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D

Dermatology
Venetia Lo, Farheen MU58alli and Nancy Xi, chapter editors Christophel' Kitamura and Michelle Lam, associate editors Janine Hutson, EBM editor Dr. Perla Lansang, staff editor
Introduction to Skin . . . . . . . . . . . . . . . . . . . . . 2 Skin Anatomy Skin Function Definitions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Primary Morphological Lesions Secondary Morphological Lesions Other Morphological Lesions Patterns and Distribution Differential Diagnoses of Common Presentations . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Common Skin Lesions ................... 6 Cysts Fibrous Lesions Hyperkeratotic Lesions Keloids Pigmented Lesions Vascular Lesions Acneiform Eruptions .................... 12 Acne Vulgaris/Common Acne Perioral Dermatitis Rosacea Dermatitis (Eczema) .................... 14 Asteatotic Dermatitis Atopic Dermatitis Contact Dermatitis Dyshidrotic Dermatitis Nummular Dermatitis Seborrheic Dermatitis Stasis Dermatitis Lichen Simplex Chronicus Papulosquamous Diseases ............... 18 Lichen Planus Pityriasis Rosea Psoriasis Vesiculobullous Diseases ................ 20 Bullous Pemphigoid Dermatitis Herpetiformis Pemphigus Vulgaris Porphyria Cutanea Tarda Drug Eruptions ........................ 22 Drug Hypersensitivity Syndrome Erythema Multiforme (EM) Stevens-Johnson Syndrome (SJS) Toxic Epidermal Necrolysis (TEN) Exanthematous Eruptions Fixed Drug Eruption Photosensitivity Eruptions Serum Sickness-Like Reaction Heritable Disorders . . . . . . . . . . . . . . . . . . . . . 24 Ichthyosis Vulgaris Neurofibromatosis Vitiligo Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 Bacterial Infections Dermatophytoses Parasitic Infections Viral Infections Yeast Infections Sexually Transmitted Infections Pre-Malignant Skin Conditions ........... 33 Leukoplakia Malignant Skin Tumours ................ 33 Basal Cell Carcinoma (BCC) Cutaneous T-cell Lymphoma Malignant Melanoma (MM) Squamous Cell Carcinoma (SCC) Alopecia (Hair Loss) .................... 36 Hair Growth Non-Scarring (Non-Cicatricial) Alopecia Scarring (Cicatricial) Alopecia Nails and Disorden of the Nail Apparatus .. 38 Nail Plate Changes Surface Changes Colour Changes Nail Fold Changes Skin Manifestations of Systemic Disease ... 39 Autoimmune Disorders Endocrine Disorders HIV-related Malignancy Others Pediatric Exanthems .................... 40 Miscellaneous Lesions .................. 41 Angioedema and Urticaria Erythema Nodosum Pruritus Wounds and Ulcers Common Medications ................... 43 Sunscreens and Preventative Therapy Topical Steroids Dermatologic Therapies References . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

Toronto Notes 2011

Dermatology Dl

D2 Dermatology

Introduction to Skin

1'oroDio

2011

Introduction to Skin
Skin Anatomy
A

-------------------------------

l.tyen of till Epl-.15 "WomW.. Lte6etli'lg lkrl lulll$"

F"IJira 1. Crass..S.ctian Df the VariaiiS Lly.s Df Skin. Epidarmallll'(llr is datailad in A Skin

divided anatomically into epidermis, dermis, and subcutaneoWJ ti!lsue


epidermiJ

dermiJI - comprised of ronnective tissue divided into two regions:

avascular: receives .its nutrition from the dermal capillariea derived from keratinocytes with the youngest presenting at the 'base' (see layers Figure IA) cells progress from stratum basale to stratum corneum in about four weeks sttatum basale (germlnativum): mitotic figures that give rise to keratinocytes stratum spinosum (prickle cells): junctions in this layer (tonofilament5) give the epidermis i1B strength stratum granulosum: flat cells containing basophlll.c granules which characterize skin stratum lucidum: comprised of transparent layers ofpacked dead cells sttatum corneum: fiat scales of the reaistant protdn keratin other epidermal cells include melanocytes, Langerbans cells, and whl.te blood cells

paplllary: contains numerous caplllarles that supply nubients to the dermis and epidermis reticular: provides a strong structure for skin; consists of collagen bundles woven together along with elastic fibres, fibroblasts, and maaophages
subcutaneous tissue (subdermal) consists primarily ofadipose cells

Skin Appendag81

epidermal in origin; can enend into the dermls include hair, nails, and ClltaneoWI glands

Cutaneous Glands gland- part of pilosebaceoua unit, produces sebum which is secreted into the hair

follicle via the sebaceoWI duct, where It covers the skin surface (protective function) sebum has some antifungal properties found over entire skin surface except palms and soles apoalne sweat gland - apocrine duct empties into hair follicle above sebaceous gland
found in axillae and perineum main function is to produce scent (Le. pheromones) ea:rine sweat gland - not part ofpilosebaceous unit found over entire skin surface except lips, nail beds and glans penis important In temperature regulation via secretl.on of sweat to cool skin surtace

Skin Function
protection due to continuoWI recycling and avascularity of epidermis barrier to: UV radiation, nlechanicallchemi.Cal inSults, pathogens and dehydruion thermal regulation insulation tD maintain body temperature in cool environments, via hair and subcutaneous adipose tissue dissipation of heat in warm environments, via increased activity ofsweat glands and increased blood flow within dermal vascular networks sensation largest sensory organ of the body, with touch, pain, and temperature sensation metabollc function vitamin D synthesis energy storage (mainly in the form of triglyceride&)

Toronto Notes 2011

DefinitiODB

Dermatology D3

Definitions
Primary Morphological Lesions
Definition
an initial lesion that has not been altered by trauma or manipulation and has not regressed macule: flat lesion <1 em patch: flat lesion em papule: elevated, palpable lesion <1 em plaque: elevated, palpable lesion 1 em nodule: deep, palpable lesion <1 em, often dermal or subcutaneous in origin tumour: deep, palpable lesion 1 em vellicle: fluid-filled lesion <1 em bulla: fluid-filled lesion em cyst: a nodule containing semi-solid or fluid material pustule: an elevated lesion containing purulent fluid (white, grey, yellow, green) erosion: a disruption of the skin involving the epidermis alone, heals without scarring ulcer: a disruption ofthe skin that extends into the dermis or deeper; heals with scarring
't'

Descrlle LIISion wllb SCALDA


Size and lurfllce area

Colour (e.g. hyp81Pi!rment8d,

hypopigmented, ertthemltousl
Arrangement (e.g. solitary, linear,

retil:ullted. grouped, herpetiform) Lecion morphology (188 Table 1) Distribution (e.g. dermatomal,
intertriginous, synvnatricaV

asymmllriclll, follicular) Always check hair, 11111ils, mucous membranes llld iltertriginous areas

.....

',
1:111111' "

Sldn Photolypn IFIIzpllllckJ

I'IIIIIDIWI

sw ..,.... ..
SPf pniiCiiln)

SUi

Table 1. Types of Lesions

<1em Dillllllllr
Flat lesion Raised Supelficial Lesion
(e.g. freckle)

:1:1 em Diallllllllr

Wllita
D

Alwlys llllnt. nMr


tins

Patch (e.g. vitiligo)

Wllita Wllill

Alwlys lllln1, ltlulln


Siglltb1111, llaw 1111

Papule (e.g. wart) Nodule (e.g. dermatofibroma) Vesicle (e.g. herpes simplex virus (HSV))

Plaque (e.g. psoriasis) Tumour (e.g. lipoma) Bulla (e.g. bullous pemphigoid)

m
IV

Deep Palpable (dermal or subcutaneous)

I'Hbmwn Sligllt b1111, lullr lin


Blown lllraly!MM,U\1111

Bevated Fluid-filled Lesions

v
VI

Secondary Morphological Lesions


Definition

lllrkbmwn NmrU.,dllrtlln or bllck

-------------------

develop during the evolutionary process of skin disease, or created by manipulation, or due to complication of primary lesion (e.g. rubbing, scratching, infection) crust: dried fluid (serum, blood, or purulent exudate) originating from a lesion (e.g. impetigo) scale; excess keratin (e.g. seborrheic dermatitis) lichenification: thickening of the skin and accentuation of normal skin markings (e.g. chronic atopic dermatitis) fisaure: a linear slit-like cleavage of the skin excoriation: a scratch mark :uresis: pathologic dryness of skin (xeroderma), conjunctiva (xerophthalmia), or mucous membranes atrophy: histological decrease in size and number of cells or tissues, resulting in thinning or depression of the skin

Other Morphological Lesions


comedones: collection of sebum and keratin open comedo (blackhead) closed comedo (whitehead) purpura: extravasation ofblood into dermis resulting in hemorrhagic lesions; non-blanchable petechiae: small pinpoint purpura ehymosa: large flat purpura, "bruise" telangiectasia: dilated superficial blood vessels; blanchable scar: replacement fibrosis of dermis and subcutaneous tissue (hypertrophic or atrophic) wheal: a special form of papule or plaque that is blanchable and transient, formed by edema in the dermis (e.g. urticaria)

D4 Dermatology

Definitions/Differential Diagnoaea of Common Presentations

Toronto Notes 2011

Patterns and Distribution


acral: relating to the hands and feet (e.g. hand, foot and mouth disease)
annular lesions: ring shaped (e.g. granuloma annulare) follicular lesions: involving hair follicles (e.g. folliculitis) guttate lesions: lesions following a "drop-like" pattern (e.g. guttate psoriasis) Koebner phenomenon: isomorphic response, appearance of lesions at an injury site (e.g. molluscum, lichen planus, psoriasis, warts) morbilliform: a maculopapular rash resembling measles reticular lesions: lesions following a net-like pattern (e.g. livedo reticularis) satellite lesions: lesions scattered outside of primary lesion (e.g. candida diaper dermatitis) aerpignousleaions: lesions following a snake-like pattern (e.g. cutaneous larva migrans) target (iri&) lesions: concentric ring lesions, like a dartboard (e.g. erythema multiforme) other descriptive terms: discrete, clustered, linear, confluent, dermatitic, indurated

Differential Diagnoses of Common Presentations


l'$ori1S$iS Xarrthelma kerllosis Basal cell carcinoma Squamous call carcinoma Sebonheic kenrtosis Angulw cheilitis Sabonhaic darmlltilis Solar lentigo Melasma Rosacea Acne Venous lake Herpes labialis

;;

II 1i
i-

...

