting disease
- Can develop comorbidities: psoriatic arthritis, cardiovascular disease, metabolic syndrome
- May have periods of exacerbation with environmental triggers
Treatment:
- Mild-moderate disease: Topical corticosteroids, vitamin D analogs (calcipotriene), topical retinoids
- Moderate-severe disease: Phototherapy (UVB, PUVA), systemic agents (methotrexate, cyclosporine, acitretin)
- Severe/refractory disease: Biologics targeting TNF-α (adalimumab), IL-17, or IL-23 pathways 2
- Monitor for increased risk of skin cancer with PUVA therapy and immunosuppressive medications 3
Atopic Dermatitis (Eczema)
Etiology:
- Multifactorial: genetic predisposition (filaggrin mutations), immune dysregulation, skin barrier dysfunction
- Environmental triggers: allergens, irritants, stress, climate changes
Appearance:
- Acute: erythematous, vesicular, weeping lesions with intense pruritus
- Chronic: lichenification, excoriations, hyperpigmentation
- Age-dependent distribution: infants (face, extensor surfaces), adults (flexural areas)
Natural Course:
- Often begins in infancy, may improve with age
- Chronic relapsing course with flare-ups
- Associated with allergic rhinitis, asthma, food allergies (atopic march)
Treatment:
- Skin hydration: Regular use of emollients, gentle cleansers
- Anti-inflammatory: Topical corticosteroids (acute flares), topical calcineurin inhibitors (maintenance)
- Severe disease: Phototherapy, systemic immunosuppressants, dupilumab (IL-4/IL-13 inhibitor)
- Adjunctive: Antihistamines for pruritus, antibiotics for secondary infections
Seborrheic Dermatitis
Etiology:
- Associated with Malassezia yeast overgrowth
- Abnormal skin barrier function and inflammatory response 4
- Genetic predisposition
Appearance:
- Erythematous patches with greasy, yellowish scales
- Common locations: scalp (dandruff), nasolabial folds, eyebrows, chest, behind ears
- May have mild pruritus
Natural Course:
- Chronic with fluctuating severity
- Often worsens with stress, seasonal changes (winter)
- May improve with age
Treatment:
- Scalp: Antifungal shampoos (ketoconazole, selenium sulfide, zinc pyrithione)
- Face/body: Low-potency topical corticosteroids, topical antifungals
- Maintenance: Regular use of antifungal products to prevent recurrence
- Severe cases: Short courses of oral antifungals
Contact Dermatitis
Etiology:
- Irritant contact dermatitis: direct damage to skin from irritants
- Allergic contact dermatitis: delayed hypersensitivity reaction (type IV)
Appearance:
- Erythema, vesicles, bullae in patterns corresponding to exposure
- Pruritus, burning sensation
- Common allergens: nickel, fragrances, preservatives, plants (poison ivy)
Natural Course:
- Acute onset after exposure (irritant) or 48-72 hours after exposure (allergic)
- Resolves with avoidance of causative agent
- May become chronic with repeated exposure
Treatment:
- Primary: Identification and avoidance of triggers
- Acute lesions: Topical corticosteroids, cool compresses
- Severe cases: Systemic corticosteroids, antihistamines for pruritus
- Prevention: Barrier creams, protective clothing
2. Infectious Dermatoses
Cellulitis/Erysipelas
Etiology:
- Bacterial infection (primarily group A streptococci, sometimes Staphylococcus aureus)
- Entry through breaks in skin barrier
- Risk factors: venous insufficiency, lymphedema, obesity, diabetes 1
Appearance:
- Cellulitis: diffuse, spreading erythema, warmth, tenderness, edema
- Erysipelas: well-demarcated, raised erythematous plaques, often on face or lower extremities
- Systemic symptoms: fever, chills, lymphadenopathy 1
Natural Course:
- Acute onset with rapid spread if untreated
- May lead to bacteremia, sepsis if severe
- Recurrent episodes can cause lymphatic damage and chronic lymphedema
Treatment:
- Mild-moderate: Oral antibiotics (penicillinase-resistant penicillins, cephalosporins)
- Severe/systemic symptoms: Intravenous antibiotics
- Recurrent cases: Prophylactic antibiotics, treatment of predisposing factors
- Supportive: Elevation, rest, warm compresses 1
Fungal Infections
Etiology:
- Dermatophytes (tinea), yeasts (Candida), or molds
- Risk factors: humidity, occlusion, immunosuppression, diabetes
Appearance:
