Dermatology

(<0.5cm)
GENERAL DIAGNOSIS & SYMPTOMATOLOGY E.g., acne, impetigo, furuncles
Encapsulated fluid-filled or a
STEPS FOR A DEFINITIVE DIAGNOSIS Cyst semisolid mass in the SC tissue
• Physical examination (The Skin Exam) or dermis
• Complete history and review of systems SECONDARY LESIONS
• Laboratory tests Loss of epidermis, does not
extend into dermis
• Histopathological analysis Erosion
E.g., ruptured chickenpox vesicle
OUTLINE OF PE AND HISTORY
Loss of skin through epidermis
STEPS OF SKIN EXAM and healing results in scar
Ulcer formation
• Note: In examination, patients with highly focused complaint E.g., stasis ulcer
such as a single wart or acne may not require a comprehensive
skin examination A split in all epidermal layers of
Fissure skin
Table 1. Steps of the Skin Exam
STEP DESCRIPTION E.g., athlete’s foot
Preparation Room with adequate lighting (bright, white, sunlight)
Examination Entire skin surface and mucous membranes Diminution of epidermal surface
with skin looking thinner and
Palpation Determine if lesion is flat or elevated
more translucent than normal
Texture Texture and presence of scale by use of magnifying glass Atrophy
May result in wasting or
Size Solitary lesions, record size in chart
depression of skin surface
Press with glass slide to differentiate between blanching
Diascopy E.g., arterial insufficiency
erythema and non-blanching purpura
Loss of outer skin layers from
SKIN SIGNS Excoriation
scratching or rubbing
TYPE OF LESIONS E.g., scratched insect bite
Table 2. Type of Lesions Collection of serous exudate and
TYPE DESCRIPTION ILLUSTRATION debris on the surface of damaged
PRIMARY LESIONS Crust or absent outer skin layers

Localized color changes with E.g., impetigo

Macule <1cm in diameter Compact portion of
E.g., freckle desquamating stratum corneum
Localized color changes with Scale (size, thickness, consistency)
>1cm in diameter E.g., psoriasis scale, pityriasis
Patch rosea scale
E.g., vitiligo, stage 1 of pressure
ulcer
Solid elevation or depression with Epidermal thickening &
<1cm in diameter Lichenification roughening of skin with increased
Papule visibility of skin surface furrows
E.g., warts, elevated nevi,
seborrheic keratosis
Collection of fibrous tissue that
Solid elevation or depression with forms to replace lost epidermal &
>1cm in diameter dermal tissue
Plaque Scar
E.g., psoriasis, eczema, pityriasis E.g., surgical scar, acne scar
rosea Keloid: augmentation of scar
Palpable lesion >1cm tissue
Extend deeper into dermis or SC
Nodule tissue COLOR
E.g., lipoma, erythema nodosum, Table 3. Color
melanoma, hemangioma COLOR DESCRIPTION ILLUSTRATION
Caused by vascular dilatation
Same as nodule >2cm
Tumor
Rosacea: erythematous papules
E.g., carcinoma on cheeks, nose, forehead with
Localized edema in epidermis sparing of periorbital & perioral
causing red/pale irregular skin (no comedones)
Wheal elevation Erythema
E.g., insect bite, hive,
angioedema
Fluid-filled elevated mass (<1cm) Exfoliative dermatitis (exfoliative
Vesicle E.g., herpes simplex, herpes erythroderma) – generalized
zoster, chickenpox, scabies
Same as vesicle (>1cm)
E.g., contact dermatitis, large 2nd
Bullae
degree burns, bullous impetigo,
pemphigus
Pustule Pus-filled vesicle or bullae
Dermatology
SLE – malar rash;
dermatomyositis – heliotrope rash

Violaceous, purplish, reddish-

brown lesions caused by
extravasated RBCs
Usually seen in cases of vasculitis
Purpura and lesions do not blanch with
diascopy
Pigmented purpuric dermatosis –
reddish-brown clusters of pinpoint
hemorrhages

