Dermatology 1 CAM I 2025 (1) (1) PDF

DERMATOLOGY 1 Professor Jacobus, MSBS, PA-C South College Where Dreams Find Direction  TOPICS Papulo-squamous diseases: (papules and plaques) dermatitis, eczema, drug eruptions, lichen planus, pityriasis rosea, psoriasis Desquama...

DERMATOLOGY 1 Professor Jacobus, MSBS, PA-C South College Where Dreams Find Direction  TOPICS Papulo-squamous diseases: (papules and plaques) dermatitis, eczema, drug eruptions, lichen planus, pityriasis rosea, psoriasis Desquamation: erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis Vesicular bullae: pemphigoid, pemphigus Acneiform lesions: acne vulgaris, rosacea, folliculitis  INSTRUCTIONAL OBJECTIVES Identify and describe the etiology, epidemiology, clinical features, differential diagnosis, and management of selected skin disorders. Identify and accurately describe skin lesions using standard terms: Number: single, multiple Pigmentation/color: white, flesh colored, pink, pearly, erythematous, tan-brown, salmon, black, purple, violaceous, and yellow  INSTRUCTIONAL OBJECTIVES Identify and accurately describe skin lesions using standard terms: (Continued) Shape and arrangement: annular, round/discoid, linear, oval, iris/target, zosteriform, serpiginous, stellate, reticulate, and morbilliform Texture: consistency, mobility, temperature, tenderness, depth Borders/margins: well-defined, ill-defined  INSTRUCTIONAL OBJECTIVES Identify and accurately describe skin lesions using standard terms: (Continued) Type: Primary lesions (including macule, tumor, patch, wheal, papule, vesicle, plaque, bulla, nodule, pustule, cyst, and telangiectasia) or secondary lesions (crust, fissure, scale, ulcer, lichenified, keloid, erosion, hypertrophic scar, atrophy, and excoriation) Arrangement/location/distribution: localized, regional, and generalized Associated changes Skin layers Epidermal layers Skin cell formation  Dermis Contains : hair follicles, nerve endings, sweat glands and connective tissue  Skin cell formation 4 steps 1: cell division: Keratinocytes divide in the deepest (basal) layer 2:cell differentiation: as cells move up in the dermis, they change shape and composition 3: keratinization: cells secrete keratin proteins and lipids to form a matrix that protects the skin and gives it strength 4: desquamation: the outer most layer of skin cells die and shed off from the skin TO  SKIN EXAM Be thorough! When possible, examine patient in a gown Good lighting (consider magnification) Check scalp, palms, soles, nails Look for lesions that look different from other lesions on their body Notice texture, turgor, color Document any findings in detail/photo and monitor for changes over time Take a picture and compare in 6 mo/ 1 yr with another picture  APPROACH TO DIAGNOSIS Primary & secondary lesions Characteristics of skin lesions(CLAMPS TN) 1. Color 2. Location/distribution (extent, pattern) 3. Arrangement (grouped vs disseminated & confluence (yes or no) 4. Margination (well- or ill-defined) 5. Palpation (consistency, temperature, mobility, tenderness, depth) 6. Shape 7. Type (ie, papule, macule, pustule) 8. Number: single vs multiple (# of lesions) MACULE Non-palpable < 1 cm diameter Varied pigmentation from surrounding skin No elevation or depression Patch: macule > 1cm diameter PAPULE Palpable < 1 cm diameter Isolated or grouped Pustule: small, circumscribed papule contains purulent material PUSTULE Circumscribed superficial cavity with purulent exudate Exudate: white, yellow, greenish-yellow, or hemorrhagic PLAQUE Plateau-like elevation. Ex/ psoriasis Lichenification -less defined large plaque that is thickened with rough skin Patch- flat or barely elevated plaque Ex/ atopic dermatitis/ eczema NODULE Palpable, solid, fatty or cystic, round or ellipsoidal Larger than papule (1-2 cm) Think of it as a large papule Tumor: nodule > 2 cm WHEAL Irregularly-shaped, elevated, edematous Erythematous or paler than surrounding skin Well-demarcated borders but not stable Disappears within 