Spider niMis Malanocytic niMIS Dysplastic niMIS Lichen planus l'$orillsis

Candidiasis Tinea inguinllis Psoriasis

Oermatufibroma

'-----l'$orillsis Lichen simplex chronicus-----.../ '-----Malignant melanoma (in women) '-----Ichthyosis

Status dermllilis-----__,
Venous leg u l c e r - - - - - - " f

Figura Z. Common Lesions Basad on Anatomical Distribution

Toronto Notes 2011

Differential Diagnosea of Common Presentations

Dermatology D5

Table 2. Differential Diagnosis of Common Presenting Proble


Lesion Brawn Macule lnfaclious lniiiiiiiiiiDry Drug/Toxin UV radiation, lentigo,

Misc:lll1111aus
Congenital: spats. congenital nevus, epidennaVjunctional news Neoplasia: lentigo maligna, malignant melanoma. pigmented basel cell carcinoma (BCC) Other: melasma/chloasma ("mask of pragnancyj Vascular: hemangioma, pyogenic granuloma Other: dermatofibroma, miaria rubra

Post-inllammatory hyper-piiJTientation

freckle

Diac111fB Red Papule

Folliculitis Furuncle Scabias

Acne vulgaris Lichen planus Rosacee Psoriasis Urticaria


Denna1itis (atopic, corrtact, nunvnular, seborrtJeic) Discoid lupus lichen planus Psoriasis Acute contact dermatitis Dyshidrotic eczema

Bites/stings

Red Scides

Pityriasis rosea Secondary syphlis

Gold

Neoplastic: mycosis fungoides

Tilea

Vasida

Cat-5cratdl disease Impetigo Viral: HSV, mster, varicella, molluscum, coxsackie Scabias Bulousirrigo

Other: dermatits herplllifcrmis, paqilyria cutanee tanla

Bullae

Acute dermatitis Erythema Multifonne (EM) Stsvan-Johnson Syndrome (SJS) Toxic Epidennal Necrosis (ltN) Systemic ILPJS erythematosus (SLE)

Fixed drug eruption

Autoimmune: bullous pemphi!JJS vulgaris Other: harplllifcrmis, poqilyria cutanea tanla

Pullule

C!lldida Dennatophyte Impetigo Sepsis Varicalla Aspergllosis

Acne vulgaris Rosacee Dyshidllllic dermatitis Pustular folliculitis Pustular psoriasis


Allergic stomatitis EMISJS/TEN lichen planus Seronegatives, SLE Recummt aphthous stomatitis Beh!;et's disease

Acute gannlizud 8Xilllhematous (usually secondary to drug reaction)

Other:

5Uppurativa

Oral Ulctr

CMV
Coxsackie Cryptococcosis HSVJllZV Hill, TB, Sypiilis

Chemotherapy Radiation therapy

Autoimmune: pgus vulgaris Congenital: XXV Hematologic: siclde cell disease Neoplasia: BCC, squamous cell carcinoma (SCC)

Skin Uk:

Plague Syphilis

TB

RA, Slf, vasculitis Ulcanrtiva colitis (pyoderma geniJI!Ilosum)

Tularemia

Autoimmune: necrobiosis lipoidica diabaticorum (e.g. OM) Congenital: XXV Hematologic: siclde cell disease Neoplasia: sec Vascular: artarial, neurotropic, prassura, venous. alilthous, leukoplakia, traumatic

D6 Dermatology

Common Skin Lesions

Toronto Notes 2011

Common Skin Lesions


Cysts
T1ble 3. Cysts
Epidennal Cyst [Sebaceous)
Clinicll Pilar Cyst (nichile11mal) Multiple, hlr'd, varying simd nodules under 1he scalp, lacks centnll punctum

Dennoid Cyst
Most commonly found lllllllenll third of eyebrow or midline under nose

Ganglion Cyst Usualy solilary, rubbery, tnJnslucent; a clear gelatinous viscous ftuid may be axtrudad

Milium

Preseltatilll

Round, yellowlllash coloured, slow growing. mobile, firm, fluctuant, nowle or tumour

1-2 mm superficial,

whit& to yellow
subepidermal papules occuring on eyelids, cheeks, forehead Wrthin pilosebaceous follicles Small epidennoid cyst, primarily arising from pluripotential cells in epidermal oradnaxal epithelium Secondary to blistering. ulceration, trauma, topical corticosteroid atrophy, or cosmetic procedures

Plthophpialagy

Epithelial cells displaced into delmis, epidermal lining becomes filled with ksrlllin and lipid-rich debris May be post-tnJLITIIItic

Thick walled cyst lined with stratified squamous epithelium and filed with dense lanlin ldioplllhic Post-tnJuma

Rare, congenital hamartomas, which arise from inclusion of epidermis along embryonal cleft closure lines, craating athick walled cyst filled with dense ksl'lllil

Cystic lesion that originates from joint or tendon sheath, called B mucous cyst when found on fingertip Associllled with osteoarthritis

Epidemialagy

Most common cuta1eous cyst in youth - mid age

znd most common Rare cutllleous cyst F>M


lfnasal midline, risk of axt8nsion intoCNS

Older age

Any age 40-511% of infants


In nevuborns, 1ponbll8ously molvel in first 4weeks of life

Clinical Couna

Central punctum may Rupture causes rupture (foul, cheesy pain and odour, creamy colour) inflammlllion and produce inflammlllory reaction Increase in siza and number aver time. especially in pregnancy Excise complel!ly before it becomes infected Excision

Stable

Mlniglllllll:

Excision

Drainage :!: steroid injection if painful Compression daly for6weeks Excision if bothersome

Incision and expression of contents Laser ablation and Multiple facial miia responds to topical retinoid therapy

Fibrous Lesions
DERMATOFIBROMA Clinical Presentation button-like, firm dermal papule or nodule, skin-coloured to red-brown colouring majority are asymptomatic but may be pruritic and/or tender site: legs > arms > trunk dimple sign: lateral compression causes dimpling of the lesion Pathophysiology benign tumour due to fibroblast proliferation in the dermis Etiology unknown; often associated with history of minor trauma (e.g. shaving or insect bites) Epidemiology adults, F>M Differential Diagnosis dermatofibrosarcoma protruberans, malignant melanoma, Kaposi's sarcoma. blue nevus

Toronto Notes 2011

Common Skin Lesions

Dermatology D7

Investigations biopsy if diagnosis is uncertain Management no treatment required excision or cryosurgeryifbothersome SKIN TAGS Clinical Presentation small (1-1 0 mm), soft, skin-coloured or darker pedunculated papule, often polypoid sites: eyelids, neck. axillae, inframammary, and groin Pathophysiology benign outgrowth of skin Epidemiology middle-aged and elderly, F>M, obese Differential Diagnosis pedunculated seborrheic keratosis, compound or dermal melanocytic nevus, neurofibroma Management excision, electrodessication, cryosurgery
'. I

..

lldn tap are lcnawn ..


Acrochordon Fibroepilhalial polyps Soft fibromllli Pedunculated lipofibromas Clllaneous papillomas

Hyperkeratotic Lesions
SEBORRHEIC KERATOSIS Clinical Presentation well-demarcated waxy papule/plaque with classic "stuck onD appearance large variety in colour, size and shape over time lesions appear more warty, greasy and pigmented sites: face, trunk, upper extremities (may occur at any site except palms or soles) Pathophysiology very common benign epithelial tumour Epidemiology unusual <30 years old autosomal dominant inheritance Differential Diagnosis malignant melanoma (lentigo maligna, nodular melanoma), melanocytic nevi, pigmented basal cell carcinoma, solar lentigo, spreading pigmented actinic keratosis Investigations biopsy only if diagnosis uncertain Management none required, for cosmetics only liquid nitrogen, curettage ACTINIC KERATOSIS (SOLAR KERATOSIS) Clinical Presentation ill-defined, scaly erythematous papules or plaques on a background of sun damaged skin (solar heliosis) sandpaper-like, gritty sensation felt on palpation sites: areas of sun exposure (face, ears, scalp ifbald, neck, sun exposed limbs) Pathophysiology UV radiation damage to keratinocytes from repeated sun exposure (especially UVB) can develop into squamous cell carcinoma (1-10%)

D8 Dermatology

Common Skin Lesions

Toronto Notes 2011

.....

