MD Notes

creation date: 2026-04-28 18:51
tags: Assessments

Dermatology Lesions

Background

Evaluation of skin lesions should consider elements of the history including:

  • Presence of infectious symptoms
  • Onset and duration
  • Past medical history
  • Precipitating events
  • Changes/evolution

Lesions

Benign

Acrochordons (Skin Tags)

Clinical Findings
  • Soft, flesh-coloured pedunculated papules
  • Located in skin folds (neck, axillae, groin, eyelids)
  • Range from 1mm to >1cm
  • Non-tender, easily moveable
  • Multiple lesions common
Pathophysiology
  • Benign fibrovascular polyps from superficial dermis
  • Friction at skin folds + hyperinsulinemia stimulates fibroblast/keratinocyte proliferation
  • Strongly associated with obesity and metabolic syndrome
Diagnosis/Treatment
  • Clinical diagnosis
  • Snip excision, electrocautery, or cryotherapy if symptomatic
  • Consider metabolic risk review given obesity and diabetes.
Differential Diagnosis
  • Intradermal nevus
  • Neurofibroma
  • Small seborrheic keratosis
Benign Melanocytic Nevus (Compound/Congenital-Pattern)

Clinical Findings
  • Well-defined, symmetric, uniformly pigmented papule
  • Tan to brown color, smooth or slightly raised
  • Stable size and appearance over years
  • Clear borders without irregularity
  • Usually <6mm
Pathophysiology
  • Benign proliferation of melanocytes at the dermoepidermal junction and/or dermis
  • Stable lesion due to oncogene-induced arrests
Diagnosis/Treatment
  • ABCDE review and dermoscopy
  • Photograph and monitor if stable and symmetric
  • Excisional biopsy if evolution, asymmetry, irregular pigment, or bleeding
Differential Diagnosis
  • Dysplastic nevus
  • Melanoma
  • Seborrheic keratosis
Blue Nevus

Clinical Findings
  • Well-defined blue-gray to blue-black papule or nodule
  • Smooth surface, usually <1cm
  • Most common on dorsal hands, feet, scalp, sacrum
  • Stable, present since childhood or young adulthood
  • Firm on palpation
Pathophysiology
  • Dermal melanocyte proliferation creates blue-gray color via the Tyndall effect
  • Melanocytes in dermis due to arrest during neural crest migration to epidermis
Diagnosis/Treatment
  • Dermoscopic assessment and baseline photo if longstanding and stable
  • Excisional biopsy if new change, growth, bleeding, or diagnostic uncertainty
Differential Diagnosis
  • Melanoma
  • Combined nevus
  • Pigmented dermatofibroma
Cherry Angiomas

Clinical Findings
  • Bright red, dome-shaped papules 1–5mm
  • Blanch completely with pressure
  • Most common on trunk
  • Increase in number with age
  • Bleed readily if traumatized
Pathophysiology
  • Benign proliferation of superficial capillaries that increases with age due to increased VEGF expression
Diagnosis/Treatment
  • Clinical diagnosis
  • Reassure if typical
  • Electrocautery or laser if bleeding or cosmetically bothersome
Differential Diagnosis
  • Pyogenic granuloma
  • Angiokeratoma
  • Amelanotic melanoma
Dermatofibroma

Clinical Findings
  • Firm, slightly raised brownish papule
  • Positive dimple sign (puckering on lateral compression)
  • Hyperpigmented center, paler periphery
  • Most common on lower legs
  • Slightly tender on palpation
Pathophysiology
  • Benign fibrohistiocytic reaction, often after minor trauma or insect bite, producing a firm dermal nodule with dimpling
  • Dimpling due to tethering of epidermis to underlying fibrous nodule
Diagnosis/Treatment
  • Clinical diagnosis including dimple sign
  • Reassure if classic and stable
  • Biopsy if enlarging, atypical, painful, or diagnostically uncertain
Differential Diagnosis
  • Epidermoid cyst
  • Dermatofibrosarcoma protuberans
  • Nodular melanoma
Epidermoid Cyst

Clinical Findings
  • Smooth, dome-shaped skin-colored nodule
  • Central punctum (key feature)
  • Cheesy, malodorous contents if expressed
  • Tender and red if inflamed/ruptured
  • Mobile unless previously ruptured
Pathophysiology
  • Keratin-filled cyst from follicular infundibulum obstruction or epidermal implantation
  • Rupture triggers inflammation and malodorous drainage
Diagnosis/Treatment
  • Clinical diagnosis
  • If acutely inflamed, consider I&D or intralesional steroid
  • Definitive treatment is complete excision of cyst wall once quiescent
Differential Diagnosis
  • Sebaceous cyst (oily, yellow sebum due to oil glands)
  • Pilar cyst
  • Abscess
  • Lipoma
Infantile Hemangioma