24-48 hours Multiple wheals/rash = urticaria “hives, whelps” VESICLE / BULLA Blister Vesicle 0.5 cm Well-defined Roof is thin Serum and blood SECONDARY SKIN LESIONS Crust-dried serum, blood, or exudate Scales-flakes Erosion-epidermis defect (heals without scar) ex/scrape Ulcer-defect in dermis or deeper (heals with scar) usually indented Scar-fibrous tissue replacement Atrophy-diminution of some or all layers of skin Keloid scars  DESCRIBING SKIN LESIONS Systematic approach/format: (CLAMPS TN) 1. Color 2. Location/distribution (extent, pattern) 3. Arrangement (grouped vs disseminated & confluence (yes or no) 4. Margination (well- or ill-defined) 5. Palpation (consistency, temperature, mobility, tenderness, depth) 6. Shape 7. Type (ie, papule, macule, pustule) 8. Single vs multiple (# of lesions) DESCRIBING SKIN LESIONS Systematic approach/format: 1. Color 2. Location/distribution (extent, pattern) 3. Arrangement (grouped vs disseminated & confluence (yes or no) 4. Margination (well- or ill-defined) 5. Palpation (consistency, temperature, mobility, tenderness, depth) 6. Shape 7. Type (ie, papule, macule, pustule) 8. Single vs multiple (# of lesions)  DESCRIBING SKIN LESIONS Systematic approach/format: 1. Color 2. Location/distribution (extent, pattern) 3. Arrangement (grouped vs disseminated & confluence (yes or no) 4. Margination (well- or ill-defined) 5. Palpation (consistency, temperature, mobility, tenderness, depth) 6. Shape 7. Type (ie, papule, macule, pustule) 8. Single vs multiple (# of lesions) DESCRIBING SKIN LESIONS Systematic approach/format: 1. Color 2. Location/distribution (extent, pattern) 3. Arrangement (grouped vs disseminated & confluence (yes or no) 4. Margination (well- or ill-defined) 5. Palpation (consistency, temperature, mobility, tenderness, depth) 6. Shape 7. Type (ie, papule, macule, pustule) 8. Single vs multiple (# of lesions) DESCRIBING SKIN LESIONS Systematic approach/format: 1. Color 2. Location/distribution (extent, pattern) 3. Arrangement (grouped vs disseminated & confluence (yes or no) 4. Margination (well- or ill-defined) 5. Palpation (consistency, temperature, mobility, tenderness, depth) 6. Shape 7. Type (ie, papule, macule, pustule) 8. Single vs multiple (# of lesions)  DESCRIBING SKIN LESIONS Systematic approach/format: 1. Color 2. Location/distribution (extent, pattern) 3. Arrangement (grouped vs disseminated & confluence (yes or no) 4. Margination (well- or ill-defined) 5. Palpation (consistency, temperature, mobility, tenderness, depth) 6. Shape 7. Type (ie, papule, macule, pustule) 8. Single vs multiple (# of lesions) DESCRIBING SKIN LESIONS Systematic approach/format: 1. Color 2. Location/distribution (extent, pattern) 3. Arrangement (grouped vs disseminated & confluence (yes or no) 4. Margination (well- or ill-defined) 5. Palpation (consistency, temperature, mobility, tenderness, depth) 6. Shape 7. Type (ie, papule, macule, pustule) 8. Single vs multiple (# of lesions) HISTORY Demographics: age, race, sex, occupation, hobbies (chemical/toxin exposure?) Constitutional symptoms (acute vs chronic) History of skin lesions (OLD CARTS) HPI PMHx FHx: skin cancer, skin disorders SocHx SexHx HX OF SKIN LESION 8 Key Questions (OLD CARTS) 1. When did lesion appear (1st noticed)? 2. Where did lesion appear (site of onset)? 3. Does it come and go or is it constant? 4. Does it itch, hurt, or bleed? 5. How has it spread (pattern/evolution)? 6. How have individual lesions changed)? 7. What are provocative factors? 