Ephelids (freckles): ↑melanin in

basal layer and come & go with
the weather (sunny)

Lentigo: ↑melanin in basal layer

with ↑melanocytes; permanent MARGINS
Hyper-
pigmentation Melasma: diffuse light or dark
brown hyperpigmentation
Skin biopsy: pigment
incontinence, melanin in basal &
suprabasal keratinocytes, and
melanin in dermis within
melanophages
Common among women who had
been pregnant or taking OCPs
↓pigment production in epidermis
ARRANGEMENT
Hypo- Pityriasis alba & pityriasis
pigmentation versicolor (Malassezia globose,
azelaic acid)
Loss of pigmen characterized by
De- absence of melanocytes in
pigmentation epidermis
Vitiligo

PALPATION
• Consistency, temperature (warm or cool), mobility, tenderness,
depth of lesion (dermal or SC)

DISTRIBUTION
SHAPE
Dermatology
Male pattern baldness (M-shape)
Androgenetic mediated by androgen-sensitive
alopecia follicles in genetically susceptible
males

Gray patch type (Trichophyton &

Microsporum sp) common in pre-
adolescents

Tinea capitis
Large, round, hyperkeratotic scaly
plaque of non-scarring alopecia & (+)
green fluorescence on Wood’s lamp

SCARRING ALOPECIA
Kerion; characterized by boggy,
purulent, inflamed nodules and
Tinea capitis plaques
Posterior CLAD
Chronic cutaneous lupus
erythematosus
Well-demarcated inflammatory
plaques that develop into atrophic
scars
Discoid lupus
erythematosus
SKIN SYMPTOMS Examination of conchal bowls for
• Pruritus: most common cutaneous symptom patulous follicles (ears) – scalp
o Inflammatory dermatoses (atopic dermatitis, lichen involvement
simplex chronicus, lichen planus, nummular eczema)
o Vesicular & bulbous disorders NAIL
o Infestations, malignancy, immune/autoimmune • Nail concerns
disorders o Changes in color, clubbing, ingrown nails, splinter
• Pain hemorrhages
HAIR o Periungual changes (swelling, redness)
• Hair concerns o Nodules, masses
o Texture, oily/dry, amount, color, distribution o Nail deformities (pits, grooves, ridges, splitting)
o Presence of parasite, fungal, bacterial infection, o Absence of nails
scaling, foul odor, hair loss, bald spots Table 6. Nail Concerns
• Alopecia: common clinical complaint NAIL CONCERN DESCRIPTION ILLUSTRATION
Beau’s lines – transverse grooves
Table 4. Alopecia across fingernail moving distally
NONSCARRING SCARRING/CICATRICIAL with nail growth
Alopecia areata/totalis/universalis Tinea captitis From viral infections (e.g., HFM
Onychomadesis
Androgenic alopecia Discoid lupus erythematosus disease) in children
Hair follicle is NOT permanently Conditions that lead to irreversible cessation Single nail (traumatic) vs multiple
damaged of hair cycling & permanent hair loss nails (systemic causes, acute
stress)
Table 5. Types of Alopecia
Bulbous enlargement & broadening
ALOPECIA DESCRIPTION ILLUSTRATION of fingertips
NON-SCARRING ALOPECIA Clubbing Lovibond’s angle > 1800
Inherited (autosomal dominant) vs
Patchy hair loss on discrete scalp acquired (cardiac, pulmonary, GIT)
areas associated with autoimmune
diseases (e.g., thyroid disease,
vitiligo)
Alopecia areata Onychoschizia - lamellar dystrophy
(transverse splitting) vs
Nail splitting
onychorrhexis - brittle nails
Exclamation point hairs (longitudinal ridging)