, ...-----------------,

Epidemiology
common with increasing age, outdoor occupation, M>F skin phototypes I-III (see sidebar, D3), rare in darker skin as melanin is protective

TYPIM of Actinic ICerato- lAICal Erythemato - typical AK leaion Hypartruphic- thickllr, rough papultl pi aqua Clllllneous horn- finn hyparbmotic outgrowth Actinic chaillil - confluant AKa on the lip Pigmented - flat. ten-brown, scaly plaque Spreallng pigmtntlld ProliflndiVI
CanjunctiVIII- pinguecula, pturyuium

Differential Diagnosis
SCC in situ. superficial BCC, seborrheic keratosis, cutaneous lupus erythematosus

Investigations
biopsy lesions that are refractory to treatment

Management
destructive: liquid nitrogen, electrodessication and curettage pharmacotherapy: Efudex (5-fluorouracil) cream for 2-3 weeks, Aldara (imiquimod) cream for 8-10 weeks

KERATOACANTHOMA Clinical Presentation


rapid growing, firm, dome-shaped, erythematous or skin-coloured nodule with central keratin-filled crater, resembling an erupting volcano often spontaneously regresses within a year, leaving a scar sites: sun-exposed skin

Pathophysiology
epithelial neoplasm with atypical keratinocytes in epidermis considered a low grade variant of sec

Etiology
HPV, UV radiation, chemical carcinogens (tar, mineral oil)

Epidemiology
>50 years, rare <20 years

Differential Diagnosis
treat as SCC until proven otherwise, hypertrophic solar keratosis, verruca vulgaris

Management
surgical excision

CORNS

.....

.. ,
black speckled central appearance dua to ttnmbosed capillarias. Planter warts destroy dennatoglyphics (apidamnal ridges).

Clinical Presentation firm papule with a central, translucent, cone-shaped, hard keratin core
painful with direct pressure sites: most commonly on dorsolateral fifth toe and dorsal aspects of other toes

Cams VI. W.rts VI. Cilia Cams h11V8 a whitish yellow centrll translucent kllratinous core. Painful with direct pressure. Warts blaed with paring and have a

Pathophysiology
localized hyperkeratosis induced by pressure on hands and feet

Epidemiology
F>M, can be caused by wearing high-heeled shoes with a tapered toe

Differential Diagnosis
tinea pedis, plantar warts

Callouses have layers at yellowish kntin FWMiad with parilg. Thare

are no thrombosed capillaries or interruption of apidannal ridges.

Management
relieve pressure with padding or alternate footwear paring, curettage

Toronto Notes 2011

Common Skin Lesions

Dermatology D9

Keloids
Clinical Presentation

firm, shiny, skin-coloured or red-bluish papules/nodules that most often arise from Qltaneous injury (e.g. piercing, surgical scar, acne), but may appear spontaneously extends beyond the margins of the original injury, and may continue to expand in size for years with claw-like extensions can be pruritic and painful sites: earlobes, shoulders, sternum, scapular area
Pathophysiology excessive proliferation of randomly organized collagen fibers following trauma to skin differentiated from a hypertrophic scar which is confined to the borders of the original injury Epidemiology predilection for darker skin M=F, all age groups Management intralesional corticosteroid injections cryotherapy silicone compression

.... .----------------.
Klleldl VI. HypM'II'Opblc Scan Keloln: extend bevond marvins of original injury ike

'.. '

ext111sions
0

ltypartropllic HUI: Confined to

original margins of injury

Pigmented Lesions
Tabla 4. Comparison of Pigmented Lesions

Ephllidel(fnlckll
Clinical l'mentldian Smaii(<Smm)walldemai'CIIIed light brown macules Sites: suiHIXj)Osed skin

Salu LBntiga
(Uv.Spatl

MDngallnSpat

Becbr's Nevus
Hairy, light brown macule/ patch with a papular verruCilus surface Silas: trunk and shouldars Pigmented hamartoma with incraased melanin in basal cells

....

''
stain I
coagulants, staroids, hemosiderin

Wall demarcal8d brown' CongenitaiiJliY-blue black irregular macules macule ccmnonly on Sites: sun.exposed skin lumbosacral area

DDxaf lfn*piFI...... rMIW. PurpUIII (1.g. solar, NOA. anti-

Post-inftamrnatory
Meluma

Increased melanin wilhin Benign melanocytic Ectopic melncytes basallllya" kllratinacytas proliferation in diiTIIillin dermis second!ly to sun epidennal junction due to exposure chronic sun exposure Skin phatotypes I and II

Melanom Find drug 11111ption

Most Cllmmon in Caucasians >40 yea'S Skin phatcrtype

99% occurs in Asian and Aboriginal ilfa1ts

M>F

Often beCilmBS noticeable at puberty


Hairy Cllngsnital melanacytic nevus Hair growth follows onset of pigmentation Cosmalic management (usually too large to remove)

Diagnosis

Junctional nevi Juvenie lentigines

sebonheic keratosis,
solar keratosis

Lsntigo maligna.

Ecc:hyma&i&

Clinical Course andMMBgamant

Laser therapy, shave No treatment required Multiply and dlrtl!n with excisions, ayatherapy sun exposure, fade in

Usually fades in early childhood but may persist into adullthoad

wilter
Sunscreens may prevent the appearance

of new freckles

SEBORRHEIC KERATOSIS (see Hyperkeratotic Lesions section, D7) NEVOMELANOCYTIC NEVI (NMN) (see Table 5) common mole be suspicious of new pigmented lesions in individuals >40 years average number of moles per person: 18-40 3 stages of evolution: junctional NMN: macular; arise at dermal-epidermal junction compound NMN: papular; nevus cells invade the papillary dermis dermal NMN: skin coloured papules (no longer hyperpigmented); nevus cells completely migrate into dermis

DIO Denoatology

Common Skin Lesions


Table 5. Nevomelanocytic Nevi Classification
Type CanQIRillll

Toronto Notes 2011

Alii of Onset
Birth

Clinicll Plwstnbdi111

Hislalagy

MIRIIIIIJient

NMN

Newmel111ocytes in Surgical excision huspiciaus, Sharply demarcated pi!Jnented brown with rep.-/irregular epidermis (dusters) and due ID increased risk of contours coarse han dermis (strands) melanoma Rule aut leptomeningeal involvement an heacVneck Bani!JI neoplasm of pigmentforming news cell Well circumscribed, round, uniformly pigmented maculesf papulas <1.5 em Classified according to of news cells Melanocytes Ill: epidermal junction abova basement membrane Excisianal biopsy required

Acquired

NMN

Early childhood ID age 40 Involute by age60

if an scalp, sales, mucous


membranes, anogenital na, or varied colaurs, borders, bleeding, exposed ID trlluma Same as above

JunctiaMI

NMN

Flat, bordered, uniformy Childhood Majority tan-dark brawn, sharply demarclll:ed progress to smooth macule compound news

Campound

NMN

Any age

Domed, regularly bordered, smooth, Melanocytes Ill: roLild, tan-dark brawn papule epidermal junction; Face, trurt. extremities, scalp migration into dermis NOT found an palms or soles Soft, dome-shaped, skin-calouned ID tarv'brown papules or nodules, often with te1111giectasia Sites: face, neck Melanocytas exclusively in dermis

Same as above

DennaiNMN

Adults

Same as abova

Dpplatic

Childhood

Variegated macule/papule
irregular indistinct rnelanocytes in the basel cell layer >6mm Risk factors: positive family history

NMN

and proliferation of melanocytes extending beyond dermal cornpertment of 1he nevus Often with region of adjacent nasts Dermal or Clllq)Ound newcellular news surroLilded by hypomelanosis, lymphocytes, histocytes

Follow qZ-6 months with colour phatograli!s for changes Excisional biopsy if lasion changing or highly atypical

HaloNMN

First 3 dacadas

Brawn ovaVraund papules surrounded by hypamelanosis Same sites as neocellular news Sponteneous involution 111Q18S$ion of centrally loclll:ad pigmented nevus

Nona required Excision if colour variegated or irregular borders Associated with vitiligo, mlll:a&tatic rnelanama

Childhood 111d lkliformly blue to blue-black late adolescence macule/papule with smooth border <6mm

Pigmented melanocytes Remove if sudden onset and mallllophages in or has chlllged dermis

Vascular Lesions
Table &. Vascular Tumoura Compared to Vascular MaHonnationa
V.Cullr TUIIOUII
Dllfiniti111
l're.ICIIII: Birth

Vascullr M111Drmilli1111
Normal endothelial tumovar 1DD% Ill: bi'lh (nat always obvious) 1:1 Proportionate growth (can expand)

Endothelial Usually postnatal 1:3-1:5 Phases:

M:F

Natural History

lnwkrtilg lnwkrted

HEMANGIOMAS Clinical Presentation is a vascular tumour, defines as benign proliferation of vessels in the dermis is red or blue, nodular and blanches with pressure includes: cavernous hemangioma, capillary/infantile hemangioma, spider hemangioma

Toronto Notes 2011 Table 7. Vascular Tumours


H1111111ioma Capillaryjlnflntie

Common Skin Lesions

Dermatology Dll

Spid Algioma
(Campbell tellngiectalial Central rad arlllriole with slender branches, faintly pulsatile, blancheble face, foraa11115, andhends

!spider llrlwberry
IIMII)

Cllany Angioma (Demoi'JIIn lpDI)


Bright rad to deep IIIIII'DDII, domesheped vascular papules, 1-5 mm Sita: tJUnk Less friable compedto pyogenic granulomas Benign vascular naoplasm

Pyogenic QoanuiORII Bright rad, domeshaped sessile or pecllnculated nodule Sites: fingers, lips, mouth, tJUnk. toe& DDx: glomus tumoW", nollllll' malignant melanoma, noclliii'BCC

Clinh:al Prealllbdion

Sllh. compressible, Congenital racilblue bluish. subcutaneous nodules mass that feels Iiiii! a bag of wonns when palpated Site: anywhere (distribution may indicate underlying cranial abnormality)

sec,

....