Clinical Findings
  • Absent or faint at birth, appears weeks 1–4 of life
  • Bright red, strawberry-like papule or plaque
  • Rapid growth phase over first year
  • Gradual spontaneous involution over years
  • Superficial (bright red) vs. deep (bluish, compressible) subtypes
Pathophysiology
  • Postnatal endothelial proliferation with a rapid growth phase followed by gradual involution over years
Diagnosis/Treatment
  • Assess for ulceration, visual obstruction, airway risk, and high-risk site involvement
  • Observe if uncomplicated
  • Oral propranolol is first-line if function-threatening or ulcerated
Differential Diagnosis
  • Congenital hemangioma
  • Vascular malformation
  • Pyogenic granuloma
Keloid

Clinical Findings
  • Raised, firm, rubbery scar that extends beyond wound margins
  • Progressive growth over time (distinguishes from hypertrophic scar)
  • Pruritic and sometimes painful
  • Hyperpigmented, shiny surface
  • Predisposition in darker skin types; earlobes, sternum, shoulders common sites
Pathophysiology
  • Abnormal wound healing with excess collagen deposition extending beyond the original injury margins
Diagnosis/Treatment
  • Clinical diagnosis
  • First-line: intralesional triamcinolone ± silicone/pressure therapy
  • Avoid simple excision alone due to high recurrence risk
Differential Diagnosis
  • Hypertrophic scar
  • Dermatofibroma
  • Epidermoid cyst
Keratoacanthoma

Clinical Findings
  • Rapid growth over 6-8 weeks
  • Dome-shaped, flesh-colored nodule with central keratin-filled crater
  • Symmetrical “volcano-like” architecture
  • Sun-exposed skin in elderly, fair-skinned patients
  • May spontaneously involute over months
Pathophysiology
  • Rapidly proliferating crateriform squamoproliferative lesion on sun-damaged skin, regarded as a well-differentiated SCC variant
Diagnosis/Treatment
  • Excisional biopsy/complete removal (indistinguishable from SCC clinically)
  • Histology guides further margins or surveillance
Differential Diagnosis
  • Cutaneous squamous cell carcinoma
  • Verruca
  • Nodular BCC
Keratosis Pilaris

Clinical Findings
  • Multiple small (1–2mm) rough follicular papules
  • Keratinous plug within follicle
  • Mild perifollicular erythema
  • Posterior upper arms and anterolateral thighs (classic sites)
  • Worsens in winter and low humidity; non-pruritic
Pathophysiology
  • Follicular keratin plugging causes rough small papules on extensor surfaces, often worse with dry weather
Diagnosis/Treatment
  • Reassure; benign chronic condition
  • Moisturizers plus keratolytics (urea, lactic acid, or salicylic acid)
  • Gentle skin care and avoid over-scrubbing
Differential Diagnosis
  • Folliculitis
  • Lichen spinulosus
  • Phrynoderma
Lipoma

Clinical Findings
  • Soft (consistency similar to tip of nose), doughy, compressible subcutaneous mass
  • Mobile and “slips” under finger
  • Not attached to overlying skin
  • Typically non-tender
  • Slow growing, usually 1–5cm
Pathophysiology
  • Benign tumour of mature adipocytes in subcutaneous tissue
Diagnosis/Treatment
  • Clinical diagnosis
  • Ultrasound if deep, fixed, large, painful, or rapidly enlarging
  • Excision only if symptomatic or uncertain
Differential Diagnosis
  • Epidermoid cyst
  • Angiolipoma
  • Liposarcoma
Seborrheic Keratosis

Clinical Findings
  • “Stuck-on” verrucous/waxy papules or plaques
  • Variable pigmentation (tan to dark brown)
  • Rough, pasted-on appearance
  • Horn cysts on dermoscopy
  • Common on trunk, face, extremities in older adults
Pathophysiology
  • Benign clonal proliferation of epidermal keratinocytes
  • Somatic mutations accumulates with aging
  • No UV-dependent mechanism or malignant potential
Diagnosis/Treatment
  • Clinical diagnosis with dermoscopy
  • Reassure if classic
  • Cryotherapy/curettage if irritated or cosmetically bothersome; biopsy if atypical or rapidly changing
Differential Diagnosis
  • Solar lentigines
  • Pigmented BCC
  • Melanoma

Pre-malignant / Malignant

Actinic Keratosis

Clinical Findings
  • Rough, sandpaper-textured papules/patches
  • Erythematous base with adherent scale
  • On chronically sun-exposed skin (scalp, face, dorsal hands, forearms)
  • Background photoaging and solar damage
  • Tender when palpated
Pathophysiology
  • Chronic UV damage causes mutation and atypia of epidermal keratinocytes
  • Premalignant lesion on the SCC spectrum
  • Progression risk rises with immunosuppression
Diagnosis/Treatment
  • Full skin exam for field cancerization
  • Cryotherapy for discrete lesions or field therapy with 5-FU/imiquimod if extensive
  • Biopsy any thick, tender, or indurated lesion
Differential Diagnosis
  • SCC in situ/Bowen disease
  • Superficial BCC
  • Seborrheic dermatitis
Basal Cell Carcinoma (Nodular Type)