- Tinea corporis: Annular, erythematous patches with central clearing and active border
- Tinea pedis: Maceration, scaling between toes or moccasin distribution
- Tinea capitis: Scaling, alopecia, black dots
- Candidiasis: Erythematous patches with satellite pustules in moist areas
Natural Course:
- Gradually spreading if untreated
- May become chronic without proper treatment
- Secondary bacterial infections can occur
Treatment:
- Localized superficial: Topical antifungals (azoles, allylamines)
- Extensive/hair/nail involvement: Oral antifungals (terbinafine, itraconazole)
- Prevention: Keeping skin dry, avoiding shared items, proper foot hygiene
Viral Infections
Etiology:
- Common viruses: Human papillomavirus (warts), Herpes simplex, Varicella-zoster
Appearance:
- Warts: Hyperkeratotic papules with thrombosed capillaries
- Herpes simplex: Grouped vesicles on erythematous base, often perioral or genital
- Herpes zoster: Painful, unilateral vesicles in dermatomal distribution
Natural Course:
- Warts: May spontaneously resolve or persist for years
- HSV: Recurrent episodes with triggers (stress, UV, illness)
- Zoster: Acute episode with potential for post-herpetic neuralgia
Treatment:
- Warts: Destructive methods (cryotherapy, salicylic acid), immunotherapy
- HSV: Antiviral medications (acyclovir, valacyclovir), suppressive therapy for frequent recurrences
- Zoster: Early antiviral therapy, pain management, vaccination for prevention
3. Neoplastic Conditions
Actinic Keratosis
Etiology:
- UV-induced dysplastic epidermal lesions
- Precursor to squamous cell carcinoma
- Risk factors: fair skin, chronic sun exposure, older age
Appearance:
- Rough, scaly, erythematous macules or patches
- Often multiple lesions in sun-exposed areas
- May have yellow or brown crusting
Natural Course:
- Slow progression
- 0.1-10% risk of progression to squamous cell carcinoma
- May spontaneously regress or persist
Treatment:
- Localized lesions: Cryotherapy, curettage
- Multiple lesions: Field therapy with 5-fluorouracil, imiquimod, ingenol mebutate
- Extensive disease: Photodynamic therapy 1
- Prevention: Sun protection, regular skin examinations
Basal Cell Carcinoma
Etiology:
- UV radiation damage to basal cells
- Risk factors: fair skin, sun exposure, radiation, immunosuppression
Appearance:
- Pearly, translucent papule with telangiectasias
- May have central depression, ulceration, or rolled borders
- Common locations: sun-exposed areas (face, ears, neck)
Natural Course:
- Slow-growing, locally invasive
- Rarely metastasizes but can cause significant local destruction
- Recurrence risk after treatment
Treatment:
- Standard: Surgical excision, Mohs micrographic surgery
- Superficial/low-risk: Electrodessication and curettage, cryotherapy
- Alternative: Topical imiquimod, 5-fluorouracil, photodynamic therapy for superficial BCC 1
- Advanced/inoperable: Hedgehog pathway inhibitors
Melanoma
Etiology:
- Malignant transformation of melanocytes
- Risk factors: UV exposure, fair skin, multiple nevi, family history, prior melanoma
Appearance:
- ABCDE criteria: Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolution
- May arise from existing nevus or de novo
- Subtypes: superficial spreading, nodular, lentigo maligna, acral lentiginous
Natural Course:
- Can grow rapidly with early metastasis
- Prognosis depends on depth (Breslow thickness), ulceration, mitotic rate
- Potential for distant metastasis
Treatment:
- Primary treatment: Wide local excision with appropriate margins
- Advanced disease: Sentinel lymph node biopsy, lymph node dissection
- Metastatic disease: Targeted therapy (BRAF/MEK inhibitors), immunotherapy (checkpoint inhibitors) 1
- Prevention: Sun protection, regular skin examinations, surveillance of high-risk patients
4. Papulosquamous Disorders
Lichen Planus
Etiology:
- T-cell mediated autoimmune reaction against basal keratinocytes
- Triggers: medications, hepatitis C, stress
Appearance:
- Violaceous, flat-topped, polygonal papules with white reticulated surface (Wickham's striae)
- Common locations: flexor wrists, oral mucosa, genitalia
- May have nail changes, scalp involvement (lichen planopilaris)
Natural Course:
- Self-limited in most cases (6-18 months)
- Oral and genital lesions may persist longer
- Post-inflammatory hyperpigmentation common
Treatment:
- Localized cutaneous: Topical corticosteroids, calcineurin inhibitors
- Widespread/severe: Systemic corticosteroids, oral retinoids, phototherapy
- Oral lesions: Topical corticosteroids, intralesional injections
Pityriasis Rosea
Etiology:
- Possibly viral (human herpesvirus 6 and 7 implicated)
- More common in young adults
Appearance:
- Herald patch: solitary, oval, salmon-colored patch with collarette scale
- Secondary eruption: smaller similar lesions following skin lines in "Christmas tree" pattern
- Mild pruritus common
Natural Course:
- Self-limited, resolves within 6-12 weeks
- Rarely recurs
- Post-inflammatory hyperpigmentation may persist, especially in darker skin types
Treatment:
- Mild cases: Symptomatic relief with antihistamines, moisturizers
- Moderate-severe pruritus: Topical corticosteroids
- Widespread/severe: UVB phototherapy, oral antivirals (controversial)
5. Acne and Rosacea
Acne Vulgaris
Etiology:
- Multifactorial: follicular hyperkeratinization, increased sebum production, Cutibacterium acnes proliferation, inflammation 4
- Hormonal influences (androgens)
- Genetic predisposition 4
Appearance:
- Comedones (open and closed), papules, pustules, nodules, cysts
- Common locations: face, chest, back, shoulders
- May have post-inflammatory erythema or hyperpigmentation, scarring
Natural Course:
- Peak incidence in adolescence, may persist into adulthood
- Hormonal fluctuations can trigger flares
- Potential for scarring with severe or manipulated lesions
Treatment:
- Mild: Topical retinoids, benzoyl peroxide, topical antibiotics
- Moderate: Combination topical therapy, oral antibiotics
- Severe/nodular: Oral isotretinoin (monitor for adverse effects including dry skin, teratogenicity, mood changes) 5
- Hormonal: Combined oral contraceptives, spironolactone for females
Rosacea
Etiology:
- Neurovascular dysregulation, innate immune system dysfunction
- Triggers: sun exposure, heat, spicy foods, alcohol, stress
Appearance:
- Erythema, flushing, telangiectasias (erythematotelangiectatic type)
- Papules, pustules (papulopustular type)
- Phymatous changes: tissue hyperplasia, sebaceous gland enlargement
- Ocular involvement: blepharitis, conjunctivitis
Natural Course:
- Chronic with periods of exacerbation and remission
- Progressive without treatment
- Psychological impact due to facial appearance
Treatment:
- Trigger avoidance: Sun protection, avoiding known triggers
- Erythematotelangiectatic: Topical alpha-adrenergic agonists (brimonidine, oxymetazoline)
- Papulopustular: Topical metronidazole, azelaic acid, ivermectin; oral antibiotics (tetracyclines)
- Phymatous: Surgical intervention, laser therapy
- Ocular: Lid hygiene, topical/oral antibiotics, artificial tears
Clinical Pearls and Pitfalls
Diagnostic challenges in skin of color:
- Erythema may be difficult to appreciate in darker skin tones
- Post-inflammatory hyperpigmentation more common and persistent
- Different prevalence patterns: keloids, melasma, and follicular disorders more common 6
Dermoscopy as diagnostic aid:
- Non-invasive technique to visualize subsurface skin structures
- Helpful for differentiating pigmented lesions, inflammatory conditions, and infections 7
Steroid-related complications:
- Topical steroid overuse can lead to skin atrophy, telangiectasias, striae
- Use appropriate potency for location and duration
- Consider steroid-sparing alternatives for chronic conditions
Treatment adherence:
- Simplify regimens when possible
- Address psychological impact of visible skin conditions
- Consider vehicle preferences (creams, ointments, foams, solutions)
Referral indications:
- Uncertain diagnosis or poor response to treatment
- Suspected skin malignancy
- Severe or widespread disease requiring systemic therapy
- Need for procedural interventions
By understanding the etiology, appearance, natural course, and treatment options for these common dermatologic conditions, primary care physicians can effectively manage many skin disorders and appropriately refer complex cases to dermatology specialists.