,,

Plthaphysiolagy Deeply situated Congenital benign IJ'Oiifaration of thick vascular prolifaration walled blood VliSSals of andotheliallining (consumptive thrombocytopenia if hemangioma enlll'ges rapidyl Can be part of PHACES syndrome

Associated with hyparastrogllic sta111 (e.g. in hepatocelhjll' disease, pregnancy, oral contraceptive pill)

Rapidly developing hamangioma Proliferation of capilaries with erosion of epidennis and neutrophilia

A1pider angiOiflll will blanch when the tip of I papan:lip is applied to 1h; Clll1lr8 of tha la1ion.

......

,,.__________________ ,

Pyovenil: is amisnomer: it i5 neither pyogenic nor Q1111Uiumatou1.

Epideftology
Clinical Coune

Can be congenital Most appear Iller Can ulcenrte Persists, generally do not involute Appears shortly Biter 9 months. increases il size over months, than regresses 511% of lesions resolva spontaneously by 5 years Consider excision f not gone by schoal age. 10% require treatment due to functional impainnent (viSUIII compromise, airway obstruction, high output cardiac fllilura) or cosmesis Propanolal; systemic corticosteroids lnCR!IIse in rurmer overtime

>30 years old Lesions bleed frequently and persist for months

<30 years old

Management

Surgical removal

8ectro or laser Usually no surgery treatment needed Systemic Laser or electrocautery corticosteroids and IN F-a may be for small lesions indicated for rapidly Excision Df large growing lesions lesions if necessii'Y

Surgical excision with histologic exanilation Electrocautery; laser; cryotherapy

VASCULAR MALFORMATIONS 1. Nevus flammeus (Port-wine stain) Clinical Presentation

red to blue macule present at birth that follows a dermatomal distribution, rarely crosses midline most common site: nape of neck
Pathophysiology

congenital vascular malfonnation of dermal capillaries; associated with Sturge Weber syndrome (Vl, V2 distribution)
Management

laser or camouflage (ie. make-up)


2. Nevus simplex (salmon patch) Clinical Presentation

pink-red irregular patches midline macule on glahella known as Angel Kissn; on nuchal region known as stork Bites present in 1/3 of newborns majority regress spontaneously

Pathophysiology

congenital dilation of dermal capillaries


Management

no treatment required

Dl2 Denoatology

Acneiform Eruptions

Toronto Notes 2011

Acneiform Eruptions
Acne Vulgaris/Common Acne
Clinical Presentation a common inflammatory pilosebaceous disease categorized with respect to severity Type I - comedonal, sparse, no scarring Type II - comedonal. papular, moderate :t: little scarring Type III - comedonal, papular, and p10tular, with scarring Type IV - nodulocyatic acne, risk of severe scarring predilection sites: face, neck, upper chest, and back Pathogenesis o follicular hyperkeratinization blocks the secretion of sebum (comedones) o androgens stimulate sebaceous glands to produce sebum o anaerobic diphtheroid Propionibacterium acnes bacteria contains lipase, which converts sebum to free fatty acids and produces pro-inflammatory mediators
Type II - Papular

Type I - Com1donal

Epidemiology age of onset in puberty (10-17 years in females, 14-19 years in males) more severe in males than in females incidence decreases in adulthood genetic predisposition: majority of individuals with cystic acne have parent(s) with history of severe acne Differential Diagnosis o folliculitis, keratosis pilaris (upper arms, face. thighs), perioral dermatitis, rosacea
Type Ill - Pustular

Management o see Table 8


Table B. Acne Treatments and Mechanisms of Action
Drug Name MILD ACNE: Topical Therapies Mechanism of Adi111 Lincosamide antibiotic; mibib; protuin synthesis Macrolide antibiotic; inhibits protein synthesis Prolain oxidant bactericidal &Ifact

dindmycil [e.g. Dllacin

Generally regarded as un&afu in lactation Local skin reactions include bumin{l peeling, dryness, erythema Dry skin, contact dennalilis Apply to the point of ctyness and erytluma, but not discomfort See above

Type IV- Nodulocptic


C Shelley Olen & Klislino Neuman, 2010

erytlnmycin benzoyl p.-oxide

Figure 3. Types of Acne

....

, ,.----------------.

BenzaCiin gel

1% clindamycin and 5% benzoyl peroxide

+ benzoyl peroxide [Bemamyci1.,


ldapal11111 [a.g. lliffllrin"l
lnlliaain [a.g.

3% etVihromycin and 5% benzoyl peroxide See above Comadolytic Comedolytic

Acna Myt... Dellunklld

Eating greasy food and chocolate does not CIIUII8 or WQIQIIICne Blackhllda (comldones)al'l black because of oxidimd melanin. not dirt

Lass irrilllting thenlrlltiloin. No intnction with sun


Sun sensitivity and irritation

llltin-A8

MODERA1E ACNE: Aftar topical treatments hiiVB failed, add oral antibiotics, such as tstracycline {500 rng PO daily to bid), or erythromycin [500 mg PO bid). Antibiotics require months of use before assessing ellicacy. Consider honnonaltherapy, includilg antiantt"ogens tllnlcycline Systemic antibiotic Cyproterone: potent anti-androgenic, progestogenic and antigonedatmphic activity Use caution with ll!{lard to drug interactions: do not use isobetinoin After 35 years of age, estrogerv'progesterane should ort{ be considered in exceptional circumstences, cal'tlfully wBighilg the risk/benefit ratio with physician guidn:e

....

,}----------------.

.A.. Exacertladng flelllrs


Systemic medications: lithium, phenytoi1, steroids, halog..,., ll!drogens, iodides, bnJmides, daiiiZol Topicllavem: mroida, !ani, ointments, oily cosmatics Mechanical prenure or occlusion, such II leaning fac1 on hand& Emational slnla

c:ypratBroae al:llatMthi estradial [Dilllll-35.,

Ethinyl Bltnldal: inc11111sas IIIVBI of SilK


hannane bilKing globulin [SHBG), reducing circulating plasma levels of antt"ogens

Toronto Notes 2011

Acneiform Eruptiona

Dermatology D13

Tabla 8. Acne Traatmants and Mechanisms of Action Icontinued)

Dnlg Nama Mechanilm of Adi111 Nllllll SEVERE ACNE: Consider systemic retinoids after above 1realments have failed Retinoid that inhilils sebaceous function and regluates keratinization Teratoganic: contraindicated during pregnancy,
unsale in lactation; reliable contraception is necess!rf

....._._______________ ,
IIOhlinoin and Lipids r.ports indicabl isDirltinoin-

Signed informed co115811t is needed when pllllicribing Baseline lpid profile, hepatic enzymes and before treatment May transiently exacerbate acne May cause depnession Drug may ba discontinued at 1620 weeks whan nodule count has !hipped by >711% A second course may be initiated r 2months pm Refractory cases may require 3 or more courses of isotretiloin

inducad hypurtriglycaridsmia can be succnsfully controlled with concurrent hypolipidernic therapy.

ea..

Perioral Dermatitis
Clinical Presentation discrete erythematous micropapules that often become c:ontluent, forming inflammatory plaques on perioral and periorbital skin c:ommonly symmetrkal, rim of sparing around vermilion border of lips aggravated by topical glucocorticoids Epidemiology 15-40 years old predominantly females Differential Diagnosis dermatitis, rosacea. acne vulgaris Management topkal: metronidazole 0.7596 gel or 0.75-1')6 cream to area BID systemic: tetracycline

Rosacea
Clinical Presentation chronic: acneiform, inflammatory skin disease flushing (transient erythema) with a burning sensation is common initially, however nontransient erythema is the c:ommonest sign of rosac:ea dome-shaped red papules pustules, contributing to a florid. ruddy complexion differentiated from acne by the absenc:e of c:omedones sites typically affected: convexities of the central face (forehead. nose, cheeks and chin) may also affect the scalp, neck, and the upper part ofbody characterized by remissions and exac:erbations all forms of rosacea can progress from mild to moderate to severe in longstanding rosacea. signs of thickening, induration, lymphedema in the skin phyma: a distinct swelling caused by lymphedema and hypertrophy of subcutaneous tissue, particularly affecting the nose (rhinophyma) ocular manifestacions: conjunctivitis, keratitis, iritis exacerbating factors: heat, cold. wind. sun, stress, drinking hot liquids, alcohol, caffeine, spices (triggers of vasodilatation) Pathophysiology
unknown

....._._______________ ,
Guidll&nN fw IIIII Diagnasis of lloACIIII Presence af ana or mare af 1he folowing primary features:

Flulhing (transient erythema)

Tallngiactasil

Nontl'll1sient erythema Papulus and puldul811

May includu onu or mare af the fallowing secondary features: Burning or slingilg
Dry lpjlllllr&rlCB

Edema Phymatous ch11111es Ocular m1111ifa!Biions Periphelllllocation

Epidemiology although found in all skin types, highest prevalence in fair-skinned people 30-50 years old
F>M

D14 Denoatology

Acneiform Erupti0ll8/Dermatitis (Eczema) Management

Toronto Notes 2011

......

t-----------------,

Sulltypelnd V.ri....