Clinical Findings
  • Pearly, translucent papule with rolled borders
  • Surface telangiectasia
  • Easy bleeding with minor trauma
  • Slow-growing over months to years
  • Almost exclusively on sun-exposed skin (face, nose, ears)
Pathophysiology
  • UV-driven malignancy of basal keratinocytes with hedgehog-pathway dysregulation causes pearly telangiectatic papules that bleed easily
Diagnosis/Treatment
  • Shave or punch biopsy for confirmation
  • Definitive treatment is excision or Mohs surgery given nasal location
  • Sun protection and skin cancer surveillance.
Differential Diagnosis
  • Fibrous papule
  • Sebaceous hyperplasia
  • Amelanotic melanoma
Melanoma

Clinical Findings
  • ABCDE criteria: Asymmetry, irregular Border, multiple colours (tan/brown/black/pink), Diameter >6mm, Evolution
  • Change in a pre-existing mole
  • Variegated pigmentation (shades of brown to black with possible pink/white areas)
  • May ulcerate or bleed spontaneously
  • Most common on back (men) and legs (women)
Pathophysiology
  • Malignant melanocytic proliferation with radial and/or vertical growth produces ABCDE features including colour variegation and irregular borders
Diagnosis/Treatment
  • Urgent excisional biopsy with narrow margins
  • Stage by Breslow depth after pathology
  • Wide local excision ± sentinel node biopsy depending on depth
Differential Diagnosis
  • Dysplastic nevus
  • Pigmented seborrheic keratosis
  • Pigmented BCC
Squamous Cell Carcinoma

Clinical Findings
  • Firm, indurated hyperkeratotic nodule or plaque
  • Ulcerated or crusted surface
  • Erythematous base, non-healing
  • Sun-exposed areas (ears, lower lip, dorsal hands, scalp in bald patients)
  • Rapid growth, tenderness, and induration suggest invasive disease
Pathophysiology
  • UV-damaged atypical keratinocytes invade the dermis
  • Immunosuppression increases risk and aggressiveness.
Diagnosis/Treatment
  • Urgent biopsy (high-risk), rapidly growing nasal lesion
  • Likely excision/Mohs after histologic confirmation
  • Examine for nodal disease if advanced features present
Differential Diagnosis
  • Keratoacanthoma
  • Hypertrophic actinic keratosis
  • Basal cell carcinoma

Inflammatory / Autoimmune

Allergic Contact Dermatitis (Urushiol/Poison Ivy Exposure)

Clinical Findings
  • Linear streaks of vesicles/bullae (hallmark of plant contact)
  • Intensely pruritic erythematous plaques
  • Distribution follows contact pattern
  • Delayed onset 24–72 hours after exposure
  • Can spread by scratching/residual urushiol (oil from poison ivy)
Pathophysiology
  • Type IV delayed hypersensitivity after plant exposure produces intensely pruritic vesicular dermatitis
Diagnosis/Treatment
  • Clinical diagnosis based on exposure pattern
  • Wash skin/clothing
  • High-potency topical steroid if localized
  • Oral prednisone taper if severe, widespread, or facial/genital involvement
Differential Diagnosis
  • Irritant contact dermatitis
  • Phytophotodermatitis
  • Arthropod bite reaction
Alopecia Areata

Clinical Findings
  • Smooth, circular/oval patches of complete hair loss
  • No scarring, scaling, or inflammation of scalp
  • “Exclamation mark” hairs at periphery (tapered proximally)
  • Nail pitting in ~10–20% of cases
  • Sudden onset, often associated with stress
Pathophysiology
  • Autoimmune T-cell attack on anagen hair follicles causes smooth round patches of nonscarring hair loss
Diagnosis/Treatment
  • Clinical diagnosis with dermoscopy if available
  • Intralesional steroid for limited disease; potent topical steroid if preferred
  • Review associated autoimmune history
Differential Diagnosis
  • Tinea capitis
  • Trichotillomania
  • Traction alopecia
Atopic Dermatitis

More details

Clinical Findings
  • Flexural distribution (antecubital/popliteal fossae, wrists, ankles)
  • Intense pruritus (“itch that rashes”)
  • Xerosis and lichenification in chronic disease
  • Dennie-Morgan lines (infraorbital folds)
  • Personal or family history of atopy (asthma, allergic rhinitis)
Pathophysiology
  • Skin barrier dysfunction (often filaggrin-related) plus Th2-skewed inflammation causes chronic pruritic flexural eczema
Diagnosis/Treatment
  • Daily emollients and trigger avoidance
  • Topical corticosteroid for flares
  • Consider calcineurin inhibitor or escalation if recurrent/moderate-severe
Differential Diagnosis
  • Allergic contact dermatitis
  • Scabies
  • Fungal infection
  • Psoriasis
Bullous Pemphigoid

Clinical Findings
  • Large, tense bullae on urticarial or erythematous base
  • Bullae do not rupture easily (subepidermal, tense)
  • Extremities and flexures most commonly involved
  • Prodrome of intense pruritus weeks before blisters
  • Elderly patients; minimal mucosal involvement
Pathophysiology
  • IgG autoantibodies against BP180/BP230 at the basement membrane produce subepidermal tense bullae, often after a prodromal pruritic phase
Diagnosis/Treatment
  • Biopsy (H&E stain + perilesional DIF)
  • High-potency topical steroid if localized; systemic steroid or steroid-sparing therapy if extensive
Differential Diagnosis
  • Bullous drug eruption
  • Linear IgA bullous dermatosis
  • Pemphigus vulgaris
Dyshidrotic Eczema (Pompholyx)