Total hair loss on the scalp, but NOT Abnormal keratinization of nail
in body hair matrix (psoriasis, atopic dermatitis,
Alopecia totalis
alopecia areata, lichen planus,
Nail pitting
Advanced form of alopecia areata trauma)
Small punctate depressions on nail
Alopecia surface
Total loss of scalp & body hair
universalis
Dermatology
Misshapen or partially destroyed Irritant contact Erythematous, moist, partially
Dystrophic
nail plates (psoriasis, dermatitis eroded patch
nails
onychomycosis, trauma)

Banded brown to black Erythematous scaly patches on

Seborrheic
pigmentation of nail (ethnic nail nose, cheeks, nasolabial folds, &
dermatitis
pigmentation) beard area

Longitudinal
melanonychia Multiple nails (benign, systemic Multiple plaques with silvery
cause) vs single nail (benign or Psoriasis white scales in symmetric
early melanoma) distribution

Hutchinson signD Multiple intensely pruritic

erythematous plaques with
MUCOUS MEMBRANES excoriations on axilla, inguinal &
• Include conjunctivae, nasal cavity, buccal mucosa, genital & Scabies
anogenital areas, inframammary,
perineal areas around umbilicus, on wrist,
interdigitations
• Check for pallor, pigmentation, erythema, swollen gums,
bleeding, petechiae, nodules/masses, erosions, lacerations, Dermatosis Multiple, small, smooth, firm,
ulcerations papulose nigra hyperpigmented papules on face
Table 7. Mucous Membrane Lesions
LESION DESCRIPTION ILLUSTRATION
Oropharyngeal area Multiple, well-defined,
Oral lichen White lacy patches, red swollen Nummular
erythematous, round, oozing
planus tissues, open sores dermatitis
plaques on extremities
May cause burning, pain
Extensive necrosis & detachment of
epidermis
2 or more sites (ocular, oral,
genital): erythema, painful erosions
SJS & TEN of lips & buccal mucosa; matting &
redness of eyes

BSA: SJS (<10%), TEN (>30%)

Life – threatening blistering disorder

characterized by acantholysis
Pemphigus resulting in intraepithelial blisters in
vulgaris MM & skin (oral cavity)
(+) Nikolsky sign

COMMON DERMATOSES
Table 8. Common Dermatoses
CONDITION DESCRIPTION ILLUSTRATION

Multiple open & closed

Acne vulgaris comedones, erythematous
pustules

Multiple erythematous scaly

Dermatophytosis plaques with advancing borders
& central clearing (pruritic)

Bacterial Firm, tender nodule with a central

infections pustule

Verruca (warts) Multiple verrucous papules

Dermatology
sodas – sunkist pineapple, mountain dew, fanta orange,
ACNE Gatorade
• Time of flare (1 month), sudden
PATHOGENESIS • Modifying factors: drug history (oral & topical), medical
history
• Monomorphous papules, no comedones usually on trunk,
shoulder, upper arms
Acneiform
eruption or
steroid acne

• Time of flare (2 months), control then flare

• Modifying factors: drug history (antibiotic intake for 2
months without relief)