Their CMraeblrimicll

of._..

nd

SUIITYPE
Flushing, persistmt central facial erytlleiTIII 1BIIIIIUiec:tnia

Papulopustular l'lnistent central facial erythema


Transient central facial papul11 or pustules or batl1
Phyml&oul

avoid topical corticosteroids cosmetic camouflage telangiectasia: treated by physical abation; electrical hyfrecators, vascular lasers, and intense pulsed light therapies phymas: treated by physical ablation or removal; paring, electrosurgery, cryotherapy, laser therapy [C02, argon, neodymium-doped yttrium aluminum garnet (Nd:YAG}] early diagnosis and prompt treatment are recommended to prevent worsening

T1ble 9. Specific RoS1ce1Treatments


!It line

Znd Line

3nl Line

Thickening skin, inegulllr surface nodularitiN and enlarvement Nose, chin, forehesd, cheeks or eers

Oral tetracyclines mg PO bid) Topical mutronidazcle Oral erytlrurnycin (250-500 mg PO bid)

Topical clildarnycin Topical eryllromycin 2% solution Topical benzoyl peroxide


Dnll metrunidamle

Oral retinoids Topicaldw"

Ocul8r Fnign body Mnsation in the eye,


burning or lllinging, dryness, itx:hing, DaJiar blumd vision, tlllangiec1ll5il. of the sclera or other parts of thleye, or periorMal edema

Ampicillin

Dermatitis (Eczema)
Definition
inflammation ofthe skin

VAliANT Gr.nulclnl8tiM
uniform size

Noninflammatory, hard. brown, yellow, or rad cutaneous papula or nodul11 of

Clinical Presentation
symptoms include pruritus and pain acute dermatitis: papules, vesicles subacute dermatitis: scaling, crusting chronic dermatitis: lichenification, xerosis, fissuring

Asteatotic Dermatitis
Clinical Presentation
diffuse, mild pruritic dermatitis secondary to dry skin very conunon in elderly, especially in the winter (a.k.a. "winter itclt") but starts in the fall

Management
skin rehydration with moisturizing routine

mild corticosteroid creams

Atopic Dermatitis
--------------------------------------

......

, ...-----------------,

Clinical Presentation
subacute and chronic eczematous reaction associated with prolonged severe pruritus distribution infant (onset at 2-6 months old): face, scalp, extensor surfaces childhood (>18 months): flexural surfaces adult: hands, feet, flexures, wrists, face, forehead, eyelids, neck inflammation, lichenification, excoriations are secondary to relentless scratching atopic palms: prominent palmar creases associated with keratosis pilaris (hyperkeratosis ofhair follicles, "chicken skin") xerosis occupational hand dryness

Trigers t.r Atopic: DIPIIIIItitia lrrimnb (dnrgentl, sol,.nts, Contact allarg &lvironmentalaeroall1r91ns (dust miiN) IIIIJiproprilrte bathing habits (long hot showers) SWe8ting

clothing, water hlrd111111)

Microbes (S. - . ) Strus

Epidemiology
frequently affects infants, children, and young adults females only slightly more at risk than males ( 1.3:1 over the age of 2 years) almost 15% of children in developed countries under the age of 5 are affected; half of these cases are diagnosed by 1 year of age associated with personal or family history of atopy (asthma, hay fever, anaphylaxis, eosinophilia) polygenic inheritance: one parent >60% chance for child; two parents >80% chance for child childhood onset and hereditary forms may be associated with a defect in the protein filaggrin the earlier the onset. the more severe and persistent the disease long-term condition with 1/3 of patients continuing to show signs of AD into adulthood

Pathophysiology
Th2 cellular response

Investigations
no gold standard for diagnosis consider: skin biopsy, immunoglobulin serum levels (often elevated serum IgE level), patch testing, and skin prick tests

Toronto Notes 2011

Dermatitis (Eczema)

Dermatology DIS

Management goal: reduce signs and symptoms, prevent or reduce recurrences/flares better outcome (e.g. less flare-ups, modified course of disease) if diagnosis made early and treatment plan individualized individualized based on age, severity, sites and extent of involvement, presence of infection, previous responses to therapy avoid triggers of AD enhance barrier function of the skin regular application of moisturizers emollients hydrate the skin and reduce pruritus twice daily application is recommended even in absence of symptoms, especially after bathing or swimming bathing promotes hydration when followed by the application of moisturizers to the skin anti-in11ammatory therapies A. topical corticosteroids effective, rapid symptomatic relief of acute flares best applied immediately after bathing control inflammation with a potent topical steroid; a milder one following resolution of acute flare systemic immunosuppression may be needed in severe cases flares may respond to systemic anti-staphylococcal therapy side effects: skin atrophy, purpura, striae, steroid acne, perioral dermatitis, and glaucoma when used around the eyes B. topical immunomodulators long-term management calcineurin inhibitors include pimecrolimus (Elide!), tacrolimus (Protopic) side effects: skin burning, transient irritation advantages of immunomodulators over long-term corticosteroid use rapid, sustained effect in controlling pruritus no skin atrophy safe for the face and neck Complications infections treatment of infections topical mupirocin or fusidic acid oral antibiotics (e.g. cloxacillin, cephalexin) for widespread S. aureus infections
lnililll amant af d i - hiltllry, extant and unrity (impact an fami!r, ..

I
Adj1nc:tiva th. .py Avoidance of triggers T11111t bacterial superinfections (topical or oral antibiotics) Antihistaminas Psychological interventions

"-tiant aducaliun, daily amullillllt uu

Ac... af flare Topical corticosteroids or topical calcinaurin inhibitor (pimacrolinus or111crolimus)

dlllrwa)

I
Dileala ramilliun (na signs symptams)

Mailtan..- tharapy is ..rsist.nt an.Vor fraqnt I'KIII'I'IIncas Use of topical corticosteroid or calcineurin inhibitor at sign offlara

long-term maintenance use of calcineurin inhibitors

Strvara rafractury dilaua Azathioprine Phototherapy Mlllhotraxate Potent topical steroids 01'11 cyclosporin P-vchotherapeutics 01'11 steroids

Figure 4. Atopic Dannltitis Treatment Algorithm


Adljad from: Blis C, at II.ICCAD II Faly.lntlmational Con1111sus Conferanca on Alopic Dermatitis II (ICCAD II): cilical updata and amntv.tmant ilmlagin.BrJilllmrltui.ZOOJ;

Dl6 Denoatology

Dermatitis (Eczema)

Toronto Notes 2011

Contact Dermatitis
Top T111 Allllrgen ldntililld by The

North Ameri01n Cont.ct Dennatitis Group

Clinical Presentation cutaneous inflammation from the interaction between external agent(s) and the skin
Tabla 11. Contact Dannatitis
Irritant Contact Dematitis

All-aic Contact Demllitis


Cel-mediated delayed {Type IV)
reaction Erythema with a pruritu& eruption, swelling.

Mechanis11 al Reaction
NckBI1.11f111 14.2 Found i11111111 Mllstclllm1'l)dyull8d
FrlgrlllC8 rratnl

Toxic injury to skin; nan-inmune mechalism Erythema, dryness. fine scale, burning .Acut8: quick reaction, &harp margins {e.g. from ecidfalkali expDSUrel Cumulative insult: slow to appear, poar1y defined margins (e.g. from sDapl. more common Majority; will occur in lllYOile given sufficient concentration of irritants Palmll' surface crf hand usually involved

Naon'rjcinsuhtl 13.1

Type al Reactian

fDiical anlibiric

llll11m of Fvru

11.8 11.7

Fnvance mix

Amix of e9rt dllarantfrlplce t:OITlponantl whicll -dMioped tDIIkrNiorallelgen tilting in COIIIIItics


ACGIIIIIDII ]JIISliYitivethdis
l:lllll'illlics

Frequancyal Canlllc:l Dannatitis

Minority; patient acquires susceptibility to allergen that parsists ildafinataly Dorsum crf hand usually involved; oftl!n discrete area of skin involvement

Diltributian
Exanlplll

Thi11111U1al

10.9

used in vaccilas, solution.

Soaps. weak alkali, detergents. organic solvents, (See sidebar! alcohol, oils Many allergens are irritants, so may coincide with irritant dermatitis Avoidance of irritants Wat compresses with Burow's solution Barrier moisturizers TopicaVoral steroids

Manqement

Sodium gold

lllldinjBWIIilry, delllistJy. thiosullltB elllCtn!Mcs

Patch blsting to dtJialmile specific allergen Avoid allergen 111d ib cross-reactants Wet COIJ1lresses soaked in Burow's solution
(drying agent)

9.3

Acobntess gu
found illl'lllll' wartpi!CII, l:lllll'illlics.