Clinical Findings
  • Deep-seated, intensely pruritic “tapioca-like” vesicles
  • Lateral aspects of fingers, palms, and soles
  • Vesicles do not rupture easily (thick overlying skin)
  • Followed by scaling, fissuring, and peeling as lesions resolve
  • Cyclic recurrences, often triggered by stress or heat
Pathophysiology
  • Recurrent vesicular hand-foot dermatitis linked to sweat, stress, atopy, or contact allergy
  • Stress causes autonomic activation and sweating which activates inflammatory cascade
  • Palmar/plantar stratum corneum results in vesicles deep in the epidermis and thus do not rupture easily
Diagnosis/Treatment
  • High-potency topical steroid and frequent emollients
  • Hand protection and trigger control
  • KOH if unilateral hand/foot to rule out dermatophyte
Differential Diagnosis
  • Tinea manuum/pedis
  • Scabies
  • Herpetic whitlow
Erosive Vulvovaginal Lichen Planus

Clinical Findings
  • Painful erosive lesions on vulvar/vaginal mucosa
  • White, lacy reticulated borders (Wickham striae) adjacent to erosions
  • Glazed erythema and friability
  • Dyspareunia and vaginal discharge common
  • Scarring and architectural distortion in chronic disease
Pathophysiology
  • T-cell-mediated autoimmune on basal keratinocytes of mucosal epithelium
  • Keratinocyte apoptosis and basal cell degeneration
  • 1-2% risk of SCC transformation
Diagnosis/Treatment
  • Vulvar biopsy if any uncertainty or cancer concern
  • High-potency topical corticosteroid is first-line
  • Gynecology/dermatology follow-up for symptom control and SCC surveillance
Differential Diagnosis
  • Lichen sclerosus
  • Chronic candidiasis
  • Vulvar intraepithelial neoplasia/SCC
Nummular Eczema

Clinical Findings
  • Coin-shaped (nummular), well-demarcated eczematous plaques
  • Vesicles, crusting, and oozing within lesions
  • Intensely pruritic, often worse at night
  • Extremities and trunk common sites
  • Chronic dry skin background; worsens in winter
Pathophysiology
  • Xerosis and epidermal barrier dysfunction lead to coin-shaped, intensely pruritic eczematous plaques
Diagnosis/Treatment
  • Emollients plus medium/high-potency topical steroid
  • KOH if annular appearance raises diagnostic doubt
  • Reduce irritants and winter xerosis
Differential Diagnosis
  • Tinea corporis
  • Plaque psoriasis
  • Allergic contact dermatitis
Pemphigus Vulgaris

Clinical Findings
  • Flaccid, easily ruptured bullae on normal-appearing skin
  • Positive Nikolsky sign (shearing normal skin causes erosion)
  • Extensive painful erosions
  • Oral mucosa almost always involved (often first site)
  • Weight loss due to painful eating
Pathophysiology
  • Autoantibodies to desmoglein 3 (and possibly Dsg1) cause intraepidermal acantholysis, flaccid bullae, and painful mucosal erosions
Diagnosis/Treatment
  • Urgent biopsy and DIF
  • Systemic corticosteroids plus rituximab or other steroid-sparing therapy
  • Address hydration, nutrition, and infection risk
Differential Diagnosis
  • Mucous membrane pemphigoid
  • Paraneoplastic pemphigus
  • Bullous pemphigoid
Perioral Dermatitis

Clinical Findings
  • Small erythematous papules and pustules clustered around the mouth
  • Characteristic sparing of a 2-5mm zone at the vermilion border
  • May extend to perinasal and periorbital areas
  • History of topical steroid use (often initially improves, then worsens)
  • Predominantly in young women
Pathophysiology
  • Topical corticosteroids impair barrier and alter microbiome
  • Barrier disruption results in innate immune activation
  • Similar mechanism to rosacea
Diagnosis/Treatment
  • Stop topical steroid and avoid heavy facial products
  • Topical metronidazole/erythromycin or pimecrolimus; oral doxycycline if extensive
  • Expect temporary rebound after steroid withdrawal
Differential Diagnosis
  • Acne vulgaris
  • Rosacea
  • Allergic/irritant contact dermatitis
Plaque Psoriasis

More details

Clinical Findings
  • Well-demarcated erythematous plaques with thick silvery-white scale
  • Predilection for extensor surfaces (elbows, knees), scalp, lower back
  • Auspitz sign (pinpoint bleeding when scale removed)
  • Koebner phenomenon (lesions at trauma sites)
  • Nail pitting and onycholysis common
Pathophysiology
  • IL-23/Th17-driven inflammation due to dysregulated innate immunity
  • keratinocyte hyperproliferation with accelerated turnover, causing sharply demarcated erythematous plaques with silvery scale
Diagnosis/Treatment
  • Confirm clinically; assess nails and joints for psoriatic arthritis
  • Topical steroid plus vitamin D analog if limited
  • Systemic therapy if extensive or joint disease present
Differential Diagnosis
  • Chronic eczema
  • Tinea corporis
  • Seborrheic dermatitis
Rosacea (Papulopustular/Erythematotelangiectatic)