Gram-negative
folliculitis

Sudden with Systemic Symptoms

• Sudden explosive onset, teenage boys
• Mild acne & sudden explosive eruption with bleeding
• Modifying factors: systemic symptoms, isotretinoin &
testosterone before
ACNE HISTORY • Most severe form, rare, painful, ulcerative form
• Systemic symptoms (fever, leukocytosis, bone pain,
Table 1. History polyarthralgia, anemia)
INFORMATION DESCRIPTION Acne fulminans • Tx: systemic & topical steroids as first line, low dose
AGE OF ONSET isotretinoin
• Ages 8-12 years old (females: menarche – 1st sign of puberty)
• Peaks at 15-18 years old, resolves by 25 years old
• Atypical acne: pediatric agne
Onset at birth to 6 weeks (visible by 2 weeks of age) and
Neonatal acne resolves within 3 months
Absent comedone (transient ↑sebum excretion rate) OCCUPATIONAL HISTORY
Onset between 6 weeks – 1 year and resolves at 1-2 years
• Gradual & localized on the back, comedones mostly in
Infantile acne True comedone (transient ↑DHEA), Tx: low-dose benzoyl covered areas with intimate contact to clothing saturated
peroxide (2.5%) with offending compound (e.g., coal tar, cutting oils)
ADULT ACNE IN FEMALES
1st outbreak at 20-35 years old, acne lesions (perioral & along
Adult acne in jawline) Occupational
females Ask about menstrual history & premenstrual flare, history of acne
amenorrhea, irregular menstrual cycles, miscarriages
Puberty – triggers sebum production & sebaceous growth
differentiation
Role of Excess production: androgens, GH, IGF-1, insulin, CRH,
hormones glucocorticoids • Within a year, gradual
Endocrine disorders: Cushing syndrome, CAH, androgen- • Modifying factors: drug history (dioxin poisoning)
secreting tumors (ovarian), acromegaly • Comedones and cysts, grayish discoloration of skin
DHEA: 4000-8000 ng/mL – CAH, >8000 ng/mL – adrenal tumor
Serum total testosterone: >150 ng/dL – ovarian source of excess
Hormonal acne Chloracne
androgens, 150-200 ng/dL – PCOS, greater – ovarian tumor
Increased LH:FSH ratio: >2.0 – PCOS
Oligo- and/or anovulation (oligomenorrhea/amenorrhea,
infertility/1st trimester miscarriage)
PCOS Clinical and/or biochemical signs of hyperandrogenism (obesity,
hirsutism, acne, acanthosis nigricans, male-pattern alopecia) IMPORTANCE OF FAMILY HISTORY
Polycystic ovaries • Post-adolescent acne: 1st degree relative (50%)
Acne genetics/
ONSET: GRADUAL OR SUDDEN • Chromosomal abnormalities, HLA phenotypes,
genetic
• Typically gradual (sudden - ~1 month, without systemic symptoms) – ask for polymorphism of human CYP450 1A1 & MUC1 gene
predisposition
drug history (drug-induced or steroid acne) • Mother’s acne history – most important prognostic factor
• Sudden with systemic symptoms – rule out acne fulminans
Sudden without Systemic Symptoms PHYSICAL EXAMINATION
• List of drugs (medications, vitamins, supplements)
Table 2. Physical Examination
Drug-induced • Testosterone, progesterone, steroids, lithium, phenytoin, PART DESCRIPTION
acne isoniazid, vitamin B-complex (B2, B6, B12)
Acne conglobata • Check for nodules & cysts, conglobate (rounded mass
• Halogens, bromides, iodides (brominated vegetable oil in
Dermatology
or ball) usually in teenage males Table 4. Acne Medications
• Discharge: foul-smelling serous, purulent, or mucoid MEDICATION DESCRIPTION (MOA)
• Keloids & atrophic scars BPO BPO → benzoic acid + O2; bactericidal, anti-inflammatory
• Tx: isotretinoin, antibiotics, intralesional steroids Topical antibiotics Topical clindamycin/erythromycin (~BPO)
Tretinoin, adapalene, tazarotene; keratolytic, anti-
Topical retinoids
inflammatory
Anti-androgenic oral Cytoproterone aceteate, OCP, spironolactone (X sebum
medications production)
• Check for telangiectasias (no comedones) Most effective acne medication, potential S/E
• History of flushing (triggers: alcohol, sunlight, hot (teratogenicity, hypertriglyceridemia, hepatotoxicity,
Oral isotretinoin
beverages, spicy food, emotional stress) depression), baseline lab results (lipid profile, liver function
tests)
Oral medications (hormonal meds, anti-androgens, oral
Rosacea
Combination isotretinoin, clindamycin, erythromycin, cyclines, steroids),
treatment topical keratolytics (topical retinoids, salicylic acid, AHA),
topical bactericidal (antibiotics, BPO cream)
Table 5. Treatment for Three Broad Categories of Acne
CATEGORY TREATMENT
• Extensive neurotic excoriations leaving crusted Comedonal/mild Topical treatment (tretinoin alone OR BPO
erosions that scar, usually in young women inflammatory acne [morning] + tretinoin [evening])
• Underlying obsession, OC personality, Moderate papulopustular Topical + oral Tx (BPO [morning] + tretinoin
Acne excoriee anxiety/personality disorder acne [evening] + doxycycline 100 mg OD)
Oral +/- topical Tx: oral isotretinoin/hormonal Tx
Severe
(women) + topical OR oral isotretinoin/hormonal
papulopustular/nodular acne
Tx (women) alone
• Papules, pustules with scaling (~acne vulgaris, no PATIENT EDUCATION
comedones)
• Setting expectations
• Localized around mouth, nose, eyes
Periorificial • History of prior or current/chronic use of topical steroids • Lack of adherence
dermatitis o Most common cause of Tx failure
o Topical agents (2-3 months) to see effect
o Therapy should be continued at least 8 weeks before
Tx response can be accurately evaluated
• Sports- or mask-induced acne (occluded by protective
gear)
• Heat, pressure, occlusion, repetitive friction, rubbing
Acne mechanica