8. What are previous treatments? (topical, systemic)  TOPICS Papulo-squamous diseases: (papules and plaques) dermatitis, eczema, drug eruptions, lichen planus, pityriasis rosea, psoriasis Desquamation: erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis Vesicular bullae: pemphigoid, pemphigus Acneiform lesions: acne vulgaris, rosacea PAPULOSQUAMOUS DISEASE Eczema / Dermatitis Drug eruptions Lichen planus Pityriasis rosea Psoriasis ECZEMA / DERMATITIS Dyshidrotic eczema Lichen simplex chronicus Nummular eczema Contact dermatitis Stasis dermatitis Atopic dermatitis Seborrheic dermatitis Perioral dermatitis  ECZEMA / DERMATITIS Inflammatory reaction of epidermis & dermis “the itch that rashes” Multiple etiologies Wide range of clinical findings Acute: pruritis, erythema, vesiculation Chronic: pruritis, xerosis, lichenification, hyperkeratosis, scaling, + fissuring DYSHIDROTIC ECZEMA Acute, chronic, & recurrent Fingers, palms, & soles (lateral fingers & toes) Sudden, deep-seated pruritic, clear “tapioca- like” vesicles Painful when erosive. May develop bullae. Treatment: strong steroids, IL steroids, PO prednisone for severe cases LICHEN SIMPLEX CHRONICUS Localized lichenification in circumscribed plaques Usually > 20 y/o, F>M Caused by repetitive rubbing & scratching Chronic, usually relapsing Common sites: scalp, neck, extensor forearms, scrotum & lower legs Thickened skin, excoriations Treatment: D/c scratching!, occlusive bandages, topical steroids, tar preps, IL steroids (small lesions), PO hydroxyzine NUMMULAR ECZEMA Chronic, inflammatory Coin-shaped plaques of grouped small papules & vesicles on erythematous base Etiology unknown Most > 50 y/o, M>F Highly pruritic m/c in legs & upper extremities Treatment: moisturizer, topical steroid, PUVA or UVB CONTACT DERMATITIS Acute or chronic Irritant: chemical (ex/hands) Soaps, detergents, solvents (Table 2-1, Fitzpatrick’s) Allergic: Nickel/jewelry, plants (Table 2-2, Fitzpatrick’s) Symptoms: Stinging, itching, burning, pain with fissures, weeps, crusting Plastics, chemical residues on clothes, plants Working in the yard? Plant exposure? Presentation: well-demarcated erythema and edema, non-umbilicated vesicles or papules Treatment: remove etiologic agent, wet dressings/Burrow’s solution (OTC,) topical glucocorticoids, PO prednisone (if severe) STASIS DERMATITIS Related to venous insufficiency PE findings: inflammatory papules, hyperpigmentation, scaly and crusted erosions in lower legs and ankles Treatment: Avoid scratching, emollients throughout the day, topical corticosteroids, wrap legs/compression stockings **This is not cellulitis** ATOPIC DERMATITIS Acute, subacute, chronic relapsing Common in infancy, itch-scratch cycle Frequent /w personal or FHx AD, allergic rhinitis, & asthma Skin barrier dysfunction, IgE reactivity ATOPIC DERMATITIS Eliciting/exacerbating factors: inhalants, microbials, aeroallergens, foods, season (winter,) and emotional stress Dry skin, pruritis “The itch that rashes”: Itch > scratch > rash > itch > scratch > rash Poorly-defined erythematous patches, papules, & plaques with or without scaling Infantile, child, & adult types Treatment (acute/chronic): avoid scratching, wet dressings, topical steroids, topical or PO antibiotics, hydration, emollients, topical calcineurin inhibitors, PO H1 antihistamines, PO steroids only for severe intractable cases SEBORRHEIC DERMATITIS Ages = infancy, puberty, 20-50 years old, M>F Chronic and relapsing Worse in fall/winter (dry environment and stress) Summer: worse in some, better in others Common in immunosuppressed = HIV, Parkinson’s, and nutritional deficiencies (zinc) Distribution = scalp, face, trunk, genitalia and body folds. “Cradle Cap”- yellow greasy scales on scalp Often seen in hair bearing regions (eyebrows, central face, scalp) – looks like dandruff Presentation = pruritis, red plaques, greasy looking. Yellowish scales may be present on areas with a plethora of sebaceous glands. Treatment options include selenium sulfide (Selsen BLUE, Head and Shoulders,) topical antifungals, tar shampoo (Neutrogena T-gel,) mild topical steroids SEBORRHEIC DERMATITIS  Perioral Dermatitis Erythematous grouped papulopustules may become plaques with scales. Can have satellite lesions. May include perinasal and periorbital skin **spares vermillion border** Most common in females 20-45 Causes: fluorinated toothpaste, topical corticosteroids Treatment: eliminate steroids and irritants (cosmetics/skin care products) topical