Clinical Findings
  • Central facial erythema (cheeks, nose, forehead, chin)
  • Telangiectasia and persistent flushing
  • Papules and pustules without comedones
  • Triggered by heat, spicy food, alcohol, sunlight
  • Rhinophyma (sebaceous hyperplasia of nose) in severe/chronic cases
Pathophysiology
  • Overexpression of genes result in pro-inflammatory cytokines
  • Neurovascular hyperreactivity causes flushing and angiogenesis
  • Demodex mites (naturally occurring skin mites) amplify immune response
  • Th1/Th17 infllammation results in papulopustular formation
Diagnosis/Treatment
  • Trigger avoidance and gentle skin care
  • Topical metronidazole, azelaic acid, or ivermectin first-line
  • Oral doxycycline if more inflammatory
Differential Diagnosis
  • Acne vulgaris
  • Perioral dermatitis
  • Cutaneous lupus erythematosus
Seborrheic Dermatitis

Clinical Findings
  • Greasy, yellowish-white scale with erythema
  • Predilection for nasolabial folds, eyebrows, scalp, external ear canals, chest
  • Chronic relapsing course
  • Worsens with stress, fatigue, neurological disease
  • Dandruff is a mild scalp form
Pathophysiology
  • Malassezia yeast metabolizes sebum triglycerides (in sebum rich areas such as face and scalp)
  • Free fatty acids from metabolized TGs disrupt skin barrier
  • Disrupted skin barrier allows for inflammatory activation
Diagnosis/Treatment
  • Ketoconazole shampoo/cream
  • Short course low-potency steroid or calcineurin inhibitor for flares
  • Maintenance antifungal for recurrent disease.
Differential Diagnosis
  • Psoriasis
  • Atopic dermatitis
  • Tinea faciei/capitis
Urticaria

Clinical Findings
  • Transient (<24h) pruritic, erythematous wheals with pale center
  • Lesions migrate and change shape
  • Surrounding erythematous flare
  • Dermographism may be present
  • Angioedema of lips/eyes/tongue possible
Pathophysiology
  • Type 1 hypersensitivity (IgE mediated) mast-cell degranulation releases histamine, prostaglandins, leukotrienes
  • Increased vascular permeability causes wheal with or without flare
Diagnosis/Treatment
  • Non-sedating H1 antihistamine; up-dose if needed
  • Assess for angioedema or anaphylaxis
  • Short steroid burst only if severe and not responsive
Differential Diagnosis
  • Urticarial vasculitis
  • Drug eruption
  • Contact dermatitis
Vitiligo

Clinical Findings
  • Chalk-white, well-demarcated, completely depigmented patches
  • Accentuated under Wood lamp (bright white fluorescence)
  • Perioral, periocular, acral, and genital predilection
  • Progresses over time
  • Associated with other autoimmune diseases (thyroid, T1DM)
Pathophysiology
  • Autoimmune destruction of melanocytes causes sharply demarcated depigmented patches
Diagnosis/Treatment
  • Clinical diagnosis
  • Wood lamp can confirm
  • Screen for associated autoimmune conditions
  • Topical steroid/calcineurin/JAK inhibitor for limited disease; nbUVB if extensive
Differential Diagnosis
  • Tinea versicolor
  • Post-inflammatory hypopigmentation
  • Pityriasis alba

Infectious

Cellulitis

Clinical Findings
  • Unilateral expanding erythema, warmth, swelling, and tenderness
  • Poorly demarcated borders (distinguishes from erysipelas)
  • Entry wound often visible (abrasion, ulcer, tinea pedis)
  • Systemic signs (fever, malaise) possible
  • Most common on lower extremities
Pathophysiology
  • Acute bacterial infection of dermis/subcutis, usually streptococcal or staphylococcal, entering through a skin break
Diagnosis/Treatment
  • Assess for abscess, systemic toxicity, and necrotizing infection
  • Start oral anti-streptococcal/anti-staphylococcal antibiotic and elevate the leg
  • Mark borders and reassess if diabetic
Differential Diagnosis
  • Deep venous thrombosis
  • Stasis dermatitis
  • Contact dermatitis
Erythema Migrans (Early Lyme Disease)

Clinical Findings
  • Expanding annular erythematous rash (>5cm) with or without central clearing
  • “Bull’s eye” pattern: central clearing with outer expanding ring
  • Appears 3–30 days after tick bite
  • Located at or near bite site (typically thigh, groin, axilla)
  • Recent tick exposure or camping/outdoor activity history
Pathophysiology
  • Local cutaneous infection with Borrelia burgdorferi after Ixodes tick exposure produces an expanding annular erythematous lesion
  • Expansion due to spirochetal spread through dermis
  • Partial central clearance due to immune response
  • Without treatment can disseminate to other systems causing complications
Diagnosis/Treatment
  • Treat clinically without waiting for serology if presentation is classic
  • Doxycycline in adults; amoxicillin as an alternative
  • Review for neurologic, cardiac, or joint symptoms
Differential Diagnosis
  • Tinea corporis
  • Cellulitis
  • Southern tick-associated rash illness (STARI)
Herpes Labialis (HSV-1 Reactivation)