• Dilated follicle that contains numerous vellus hairs and

keratin debris

Trichostasis
spinulosa

BASIC PRINCIPLES OF MANAGEMENT

Table 3. Basic Principles of Management
ACTION THERAPY
Hormonal treatment (OCPs, anti-
Decrease/inhibit sebum production
androgens, oral isotretinoin)
Normalize follicular hyperkeratinization Retinoids, salicylic acid/BHA, AHA
Reduce C. acnes proliferation Antibiotics, BPO, isotretinoin
Treat inflammation Antibiotics, retinoids, steroids, BPO
Dermatology
BENIGN & MALIGNANT SKIN LESIONS
Illustration
MELANOCYTIC TUMORS
Table 1. Benign vs Malignant Melanocytic Tumors
BENIGN MALIGNANT Histology
Common acquired
Other name/s Melanoma
melanocytic nevi
Benign tumors of nevus cells Onset: in general, after puberty (all
(moles, 2-6mm) on palms, ages, 30-70 y.o.) NON-MELANOCYTIC TUMORS
soles, nailbeds (Africans > Prevalence: Whites >> Africans,
Whites) Asians Table 4. Benign Non-Melanocytic Tumors
Women: lower extremities & trunk, CONDITION DESCRIPTION ILLUSTRATION
men: trunk (back TUMORS & CYSTS OF EPIDERMIS
Fitzpatrick’s MMRISK: moles (atypical, Cutaneous Cysts
Clinical
>5), moles (numerous, >50, >5mm), • Epidermal/infundibular cyst
features
red hair & freckling, inability to tan, • Most common
Number: Whites > Africans,
sunburn, kindred • Origin: infundibular (hair
Asians
Six signs of malignant melanoma follicle), implantation of
(ABCDE): asymmetry, irregular border, epidermis into dermis
mottled color, large diameter, ugly • Clinical features: solitary/
duckling sign – different, elevation, multiple, skin-
enlargement, evolution Epidermal
colored/yellow/white, slowly
Superficial spreading melanoma inclusion cyst
growing, round, firm, movable
Junctional, dermal, and (SSM), nodular melanoma (NM), (EIC)
Classification (1-5cm) cysts, (+) surface
compound nevi lentigo maligna melanoma (LMM), punctum in center
acral lentiginous melanoma (ALM) • Found in face, neck, torso
Table 2. Clinical Features of Benign Melanocytic Tumors (palms, soles)
JUNCTIONAL COMPOUND DERMAL • Capsule (sometimes with
Childhood, early Childhood, Adulthood (2nd or 3rd odorous, cheesy, whitish,
Onset keratinous exudate)
adolescence adolescence decade)
Type of lesion Macule Papule/nodule Papule/nodule • Any age even in infants
Size 2-6mm 2-6mm 2-6mm (nose)
Uniform tan, dark Light brown, dark Skin-colored, tan, or • Miniature epithelial cysts
Color • Superficial, w/o capsule
brown brown, black with flecks of brown
Round, dome- • Origin: infundibulum (hair
Round, slightly follicle, 10 milium), epithelial
shaped,
Shape Round or oval elevated, dome- Milium structures (eccrine ducts, 20
pedunculated/poly-
shaped or polyploid milium)
ploid
Regular, well- • Clinical features: small,
Border Regular, well-defined Regular, well-defined multiple, white, globoid, firm
defined
Smooth, Smooth, 1-2mm papules
Slight accentuation cobblestone-like, papillomatous, • Found in eyelids, cheeks,
Surface forehead
of skin markings papillomatous, may verrucous, may have
have hairs hairs • Middle age, females