metronidazole, erythromycin or pimecrolimus Perioral Dermatitis FIXED DRUG ERUPTION Adverse cutaneous reaction to ingested drug Solitary (or multiple) erythematous patch or plaque Usually asymptomatic (may have pruritis, pain, burning) Sharply demarcated macule, round or oval Initially erythematous, then dusky red to violaceous May evolve to bulla, then erosion Most common agents: TCN, sulfa, NSAIDs, barbiturates, OCPs, quinine, yellow food coloring (full list: Table 23-6, Fitzpatrick’s) Resolves in a few weeks after d/c offending agent Treatment: d/c drug, topical steroids (non-eroded), antibiotic ointment (eroded), PO steroids for severe mucosal lesions FIXED DRUG ERUPTION LICHEN PLANUS Acute or chronic inflammation involving skin or mucous membranes (In mouth/ vaginal mucousa appears white and lacy) 4 Ps: Papule, purple, polygonal, pruritic (and flat topped) Flexor creases of arms and legs 30-60 y/o, F>M Idiopathic Treatment: topical & PO steroids, cyclosporine PITYRIASIS ROSEA Acute rash, self-limited course, more common in fall Initial single, primary (“herald”) patch usually on trunk (80% of patients) Generalized secondary eruption 1-2 weeks later Fine scaling papules & patches in “Christmas tree” pattern (lines of cleavage) on back ** Resolves spontaneously in 6-12 weeks Probable etiology: reactivation HSV-7 & HSV-6 Herald patch: oval, salmon-red plaque or patch 2-5 cm with fine collarette peripheral scale PITYRIASIS ROSEA Treatment: PO or topical antihistamines, topical steroids, UVB phototherapy or natural sunlight, PO steroids PITYRIASIS ROSEA PSORIASIS History Taking/ PE findings Usually a + FHx All ages; M=F Worse with stress, obesity +/- joint pain – psoriatic arthritis Pruritic well-demarcated, erythematous plaques with silver “scales” (when scraped off reveal pinpoint bleeding) usually on knees, elbows, nails, palms, and soles of feet Causes pitting in nails PSORIASIS 2 major types: Eruptive, inflammatory, “raindrop” (guttate) Chronic stable (plaque) psoriasis Triggers: physical trauma, strep (guttate,) stress, drugs, alcohol Diagnosis Clinical Biopsy for uncertain diagnosis Differentials Eczema Lichen simplex chronicus  Guttate Psoriasis Drop-like scattered (scaly) red to pink lesions- diffuse Often preceded by strep infection Usually in children or young adults< 30; M=F May self remit in several weeks to several months May progress to plaque psoriasis 10 days. Macule > papule >vesicles and bullae Hands, feet, palms, soles, elbows, knees, mouth, torso, face, genitals Diagnosis Clinical Biopsy may help confirm ERYTHEMA MULTIFORME Treatment/Medications Topical corticosteroids, PO steroids for disabling oral lesions PO antihistamines Wet dressings Medicated (lidocaine, diphenhydramine) mouthwash for oral mucosal lesions Ophthalmology referral for ocular lesions Follow up Continuous antiviral therapy for recurrent HSV- associated EM STEVENS-JOHNSON SYNDROME (SJS) TOXIC EPIDERMAL NECROLYSIS (TEN) Acute, life-threatening mucocutaneous reaction Necrosis and detachment of epidermis Differ by % of body surface involved SJS 30% epidermal detachment (overlap 10-30%) 90% of the time, mucous membranes affected – ocular, oral, and genital Rarely present on palms/soles Idiopathic or drug-induced: anti-seizure meds, sulfa, allopurinol, NSAIDS Higher incidence in HIV & active cancer. F>M. STEVENS-JOHNSON SYNDROME (SJS) TOXIC EPIDERMAL NECROLYSIS (TEN) Presentation – usually 4 days to 4 weeks after drug exposure Fever, malaise, and arthralgias (influenza like sx) for 1-3 days…THEN… Skin is sloughing off and painful – burning, paresthesia, etc! Conjunctival burning/itching, and painful mouth lesions Lesions: ill-defined, coalescing, erythematous macules with purpuric centers or diffuse erythema; *pain out of proportion* Lesions usually start on face and thorax and symmetric Management Admit to ICU or burn center, d/c offending agent/drug IV fluids and electrolytes (treat as burn patient) Narcotics for pain Systemic glucocorticoids controversial (contraindicated late in disease course) IVIG (if started early) Surgical debridement not recommended Lasts approximately 8-12 days Source: JAMA NIKOLSKY SIGN The ability to extend the area of superficial sloughing by applying gentle lateral pressure on the surface of the skin at an apparently uninvolved site. PAthognomonic for pemphigus, TEN, Nikolsky sign video Break  TOPICS Papulo-squamous diseases: (papules and plaques) dermatitis, eczema, drug eruptions, lichen planus, pityriasis rosea, psoriasis Desquamation: erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis Vesicular bullae: pemphigoid, pemphigus Acneiform lesions: acne vulgaris, rosacea VESICULOBULLOUS DISEASE Bullous pemphigoid (Fitzpatrick’s, pg. 106) Autoimmune disease of elderly patients (60-80yrs) with pruritic, large, tense, bullae scattered but also in groups. Often starts with urticarial eruption. Don’t rupture as easily as pemphigus. Predilection- axillae, medial thigh, groin, flexor UE, lower LE, can be in mouth TX- PO, topical steroids 50-100 mg QD or immunosuppressives Bullous pemphigoid  VESICULOBULLOUS DISEASE Cont’d Pemphigus (Fitzpatrick’s, pg. 100) Chronic or acute, bullous autoimmune disease, adults 40-60 Predilection: scalp, face, chest, axillae, groin, umbilicus Usually starts in mouth, no pruritis, but burning and painful PE- vesicles and bullae, easily rupture, flaccid and weeping. + Nikolsky sign, TX- dermatologist, high dose steroids and immunosuppression VESICULOBULLOUS DISEASE Cont’d  TOPICS Papulo-squamous diseases: (papules and plaques) dermatitis, eczema, drug eruptions, lichen planus, pityriasis rosea, psoriasis Desquamation: erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis Vesicular bullae: pemphigoid, pemphigus Acneiform lesions: acne vulgaris, rosacea ACNE & RELATED DISORDERS Acne vulgaris Rosacea Hidradenitis suppurativa ACNE VULGARIS Inflammation of pilosebaceous units Seen with comedones (must have for diagnosis,) cysts, pustules and/or nodules Occurs primarily in young people on face, trunk, upper arms and sometimes buttocks Can result in pits, depressions, scars or hyperpigmentation More severe in males than females Less often in Asians and African Americans Cystic acne can be familial  ACNE VULGARIS Cont’d Factors in pathogenesis – follicular keratinization, androgens, Propionibacterium acnes Follicular plugging= (comedone) traps sebum->androgens produce more sebum-> bacteria produce inflammatory response Contributory factors- meds (lithium, isoniazid, steroids, OCP, androgens; stress; occlusion/pressure (hand on face,) cosmetics, pomade, sweat  ACNE VULGARIS Cont’d Worse in fall and winter Nodulo-cystic type can be painful Comedones – open= blackheads, closed – white heads; required for acne diagnosis Labs- none required Course- often clears by early 20’s, flares in winter and with onset of menses  ACNE VULGARIS Cont’d Treatment – long-term goal is scar prevention Remove plugging, treat bacteria Mild – topical antibiotics (clindamycin and erythromycin 3%, 5% BID) and benzoyl peroxide gels 2%, 5%, 10%) **this bleaches fabrics** can get in combo Topical retinoids ** gradual increase in strength from 0.01%, 0.025%, 0.05% cream, gel, liquid, or ointment (retinoic acid, adapalene (now OTC), tazarotene) *** can NOT use if pregnant Combination therapy works best  ACNE VULGARIS Cont’d Treatment – moderate- same regimen for minor plus PO antibiotics (Minocycline 50-100mg/d or doxycycline 50-100mg BID tapered to 5o mg/d as acne lessens.) Spironolactone 25- 50mg QD. Severe- same as above with the addition of PO isotretinoin for cystic or refractory acne.  