Clinical Findings
  • Prodrome of tingling, burning, or itching 12–24h before eruption
  • Grouped vesicles on erythematous base at vermilion border
  • Rapid progression: vesicles to pustules to crust
  • Heals over 7–10 days
  • Recurs at same site with subsequent triggers (UV, stress, fever)
Pathophysiology
  • HSV reactivates from latency in the trigeminal ganglion, causing prodromal tingling followed by grouped painful vesicles
Diagnosis/Treatment
  • Start oral antiviral early (within prodrome/first 48 hours)
  • Supportive care and avoid direct contact during active lesions
  • Consider suppressive therapy if recurrent
Differential Diagnosis
  • Impetigo
  • Aphthous lesion near vermilion
  • Contact cheilitis
Herpes Zoster

More details

Clinical Findings
  • Painful prodrome (burning, tingling) preceding rash by days
  • Unilateral dermatomal grouped vesicles on erythematous base
  • Does not cross the midline
  • Most common thoracic dermatomes (T3–L3)
  • Risk of post-herpetic neuralgia, especially in elderly/immunocompromised
Pathophysiology
  • Reactivation of latent VZV in a dorsal root ganglion causes painful unilateral dermatomal vesicular eruption
  • Risk increased by immunosuppression (age related, chemotherapy)
Diagnosis/Treatment
  • Start valacyclovir/acyclovir promptly with analgesia
  • Monitor closely given active chemotherapy
  • Urgent review if disseminated or ophthalmic/neurologic symptoms develop
Differential Diagnosis
  • HSV infection
  • Allergic contact dermatitis
  • Zosteriform metastatic eruption
Measles (Rubeola)

Clinical Findings
  • Prodrome: 3 Cs (Cough, Coryza, Conjunctivitis) + high fever
  • Koplik spots: white/gray dots on buccal mucosa (pathognomonic, appear 1-2 days before rash)
  • Maculopapular rash starts at hairline/face and spreads cephalocaudally
  • Lesions may become confluent
  • Unvaccinated child in endemic or outbreak setting
Pathophysiology
  • Paramyxovirus enters respiratory system via epithelial cells resulting in primary viremia
  • Secondary viremia seeds skin, respiratory tract, CNS
  • Viral antigens present in dermal vessels causes CD4 T cell immune response, producing rash
Diagnosis/Treatment
  • Immediate airborne isolation and public health notification
  • Confirm with PCR/serology
  • Supportive care plus vitamin A per pediatric guidance
Differential Diagnosis
  • Rubella
  • Roseola
  • Adenoviral/other viral exanthem
Molluscum Contagiosum

Clinical Findings
  • Multiple 2–5mm dome-shaped flesh-coloured papules
  • Central umbilication (pathognomonic)
  • White cheesy core can be expressed
  • Clusters in moist/intertriginous areas
  • Surrounding eczematous reaction (“molluscum dermatitis”) common
Pathophysiology
  • Poxvirus infection of epidermal keratinocytes
  • Inhibits MHC-1 expression and blocks apoptosis for local immune evasion leading to delayed immune recognition (and thus resolution)
Diagnosis/Treatment
  • Usually clinical diagnosis and watchful waiting
  • Treat if spreading with cantharidin, curettage, or cryotherapy
  • Manage associated eczema to reduce scratching
Differential Diagnosis
  • Verruca vulgaris
  • Milia
  • Folliculitis
Nonbullous Impetigo

Clinical Findings
  • Honey-colored/golden crusted erosions (pathognomonic)
  • Perioral and perinasal distribution most common
  • Fragile vesicles/pustules rupture quickly leaving crusts
  • Mildly pruritic, non-tender
  • Spreads readily by scratching/contact
Pathophysiology
  • Superficial epidermal infection (S. aureus or group A strep) causes
  • Superficial blister rupture results in honey-coloured crusts
  • Spreads by contact and autoinuoculation
Diagnosis/Treatment
  • Clinical diagnosis
  • Topical mupirocin if limited; oral antibiotic if extensive
  • Hygiene and nail trimming to reduce spread
Differential Diagnosis
  • HSV infection
  • Periorificial dermatitis
  • Excoriated eczema
Pityriasis Rosea

Clinical Findings
  • Herald patch: solitary large (2–10cm) oval erythematous patch with collarette scale, precedes rash by 1–2 weeks
  • Diffuse smaller oval patches following skin cleavage lines (“Christmas tree” pattern on back)
  • Spares face, palms, and soles
  • Mild pruritus
  • Self-resolving in 6–12 weeks
Pathophysiology
  • Likely post-viral inflammatory eruption (HHV-6/7)
  • Viral antigen triggers Th1 response
  • Herald patch from initial replication site
  • Subsequent lesions follow cleavage lines via viremic spread
Diagnosis/Treatment
  • Clinical diagnosis
  • KOH or RPR if atypical
  • Reassure; topical steroid or antihistamine for itch
Differential Diagnosis
  • Tinea corporis
  • Guttate psoriasis
  • Secondary syphilis
Plantar Warts (Verruca Plantaris)