• Trichilemmal cyst, isthmus-
catagen cyst
Illustration • Origin: isthmus of anagen
hairs, sac surrounding
catagen & telogen hairs
Pilar cyst • Clinical features: solitary/
Histology multiple (familial, autosomal
dominant), smooth, mobile,
firm, dome-shaped, 0.5-5cm
Table 3. Clinical Features of Four Major Types of Malignant Melanoma nodules/tumors, no surface
SSM NM LMM ALM punctum, easily nucleated
Race White > Blacks Blacks > Whites • Predilection for scalp
Elderly median: • Origin: sebaceous/oil cyst
Age 30-50 Median: 50 Median: 65
65 • Clinical features:
Sex Slightly F > M M=F 3M:1F steatocystoma simplex
Frequency 70% 15% 5% 5-10% (solitary, non-inherited),
Size 8-12mm 1-3cm 3-20cm 3-12cm steatocystoma multiplex
Lesion Large macule Macular or (multiple, autosomal
Plaque Nodule Steatocystomas
type or patch slightly raised dominant), yellowish to skin-
Uniformly dark colored, round, moderately
Color Mottled blue, black, Mottled firm <3mm-3cm papules/cyst
amelanotic • Predilection for chest, also
Palm, sole, toe, found in axillae, groin, trunk,
Site M: back, F: leg Face, forearms extremities
finger, subungual
Periungual Benign Hyperplastic Disorders of Epidermis
Can look like a Sun-damaged • Senile warts
Other pigmentation
pigmented skin (solar • Middle-aged (>30 y/o) & older
features (Hutchinson’s
BCC elastosis)
sign) Seborrheic • Most common epidermal
keratosis tumor of middle-aged & older
adults
• Clinical features: multiple >
single, flesh-colored/gray-
Dermatology
brown/black papules (≤1cm) chest, back, shoulder
with stuck on appearance, VASCULAR TUMOR
sharply demarcated • Juvenile capillary
• Found in head, neck, trunk hemangioma, strawberry
• Tx: cauterization nevus
• Younger-aged (<30 y/o) • Within 1st month or 1st year of
(since birth/infancy) life
• Forms: localized (nevus • Most common vascular tumor
verrucosus) – plaque or of infancy
linear, systematized (nevus • Natural history: proliferating
unius lateris, ichthyosis phase (1st 8-12 months),
hystrix) involuting (over 1-5 years)
Epidermal nevi • Multiple confluent sebaceous • Clinical features: 3F:1M,
glands Caucasians > other racial
• Clinical features: single > groups, solitary/multiple, pink
multiple, brown > gray/ black/ Capillary macules → red to purple
flesh-colored warty hemangioma nodules
papules/plaques • Found in head & neck, trunk
• Found in head, neck, trunk, • Occasionally life-threatening
extremities cases: impingement on vital
SEBACEOUS TUMOR structures (airway),
• Most common benign Kasabach-Merritt
proliferative abnormality of phenomenon
sebaceous glands (thrombocytopenic
• Multiple, giant confluent coagulopathy), shunting of
sebaceous glands blood & high-output cardiac
• Clinical features: older > failure
Sebaceous younger, multiple > solitary, • Tx: regress on its own,
hyperplasia doughnut appearance usually no need for
(yellowish/whitish/tan, intervention
umbilicated with essential Table 5. Malignant Non-Melanocytic Tumors
crater), 2-3mm papules CONDITION DESCRIPTION ILLUSTRATION