ACNE VULGARIS Cont’d PO isotretinoin – complete remission in most cases for months to years. Works by inhibiting sebaceous gland function and keratinization. ****Is extremely teratogenic*** MUST have effective contraception and 2 neg pregnancy tests prior to initiating. Can cause pseudotumor cerebri when used in combo with tetracycline. Must check lipids and transaminases prior to therapy as can cause elevated triglycerides and mild to moderate elevations of transaminases (normalize with dose reduction.) Causes extremely dry skin and mucosa. Can cause depression. ROSACEA Chronic inflammation of facial pilosebaceous units 30-50 y/o, F>M Episodic erythema, “flushing & blushing” Stages I, II, & III: persistent erythema, telangiectasias, papules, tiny pustules, nodules **Note, NO comedones** Triggered by hot liquids, spicy foods, alcohol/wine, aged cheese, exposure to sun & heat, stress Duration: days, weeks, months ROSACEA Late stage: rhinophyma, metophyma, blepharophyma, otophyma, gnatophyma Distribution: symmetric on face. Rarely on neck, chest, back, & scalp. Recurrences common; usually lifetime Treatment: Reduce or eliminate alcohol & caffeine Metronidazole gel or cream, ivermectin cream Topical antibiotics PO antibiotics better than topical (minocycline, doxycycline, TCN) in papulopustular rosacea PO isotretinoin for severe disease Surgery for rhinophyma; telangiectasia (lasers) Rosacea - rhinophyma ROSACEA  Folliculitis Inflammation or infection of superficial hair follicles Perifollicular papules and/or pustules with surrounding erythema; hair bearing skin; often pruritic More common in males Risk factors: prolonged antibiotic use, topical corticosteroids, hot tubs Etiology: most common staph aureus; hot tub-->> pseudomonas auruginosa  Folliculitis Treatment: Benzoyl peroxide wash (bleaches) topical mupirocin, clindamycin, erythromycin. If no improvement -- >PO Cephalexin. HIDRADENITIS SUPPURATIVA Chronic, suppurative Apocrine gland skin Axillae, inguinocrural, anogenital, inframammary, rarely scalp F (axillae)>M (anogenital) FHx: NC acne & HS Unknown etiology Risk factors: obesity, smoking, genetic predisp. to acne HIDRADENITIS SUPPURATIVA Lesions: tender open & double comedones, red nodules/abscesses, sinus tracts, “bridge” scars, hypertrophic & keloidal scars, contractures Pathogenesis: follicle plugging > dilated follicle & apocrine duct > inflammation > bacterial growth > extension of suppuration/tissue destruction > ulceration, fibrosis, sinus tracts > scarring HIDRADENITIS SUPPURATIVA Usual spontaneous remission at >35 y/o Treatment (combination): Intralesional steroids, then I&D abscess Prednisone for severe pain & inflammation Surgery (excision, skin grafting) PO antibiotics (chronic low-grade disease) Isotretinoin for early disease adalimumab (Humira) Psychological  INSTRUCTIONAL OBJECTIVES Identify and describe the etiology, epidemiology, clinical features, differential diagnosis, and management of selected skin disorders. Identify and accurately describe skin lesions using standard terms: Number: single, multiple Pigmentation/color: white, flesh colored, pink, pearly, erythematous, tan-brown, salmon, black, purple, violaceous, and yellow  INSTRUCTIONAL OBJECTIVES Identify and accurately describe skin lesions using standard terms: (Continued) Shape and arrangement: annular, round/discoid, linear, oval, iris/target, zosteriform, serpiginous, stellate, polycyclic, reticulate, and morbilliform Texture: consistency, mobility, temperature, tenderness, depth Borders/margins: well-defined, ill-defined  INSTRUCTIONAL OBJECTIVES Identify and accurately describe skin lesions using standard terms: (Continued) Type: Primary lesions (including macule, tumor, patch, wheal, papule, vesicle, plaque, bulla, nodule, pustule, cyst, and telangiectasia) or secondary lesions (crust, fissure, scale, ulcer, lichenified, keloid, erosion, hypertrophic scar, atrophy, and excoriation) Arrangement/location/distribution: localized, regional, and generalized Associated changes  DESCRIBING SKIN LESIONS Systematic approach/format: 1. Color 2. Location/distribution (extent, pattern) 3. Arrangement (grouped vs disseminated & confluence (yes or no) 4. Margination (well- or ill-defined) 5. Palpation (consistency, temperature, mobility, tenderness, depth) 6. Shape 7. Type (ie, papule, macule, pustule) 8. Single vs multiple (# of lesions) QUESTIONS?