Steroid cream ihydrocortisone 1%. b81lm81hasane valllllla 0.05% or 0.1% cream; bidl Systemic steroids pm (prednisone 1mg/kg. taper owr2weeksl

11*1ic8tions. flldilas, resins,plasticbGitles


ILnmiurn-15
9.0

Dyshidrotic Dermatitis
Clinical Presentation "tapioca pudding" papulovesicular dermatitis of hands and feet that coalesce into plaques, followed by painful fissuring acute stage often very pruritic secondary infection common lesions heal with desquamation and may lead to chronic lichenification sites: palms and soles dorsal surfaces ofhands and feet Pathophysiology NOT caused by hyperhidrosis (excessive sweating) emotional stress may precipitate the dermatitis Management topical: high potency corticosteroid with plastic cling wrap occlusion to increase penetration intralesional triamcinolone systemic: prednisone in severe cases antibiotics for secondary S. aureus infection

11'1111\'lhllmpoos,
mcilflllm,.

Cobak clmla

9.0

aJI'Iditianen 11111 lOIIlS Al'llldmetalfound in

linin. tDals
Blcitlllcil

8.7

AfDpic:allllfibiatic

Nummular Dermatitis
Clinical Presentation annular, coin-shaped, pruritic, erythematous plaques, dry, scaly, lichenified often associated with atopic and dyshidrotic dermatitis secondary infection common Management rnoisturization corticosteroid ointment BID

Toronto Notes 2011

Dermatitis (Eczema)

Dermatology D17

Seborrheic Dermatitis
Clinical Presentation greasy, erythematous, yellow, scaling papules and plaques in areas rich in sebaceous glands infants: one cause of"cradle cap
children: may be generalized with flexural and scalp involvement adults: diffuse involvement of scalp margin with yellow to white flakes, pruritus, and underlying erythema sites: scalp, eyebrows, eyelashes, beard, glabella, post-auricular, over sternum, trunk, body folds, genitalia

Pathophysiology possible etiologic association with Pityrosporum ovale (yeast) Epidemiology common in infants and at puberty increased incidence in immunocompromised patients (e.g. HIV) in adults, can cause dandruff (pityriasis sicca) Management face: Nizoral cream OD +mild steroid cream ODor BID scalp: salicylic acid in olive oil or Derma-Smoothe FSlotion (peanut oil, mineral oil, fluocinolone acetonide O.ol %) to remove dense scales, 2% ketoconazole shampoo (Nizoral), ciclopirox (Stieprox) shampoo, selenium sulfide (e.g. Selsun) or zinc pyrithione (e.g. Head and Shoulders) shampoo, steroid lotion (e.g. betamethasone valerate 0.1% lotion bid)

Stasis Dermatitis
Clinical Presentation persistent skin inflammation ofthe lower legs with brown pigmentation, erythema, xerosis, and scaling associated with venous insufficiency Management support stockings rest and elevate legs moisturizer to treat xerosis mild topical corticosteroids to control inflammation Complications ulceration (common in medial malleolus), secondary bacterial infections

Lichen Simplex Chronicus


Clinical Presentation chronic dermatitis resulting from continued rubbing/scratching of skin may develop secondarily to another pruritic skin disease lichenified (thickened) skin Management treat pruritus to break the itch-scratch cycle: antihistamines, topical antipruritics topical corticosteroids (extremely potent)

DIS Denoatology

Papuloaquamous Diseases

Toronto Notes 2011

Papulosquamous Diseases
Lichen Planus
Clinical Presentation
acute or chronic inflammation of mucous membranes or skin characterized by violaceous papules, especially on flexural surfaces small, polygonal, flat-topped, shiny, violet papules; resolves into hyperpigmented macules sites: wrists, ankles, muc:ous membranes in 60% (mouth, vulva, glans), nails, scalp Wickham's striae: greyish lines over surface; pathognomonic mucous membrane lesions: lacy, whitish reticular network. milky-white plaques/papules; increased risk of sec in erosions and ulcers nails: longitudinal ridging; dystrophic scalp: scarring alopecia spontaneously resolves in weeks or lasts fur years (mouth and shin lesions) Koebner phenomenon "isomorphic reaction": develops in areas oftrauma

The 6 P's uf Uch... PIPurple, Pruritic, Polygonal, Peripheral, Papules, Penis (i.e. lnjCOSil}

Epidemiology association with hepatitis C may be triggered by severe emotional stress Management
topical corticosteroids with occlusion or intradermal steroid injections short courses of oral prednisone (rarely) photochemotherapy for generalized or resistant cases oral retinoids fur erosive lichen planus in mouth

Pityriasis Hosea
Clinical Presentation
acute, self-limiting, erythematous eruption characterized by red, oval plaques/patches with central scales that do not extend to edge oflesion long axis oflesions follows parallel to ribs producing "Christmas treeD pattern on back varied degree of pruritus most start with a "Herald" patch which precedes other lesions by 1-2 weeks sites: trunk. proximal aspects of arms and legs

Etiology
suspected human herpes virus 7

Management
none required; clears spontaneously in 6-12 weeks, reassurance topical corticosteroids when post-inflammatory pigmentation is a concern

Psoriasis
It' PSORIASIS: "'-ntttion ond

Classification
1. plaque psoriasis 2. guttate psoriasis 3. erythrodermic psoriasis 4. pustular psoriasis 5. psoriatic arthritis

Pink

bleeding

(Auspitz signi/PI1ysical injury (Koebner phanomanon} Silver scale/Sharp mBrgins spots Rata Ridges with lagulsr elongation

Differential Diagnosis
atopic dermatitis, mycosis fungoides (cutaneous T-celllymphoma), seborrheic dermatitis, tinea

Itching

ArthritiiVAbscns (MunroVAu1Dimmun Slnltum corneum with nuclei Immunologic

Diagnosis
often clinical, biopsy to confirm PASI (Psoriasis Area and Severity Index) score is based on: percentage of surface area involved and the severity of symptoms (erythema, infiltration, desquamation)

Slnltum granulosum absent

Toronto Notes 2011

Papuloaquamous Diseases

Dermatology Dl9

1. PLAQUE PSORIASIS
Clinical Presentation chronic and recurrent disease characterized by well-circumscribed erythematous papules/ plaques with silvery-white scales worse in winter (lack of sun and humidity) Koebner phenomenon "isomorphic response": induction of new lesion by injury Auspitz sign: bleeds from minute points when scale is removed usually non-pruritic exacerbating factors: drugs (lithium, ethanol, chloroquine, beta-blockers), stress sites: scalp, extensor surfaces of elbows and knees, trunk, nails, pressure areas Pathophysiology decreased epidermal transit time from stratum basale to stratum corneum shortened cell cycle of psoriatic compared to normal skin TIU -mediated inflammatory response Management preventative measures avoid sunburns avoid drugs that exacerbate the condition (e.g. beta-blockers, lithium, corticosteroid rebound phenomenon, interferon} first-line treatment mainly topical, usually prescribed if less than 5-10% oftotal body surface area is involved first-line topical treatments include moderate to potent steroids, vitamin D analogues, retinoids, anthralin, coal tar, salicylic acid ifthe affected area is >10%, use topical medications as adjuncts to phototherapy or systemic drugs second-line treatment include cyclosporin, methotrexate, acitretin, phototherapy third-line treatment biologics including alefacept, etanercept, intliximab, adalimumab, ustekinumab systemic treatments should be considered if: psoriatic lesions cover >10% of total body surface area unsuccessful topical therapies psychological distress

....

't-----------------, ,

PSORIASIS: Triggers (Koebner'1 ph-menan)

lnfactions (acubl mptococcal infection


pracipitatu& guttate psoria1i1) Strass (can baa major factor in flares) Drugs (l'(slumic gmocorticoidl, and lilllium, antimlllarilll drugs, inmrferun) Alcohol ingestion

lofi:al T..-.afGrCinlic .... 1'11ri181


lllua 2
-

C<nne

2U09,

'lillniiD.
piiiiBI.

Sysllnri: IIWw alllncbnizld trills c:ampllil; tnmem IQiinst J8;ello ...

lnllnlnliln: CarlicGitiRidl. diltniJI,


corlicDIIIInlidl. Dlilllml: IIMI1igltDr a-.!aiiMIIII gbbll Talll-ny-SCIRS.I'Ior8sisaa

Wlmil D,llldmrril D+

1111d.wity illllll'l1ilnt.-lai1M1111
Ill*: Cri:llllaroidt, villnil and 1mluln peliDrmud bllbl'lllln piiM alona. A c:oriinltion at cri:OIIIsroids and villmil D Willi batllr 1hln litlmWinin D corlicoltaroils aloal. II'

Tabla , , . Topical Treatment of Psoriasis


Tnlltmlnt LWicaniB Salicylic acid 1-12%
Tar (LCD: Liquor carbonis detergans)
20% coal tar sokltion

Reduce fissure formation RemOVII seal lrllibits DNA synthesis, increases cal
tumDVI!I

Putrolatum is effectiw Poor long term compliance


Not ID be used on face or skin folds
Use appropriete potency steroid in difhmrt arees for degree of psoriasis Use on nais

....

Caldpotriol i8 a vlbunm Dd.W..tin


considerad 1o be !he most potent topical psoriatic therapy.

'.,

Calcipotriene
(Dovonax",

Binds to skin keretinocyte proliferation


1,25dihydroxyvitarrin DJ ID inhibit

with batamathasona diprupionata and is

calcipotriallll combined

Corticosteroid oinbnent

Reduce scaling end thickness Retinoid derivatiw

Tabla , 2. Systamic Tralltmant of Psorinis Tnlltmlnt Methotrexate Bone maiTIIW toxicity, hepatic cirrhosis Psoralens end long wave ultraviolet radiation (PINA) Pruritus. burning. cetaracts, skin cancer
Alopecia, cheilitis, teraiDganicity, apislaxis, xerosis, hyperlriglyeridamia

Cyclosporine
lNB and "Narrow band"INB (311312 nm)

Renal toxicity, hypertansion, immunosuppniSSion


Wall tolerated

Tabla , 3. Biologics approved in Canada Tnlltmlnt Routa Dulling Sc:hedull


etanarcept {Entnl)*
adalirrumab (Humira)*

Etfll:tinn. .