• Found in face (forehead, BASAL CELL CARCINOMA (BCC)
cheeks)
• Most common skin
• Tx: cauterization or laser malignancy, M > F
PILAR TUMOR • >40 y/o (60 y/o), white-
• Children & adults skinned individuals
• Origin: poorly differentiated • Predisposing factors: sun
hamartomas of hair germs exposure, white skin,
• Clinical features: solitary > cumulative UVR exposure,
multiple (familial, autosomal ionizing radiation, arsenic
dominant), skin-colored/ ingestion,
whitish/clear, slowly growing, immunosuppression,
Trichoepithelioma
round, firm (<1cm, 2-8mm) preexisting
papules/nodules, no central inflammatory/degenerative
umbilication processes, genodermatoses
• Found in head & neck, • Etiology: cumulative UVR
especially face (nasolabial exposure (UVB>UVA), PTCH
folds > nose, forehead, upper gene mutation (Hedgehog
lip) signaling pathway)
ECCRINE TUMORS • Tx: Mohs micrographic
• Puberty (M > F) surgery
• Hereditary & recurring,
tadpole-like structures
• Origin: adenoma of
intraepidermal eccrine duct
Syringoma • Clinical features: multiple >
solitary, small, flesh-colored/
whitish/yellowish, soft, 1-2mm
papules
• Found in lower eyelids, upper
cheeks, genitalia, thighs
TUMORS OF FIBROUS TISSUE OF THE SKIN
• Most common in children &
young adults
• Red, raised, shiny, smooth,
firm plaques
• Thickened scar line that does
NOT extend beyond original
Hypertrophic scar
site of injury
• Raised plaque
SQUAMOUS CELL CARCINOMA
• Blacks > Whites
• Variants: glabrous skin,
• Unsightly & symptomatic anogenital areas
(pruritic/painful, tenderness) (erythroplasia of Queyrat)
Keloid scar that extends beyond original Bowen’s disease
• Clinical features: sun-
site with claw-like extensions (SCC in situ)
exposed skin (face, legs) of
(pseudopods)
fair-skinned older individuals
• Found in head, neck, upper → UVR exposure,
Dermatology
unexposed skin (arsenic
ingestion), solitary, slowly
enlarging, well-defined,
erythematous scaly patch/
plaque, few mm-few cm
• D/Dx: eczema (Bowen’s
disease is NOT pruritic & also
persistently present)
• 2nd most common skin
malignancy
• More common in males
• 55 y/o, 20s-30s, middle-aged
to elderly
• White-skinned individuals
• Risk factors: increased age,
light skin pigmentation,
genetic disorders,
immunosuppression, smoking
& tobacco chewing
• Etiology: cumulative UVR
exposure (UVB > UVA),
ionizing radiation exposure,
oncogenic HPV infection (16,
18, 31), arsenic ingestion,
coal tar & various HC
exposure,
immunosuppression,
preexisting dermatoses, sites
of chronic injury or irritation
• Clinical features: malignancy
of keratinous skin cells, flat
Invasive SCC mass (patch) or large tumor,
isolated single > multiple
lesions, M > F, flesh-colored,
large, red to brown papule,
plaque, nodule, overlying
scale & crusting, shallow
ulcer with crust & raised
indurated border, raised,
fungoid, verrucous, (-)
ulceration
• Found in head, neck, &
dorsum of hands; scalp, ears,
vermillion part of lower lip (M)
• Highly (firm, hard) vs poorly
(fleshy/granulomatous, soft)
differentiated
Dermatology
LEPROSY