Clinical Findings
  • Hyperkeratotic papules on weight-bearing surfaces
  • Black dots (thrombosed capillaries) - pathognomonic
  • Disruption of normal skin lines
  • Pain with direct pressure and pinching (distinguishes from callus)
  • May coalesce into mosaic warts
Pathophysiology
  • HPV infection of plantar keratinocytes causes hyperkeratotic papules with thrombosed capillaries visible as black dots
Diagnosis/Treatment
  • Clinical diagnosis, sometimes aided by paring
  • Topical salicylic acid or cryotherapy
  • Counsel on autoinoculation and foot hygiene
Differential Diagnosis
  • Corn/callus
  • Pitted keratolysis
  • Foreign body granuloma
Roseola Infantum (Exanthem Subitum)

Clinical Findings
  • High fever (39-40 deg C) lasting 3–5 days in a well-appearing child
  • Abrupt defervescence followed immediately by rash
  • Rose-pink maculopapular rash on trunk, spreading to extremities
  • Rash non-pruritic and fades within days
  • Most common in children 6-24 months
Pathophysiology
  • Primary HHV-6/7 infection after maternal antibody wanes (~6 months of age)
  • Virus replicates in CD4 T cells causing systemic viremia and high fever
  • As viremia clears (and thus fever), immune response on skin results in transient maculopapular rash
Diagnosis/Treatment
  • Clinical diagnosis and supportive care
  • No specific treatment if well appearing
  • Review hydration and seizure history if fever was very high
Differential Diagnosis
  • Measles
  • Rubella
  • Enteroviral exanthem
Scabies

Clinical Findings
  • Intensely pruritic, worse at night
  • Linear burrows in finger webs, wrists, waistline, axillae, genitalia
  • Erythematous papules and vesicles
  • Spares head and neck in immunocompetent adults
  • Close contacts with similar symptoms (highly contagious)
Pathophysiology
  • Sarcoptes scabiei infestation triggers delayed hypersensitivity, causing nocturnal itch, papules, and burrows in classic sites
  • Initial infestation: 4-6 weeks sensitization before itch starts
  • Re-infestation: 24-48 hrs before itch
  • Type IV hypersensitivity to mite antigens, eggs, and feces
Diagnosis/Treatment
  • Treat patient and close contacts with permethrin 5% or oral ivermectin
  • Wash/dry bedding and clothing on hot cycle
  • Topical steroid/antihistamine for post-treatment itch
Differential Diagnosis
  • Atopic dermatitis
  • Papular urticaria
  • Contact dermatitis
Secondary Syphilis

More details

Clinical Findings
  • Copper-coloured papulosquamous rash involving palms and soles (classic and distinctive)
  • Generalized non-tender lymphadenopathy
  • Constitutional symptoms (malaise, low-grade fever, sore throat)
  • Condylomata lata (flat moist lesions in intertriginous areas)
  • Painless chancre history 6–8 weeks prior
Pathophysiology
  • Hematogenous dissemination of Treponema pallidum after the primary chancre stage causes systemic symptoms and a palm/sole papulosquamous eruption
Diagnosis/Treatment
  • RPR/VDRL plus treponemal confirmation
  • Treat with benzathine penicillin G (discuss desensitization or alternative if severe penicillin allergy)
  • Notify public health and treat contacts
Differential Diagnosis
  • Pityriasis rosea
  • Viral exanthem/drug eruption
  • Psoriasis
Tinea Capitis

Clinical Findings
  • Scaly patches with partial alopecia
  • Broken “black dot” hairs at follicle openings
  • Cervical lymphadenopathy common
  • Kerion: boggy, indurated, pustular inflammatory mass
  • Predominantly in prepubertal children; contagious within households
Pathophysiology
  • Dermatophyte invade hair shaft
  • Spores weaken hair causing black dot breakage
  • Kerion due to exaggerated hyper IV hypersensitivity to antigens resulting in boggy inflammatory mass (pustular)
Diagnosis/Treatment
  • Confirm with fungal culture/KOH
  • Systemic terbinafine or griseofulvin - topical therapy alone is inadequate (fungi penetrate below topical drug depth)
  • Antifungal shampoo for household contacts
Differential Diagnosis
  • Alopecia areata
  • Seborrheic dermatitis
  • Traction alopecia
Tinea Corporis

Clinical Findings
  • Annular erythematous plaque with central clearing
  • Active, scaly, slightly raised advancing border
  • Pruritic
  • Single or multiple lesions
  • KOH demonstrates branching hyphae
Pathophysiology
  • Dermatophyte infection of the stratum corneum causes an annular plaque with central clearing and a scaly advancing edge
  • Central clearing caused by neutrophil immune clearance
Diagnosis/Treatment
  • Confirm with KOH if uncertain
  • Topical terbinafine or azole cream
  • Avoid topical steroid monotherapy
Differential Diagnosis
  • Nummular eczema
  • Granuloma annulare
  • Pityriasis rosea herald patch
Tinea Versicolor