Action

sc sc
IV

Twice weBidy initially Once wery 2weeks -Every 2 months


Every 12 weeks during maintenance

+ +++
++++

Tcell

....

infliximab (Remicade)* ustekinumab (Stelara)

sc

+++++ ++++

TNF TNF TNF


IL 12/23

,,,

Mechanism of Blalogla "mab" - monoclonal antibody capt" = recaptor

'Can lim be us1D 11111 ]JI01il1ic 11111ritis

D20 Denoatology

Papulosquamous Diseases/Vesiculobullous Diaeases

Toronto Notes 2011

2. GUTTATE PSORIASIS (DROP-LIKE;


Clinical Presentation
discrete, scattered salmon-pink scaling papules sites: generalized, sparing palms and soles often antecedent streptococcal pharyngitis

Management
UVB phototherapy, sunlight, lubricants penicillin V or erythromycin if Group A beta-hemolytic SITeptococcus on throat culture

3. ERYTHRODERMIC PSORIASIS
Clinical Presentation
generalized erythema with fine desquamative scale on surface associated symptoms: arthralgia, severe pruritus may present in patient with previous mild plaque psoriasis aggravating factors: lithium, beta-blockers, NSAIDs, antimalarials, phototoxic reaction, infection

Management
hospitalization, bedrest, IV fluids, monitor fluid and electrolytes treat underlying aggravating condition, sun avoidance methotrexate, cyclosporine, UV, oral retinoids, biologics

4. PUSTULAR PSORIASIS
Clinical Presentation
sudden onset of erythematous macules and papules which evolve rapidly into pustules, very painful can be generalized or localized to palms/soles patient usually has history of psoriasis; may occur with sudden withdrawal from steroid therapy

Management
methotrexate, oral retinoids, biologics

5. PSORIATIC ARTHRITIS
5 categories asymmetric oligoarthropathy distal interphalangeal (DIP) joint involvement (predominant) rheumatoid pattern (symmetric polyarthropathy) psoriatic arthritis mutilans (most severe form) predominant spondylitis or sacroiliitis see Rheumatology; RH21

Vesiculobullous Diseases
Bullous Pemphigoid
Clinical Presentation
chronic autoimmune bullous eruption characterized by pruritic, tense, subepidermal bullae on an erythematous or normal skin base sites: flexor aspect of forearms, axillae, medial thighs, groin, abdomen, mouth (33%)

Pathophysiology
Pa11phlgus Vulauls vs. Bulous Pallphigoid
VUI(IBril intraapidarmal, flaccid lesions PemphigoiD. = D.eepar, tense lesions at the junction

IgG produced against dermal-epidermal basement membrane proteins (hemidesmosomes) leads to subepidermal bullae

Epidemiology 60-80 years old


associated with malignancy (rarely)

Investigations
immunofluorescence shows deposition of IgG and C3 in the basement membrane anti-basement membrane antibody (IgG) (pemphigoid antibody detectable in serum)

Prognosis
generalized bullous eruption heals without scarring rarely fatal

Toronto Notes 2011

Vesiculobullous Diseases

Dermatology D21

Management prednisone steroid-sparing agents (e.g. azathioprine) topical potent steroids (clobetasol) may be as effective as systemic steroids tetracycline nicotinamide is effective fur some cases dapsone for milder cases

Dermatitis Harpetiformis

-------------------------------

Clinical Presentation grouped papules/vesicles/urticarial wheals on an erythematous base. associated with intense pruritus, burning. stinging almost always excoriated, rarely seen as blisters lesions grouped, bilaterally symmetrical sites: extensor surfaces of elbows/knees, sacrum, buttocks, scalp Pathophysiology 90% have HLA B8, DRJ, DQWZ 90% associated with gluten-sensitive enteropathy (celiac) (80% are asymptomatic) 30% have thyroid disease; some have intestinal lymphoma or iron/folate deficiency Epidemiology 20-60 years old, M:F = 2:1 Management dapsone fur pruritus gluten-free diet

Pemphigus Vulgaris

----------------------------------....

Clinical Presentation autoimmune blistering disease characterized by flaccid, non-pruritic epidermal bullae/vesicles on an erythematous or normal skin base may present with erosions and secondary bacterial infection sites: mouth (90%), scalp, face, chest, axillae. groin, umbilicus N"Ikolsky's sign: sliding or rubbing pressure on skin -+ separation of epidermis Asboe-Hansen sign: pressure applied to bulla causes it to extend laterally Pathophysiology IgG produced against epidermal desmoglein 1 and 3leads to intraepidermal bullae Epidemiology 40-60 years old, higher prevalence in Jewish, Mediterranean, Asian populations paraneoplastic pemphigus may be associated with thymoma, myasthenia gravis, malignancy, and use ofD-peni.cillamin.e Investigations immunofluorescence: shows IgG and C3 deposition intraepidermally circulating serum anti-desmoglein IgG antibodies Prognosis and Clinical Course begins with mouth lesions, followed by skin lesions first localized (6-12 months) then generalized lesions heal with hyperpigmentation but no scar may be fatal unless treated with immunosuppressive agents Management prednisone 1.0-3.0 mg/kg until no new blisters, then 1.0-1.5 mg/kg until clear, then taper steroid-sparing agents: azathioprine, methotrexate, gold, cyclophosphamide, cyclosporine, intravenous immunoglobulin (IVIG), mycophenolate mofetil plasmapheresis for acutely high antibody levels

,9.----------------. "

Pe..phig Foliac An autoimmune inlrlllpidermal blistaring disease that is more SL4!erficialthan pamphigus wlgaris due to antibodies against dasmoglain I, an intracellular adhesion molecule. Appears as crusted patchas and erosions which can initially be managed topical steroids if localizld. Activa widespread disease is treated like pemphi!Jls wlgaris.

....

,"

Azatllioprin1 Thiopurine malhyltnmsfanlse(TPMT] levels should be meBSUred before starting therapy. Individuals with low enzyme activity will axpariance graatar immunosuprassion.

D22 Denoatology

Vesiculobullous Diseases/Drug Eruptions Tabla 14. Summary of Vasiculobullous Disaasas


Bullous Psnpligaid Dannllitis H.-patifannis
lgA

Toronto Notes 2011

Psnphigus Vulgaris
lgG lnlriilepidermal
Eosinaphils 111d neutrophils

Altibady

lgG

Basement mentr.me
Eosinaphils

Dermal
Neutrophils
Gluten-free diet Dapsone

Systemic steroids lmmunosupn!SSive agents Tetracycline

High dose steroids Immunosuppressive agent (e.g. lmuran8 , mycophenolic acid) Malignancy with paraneoplastic

Clobstasol
Malignancy (rarely)

Gluten enteropathy Thyroid dis811S8 lntestinallymphD1118

Porphyria Cutanea Tarda


Clinical Presentation
tense vesicles/bullae in photoexposed areas subjected to trauma facial hypertrichosis, brown hypennelanosis vesicles, and bullae in photo distribution (dorsum of hands and feet) sites: light-exposed areas subjected to trauma, dorsum of hands and feet. nose, and upper trunk

Pathophysiology
autosomal dominant or sporadic skin disorder associated with the presence of excess heme associated with alcohol abuse, DM, drugs (estrogen therapy, NSAIDs), mv, hepatitis C, increased iron indices

Epidemiology 30-40 years old, M> F Investigations urine+ 5% HCl shows orange-red fluorescence under Wood's lamp (UV rays)
24-hour urine for uroporphyrins (elevated) stool contains elevated coproporphyrins immunofluorescence shows IgE at dermal-epidermal junctions

Management
discontinue aggravating substances (alcohol, estrogen therapy) phlebotomy to decrease body iron load low dose hydroxychloroquine

Drug Eruptions
Drug Hypersensitivity Syndrome
Drug Hypena..ilivity Syndrame Trid

Exanthematous Eruption lntarnal 01'!1., lnvolvarnant

Fever

fever followed by symmetrical bright red exanthematous eruption that may lead to internal organ involvement (hepatitis, arthralgia, nephritis, pneumonitis, lymphadenopathy; and/or hematologic abnormalities) classically occurs approximately 10 days after first exposure to the drug siblings at risk most common causes: sulfonamides and anticonvulsants (phenytoin, phenobarbital, carbamazepine, lamotrigine) 10% mortality if undiagnosed and untreated

Erythema Multiform& (EM). Stevens-Johnson Syndrome (SJS). Toxic Epidermal Necrolysis (TEN)
disorders with varying presence of characteristic skin lesions, blistering and mucous membrane involvement NOTE: EM is considered to be distinct from the SJS-TEN spectrum

Toronto Notes 2011

Drug EruptiOJU

Dermatology D23

Table 15. Comparison ol Erythema Multilome, Stevens-Johnson Syndrome, Toxic Epidermal Necrolpis
E.ryt1111111

Multifanne (EMI

Stevens-Jallnson Synlhme (SJSI Toxic Epidennll NICI'IIIysis flfNI


EM with more mucous membrane invoiVI!IIII!nt "Atypical lesions": rad patch with dark purple centre "Sicker" {hilt! feverl Sheet-like epidennll detachment in < 10% {Nikolsky sign) Severe mucous membrane invoiVI!IIII!nt, and blistering "Atypical lesions": 50% have no target lesions Diffuse erythema then necrosis and sheet-like epidermal detachment in >30%

....