Clinical Findings
  • Multiple well-defined hypo- or hyperpigmented patches with fine scale
  • Trunk, shoulders, and upper arms most common
  • Scale accentuated by stretching skin
  • KOH shows “spaghetti and meatballs” (short hyphae + round spores)
  • Worsens in summer/heat; asymptomatic or mildly pruritic
Pathophysiology
  • Malassezia convers to mycelial form in warm, humid conditions
  • Produces azelaic acid which inhibits tyrosinase causing hypopigmentation
  • Inflammatory response may result in hyperpigmentation in darker skin
Diagnosis/Treatment
  • Clinical diagnosis; KOH can confirm “spaghetti and meatballs” pattern
  • Selenium sulfide or topical ketoconazole first-line
  • Explain that pigment normalization lags behind fungal clearance
Differential Diagnosis
  • Vitiligo
  • Pityriasis alba
  • Post-inflammatory hypopigmentation
Varicella (Chickenpox)

Clinical Findings
  • “Dewdrop on a rose petal” vesicles on erythematous base
  • Lesions in multiple simultaneous stages (macule, papule, vesicle, crust)
  • Centripetal distribution (face and trunk > extremities)
  • Intensely pruritic
  • Fever and malaise precede rash
Pathophysiology
  • Primary VZV infection from respiratory droplets to upper respiratory lymph nodes
  • Secondary viremia seeds skin causing keratinocyte infection and intraepidermal vesicle formation
Diagnosis/Treatment
  • Clinical diagnosis and isolation
  • Supportive care if otherwise healthy
  • Consider oral acyclovir if early and high-risk or severe
Differential Diagnosis
  • Disseminated HSV
  • Eczema herpeticum
  • Papular urticaria

Pigmentation Disorder

Solar Lentigines (sun spots)

Clinical Findings
  • Flat, well-defined, uniformly brown macules
  • 1–3cm on chronically sun-exposed areas (dorsal hands, face, forearms)
  • No elevation or palpable texture
  • Persistent (unlike freckles, do not fade in winter)
  • Background of photoaging
Pathophysiology
  • Chronic UV exposure increases melanocyte activity and melanin deposition, producing flat brown macules on sun-exposed skin
  • Excess of melanin production persists even during winter (unlike freckles)
Diagnosis/Treatment
  • Clinical/dermoscopic diagnosis
  • Biopsy any irregular, very dark, or changing lesion
  • Sun protection; optional topical lightening or laser for cosmesis
Differential Diagnosis
  • Freckles/ephelides
  • Lentigo maligna
  • Flat seborrheic keratoses
Melasma

Clinical Findings
  • Symmetric, irregular brown-gray hyperpigmented patches
  • Cheeks, forehead, upper lip, and chin distribution
  • Worsens with sun exposure
  • Predominantly in women of reproductive age, darker skin types
  • Associated with OCP use or pregnancy (“mask of pregnancy”)
Pathophysiology
  • Estrogen/progesterone upregulate genes within melanocytes
  • UV exposure and hormonal stimulation increase melanogenesis, producing symmetric facial hyperpigmentation
Diagnosis/Treatment
  • Clinical diagnosis
  • Strict photoprotection (tinted mineral sunscreen)
  • Hydroquinone/triple-combination cream
  • Reduce estrogen trigger if feasible
Differential Diagnosis
  • Post-inflammatory hyperpigmentation
  • Lichen planus pigmentosus
  • Drug-induced hyperpigmentation

Other

Neurofibromatosis Type 1 (NF1)

Clinical Findings
  • ≥6 cafe-au-lait macules (>5mm prepubertal, >15mm postpubertal)
  • Axillary or inguinal freckling (Crowe sign)
  • Multiple soft, flesh-coloured neurofibromas
  • Lisch nodules (iris hamartomas) on slit-lamp exam
  • Autosomal dominant; diagnosis by NIH clinical criteria
Pathophysiology
  • Loss-of-function of NF1 gene causes uncontrolled proliferation of neural crest-derived cells
  • Disordered melanocyte development results in cafe-au-lait macules
Diagnosis/Treatment
  • Confirm clinical criteria; genetics if uncertain
  • Ophthalmology, BP monitoring, neurologic review, and hereditary counseling
  • Remove symptomatic neurofibromas selectively
Differential Diagnosis
  • Legius syndrome
  • Schwannomatosis
  • Multiple lipomas with incidental lentigines
Spider Angiomas

Clinical Findings
  • Central red arteriole (“spider body”) with radiating thin capillaries
  • Blanches with central point pressure, refills from centre outward
  • Typically on face, neck, upper chest
  • Multiple lesions in pregnancy or liver disease
  • Resolves postpartum in most cases
Pathophysiology
  • Elevated estrogen (pregnancy, liver disease, OCP use) upregulates VEGF and nitric oxide
  • Arteriolar dilation and central arteriole dilates and feeds surrounding radially arranged capillaries
Diagnosis/Treatment
  • Reassure if isolated and pregnancy-related (benign)
  • No treatment needed unless bothersome; pulsed-dye laser is an option
  • Broader workup only if numerous or atypical; suspicion of underlying disease
Differential Diagnosis
  • Telangiectasia
  • Cherry angioma
  • Hereditary hemorrhagic telangiectasia lesions

References

Tools / Guidelines

Additional Reading