',

Lilian

Maculef/papules with central vesicles Classic bull's-eye pattern of concentric light and dart rings (target lesions) Bilateral and symmetric All lesions appear within 72 hours No edema Lesion "fixed" for at least 1 days

Erythmul multiform is 1 clinical diagno1i1. Resonabla evidence axim fur the following as precipitating factors: HSV (pqdomin1111t pl'8cipillllingfactorl
Myr;opluma ptlflllmonies

Orfviru&

scomrt As-ilt*._ San far Taxi:


Generalized with prominent face and 1nlnk involvement Palms and soles may be spared Generalized Nails may also shed

DoiSI of hands and forearms


Mucous membrane involvement (lips, 1D191e, buccal muCOSI) is possible Extremities with lace > 1nlnk lnvoiVI!IIII!nt af palms and soles Other Burning and stinging Complications Recurrences Secondary bacterial infection Constibdianal Weakn1155, malaise Symptom

Scarring, contractures, eruptive nevornelanocytic nevi, corneal scarring, blindness, phimosis and vaginal&ynechiae

Tubular necrosis and acute renal failure, epithelial erosions of trachea

Prodrome 114 days prior to High faver >38"C eruption with fever and ilness

Jbest Demllifri 2UMl;115:14S.153 S1udy: lleveio!l-.1 nlidllt updic QQrily af-il_s_lar CUll allEN and CDII1llftl 1D Simpllied AID l'lrjliolagy Score 1nd blln scaring &'jlllm. l'ltiiB To develp score IIIII evabite Diller .-.: 165 plli8IQ wi1b SJS.SJS/ItN, or TEN IIW1Id 1D the K:U. For Vllillliln,l sepnfl dltlbll8 gf 75 pltilnii\WII Ullld. llqi8CIIdand lCllll 11'l(ltJiy. rllill:rmr.tion. bulls: s-. diflrant risk fldln far dllth:
age>40y,lllllignlnl;y,lldlylrillbcM! 12D. illitiellpidennll dlllehmllll >I 11\, liMn Ural >10 mmoK,11m11 gtc >14 rrmol1.. ..t bicllil

Etiology

Infection: HSV. or Micoplasma pneumoniiJe

15% are drug-related (NSAIIls, anticorMJisants, sullcnamides, penicillins) Occurs up to 1-3 weeks alter drug exposure with more rapid onset upon rechallenge

50% are definitEly drug related <5% 1111 due to viral infection, immunization

<20 mmol'\. Expeclld . -QJI!tlllfed with IICUI 11'llltJiy (19.3 compnd fa 20'41; wlliiNS, 1he SAPS hid poor IIQ181111111111 llqlldBd ..t lttull molllily l9.1'lo VI.

Diflerentill Di111nD1i1

Giant urticaria, graooloma annulare, Scanet lever, photutoxic, eruption, Scanet lever, phototoxic eruption, myc08is fungoides, vasculitis gRift w. host disease {GVHDI. GVHD, SSSS, axluliative dermatitis staphylococcal scalded skin syndrome (SSSSI, exfoliative dermatitis, Kawasaki disease, paranaoplastic pemphigus Lesions last 2 weeks and heal without cDiflllications SyrqJIDmatic treatment {oral antihistamines, oral antacidsl Corticostaroids in severely ill (controwrsiall Prophylactic oral acyclovir for 6-12 months for herpes siiJ1llex virus (HSV)-associated EM with frequent recu1T811ces course 5% mortality Prolonged hospitalization Vllithdraw suspect drug htravenous fluids Corticostenoids (contiOV8nial) hfection prophytuis Consider IVIG

Coune;md

PragnDiia
Mulglllllllt

30% mortality due to fluid loss, regrowth of epidermis by 3 weeks, secondary infection
As for Stevens-Johnson syndrome Admit to bum unit Debride frankly necrotic tissue ConsiderMG

Exanthematous Eruptions (Maculopapular Eruptions/Morbilliform)


symmetrical, widespread, erythematous patches or plaques scales the "classic" and most common adverse drug reaction often starts on trunk or areas of sun exposure may progress to generalized exfoliative dermatitis especially if the drug is continued most common causes: penicillin > sulfonamides > phenytoin see Pediatric Exanthems, D40

Fixed Drug Eruption


sharply demarcated erythematous oval patches on the skin or mucous membranes sites: face, mucosa, genitalia reaccurs in same location upon subsequent exposure to the drug (fixed location) most common causes: antimicrobials (tetracycline, sulfonamides), anti-inflammatories, psychoactive agents (barbiturates), phenolphthalein

D24 Denoatology

Drug Eruptions/Heritable Disorders

Toronto Notes 2011

Photosensitivity Eruptions
phototoxic reaction: an exaggerated sunburn" confined to sun -exposed areas photoallergic reaction: an eczematous eruption that may spread to areas not exposed to light most common causes: chlorpromazine, doxycycline, thlazide diuretics, procainamide

Serum Sickness-Like Reaction


a symmetric drug eruption resulting in fever, arthralgia, lymphadenopathy, and skin rash usually appears 5-10 days after drug skin manifestations: usually urticaria; can be morbilliform most common causes: cefaclor in kids; buproprion (Zyban") in adults

Heritable Disorders
Ichthyosis Vulgaris
Clinical Presentation generalized hyperkeratosis leading to dry skin "fish-scale" appearance especially on extremities with sparing of flexural creases, palms and soles; scaling without inflammation Pathophysiology abnormal retention of hyperkeratosis scaling without inflammation Epidemiology 1:300 incidence autosomal dominant inheritance associated with atopic dermatitis and keratosis pilaris Management immersion in bath and oils emollient or humectant creams, and creams or oils containing urea

Neurofibromatosis

(Typal; von Rackllnghausans Disease)

Clinical Presentation diagnostic criteria includes 2 or more of the following: 1. more than 6 spots >1.5 em in an adult, and more than 5 spots >0.5 ern in a child under age 5 2. axillary or inguinal freckling 3. iris hamartomas (Lisch nodules) 4. optic gliomas 5. neurofibromas 6. distinctivebonykmon 7. first degree relative with neurofibromatosis type 1 associated with pheochromocytoma, astrocytoma, bilateral acoustic neuromas, bone cysts, scoliosis, precocious puberty, developmental delay, and renal artery stenosis Pathophysiology autosomal dominant disorder with excessive and abnormal proliferation of neural crest elements (Schwann cells, melanocytes) linked to absence of neurofibromin (a tumour suppressor gene) Epidemiology incidence 1:3,000 Management follow closely for malignancy, transformation of neurofibroma to neurofibrosarcoma excise suspicious or painful lemons see Pediatrics, P86

Toronto Notes 2011

Heritable Disordersllnfectiona

Dermatology 025

Vitiligo
Clinical Presentation
primary pigmentary disorder characterized by hypopigmentation and depigmentation acquired destruction of mdanocytes characterized by sharply marginated white patches associated with streaks of depigmented hair, chorioretinitis sites: extensor surfaces and periorificial areas (mouth, eyes, anus, genitalia) Koebner phenomenon "isomorphic response": may be precipitated by trauma
IIIIMIIIilu fer \lilgo

Coclnlle Dl!rllase ofS)'st Rev 2010; Issue 1


S1udy: Sys1imllic nMiw rl1111damiltd controllll trills. l'atillll: 3139 pllticiplrltsNtllvitiiQO. lnlelwldion: TQI)ic:al treltmenl!, lghttheRpies, 01111

trallmlnll, _.1 mlllhods. Md


tt.lpias

Pathophysiology
acquired autoimmune destruction of melanocytes

ldverseella:ls

ReiIIIII: Modnta Mdancellldsls fa' 'die usa at


tupical carticosleloids111 incM:e H17NMt IIMna allacts II'B absarwd Ntll use. Topical use r1 nan-mroidal innrlmnlllillators (i.e. tacralu),ISpllcilly in

Epidemiology
1% incidence, polygenic 30% with positive family history

alriillltianNtlllighttlimpies, lllslllabaen
liiiMIIID ildue&l'llpi(Jnllnlltian.llawiM!r.IDnR1Brrn use Rlll'llillllticaltf incrasatlia risk lor cancer. In combirlllian thenpy incUdilg somafonn hlwJ 'dla mast improvemelf. Sustained rePtJnen1atia11 (>2 YtMI lu nat bean rapaT1Id nl tlu radsllhauld ba tra1111d with caution.

Investigations
rule out associated autoimmune diseases: thyroid disease, pernicious anemia, Addison's disease, TypeiDM Wood's lamp to detect lesions: iluminates UV light onto skin to detect patches of amelanosis

Management
sun avoidance and protection topical immunomodulator (i.e. tacrolimus, pimecrolimus) or a topical steroid for 6-12 months prior to attempting phototherapy PUVA camouflage preparations "bleaching" normal pigmented areas (Le. hydroquinone 20%) if widespread loss of pigmentation

M;/1 Oemrafti2007; 143: 578

.....

IIIMIIIizlllllauWHiind Trill rl Tnlllnat

S1ully: rllllbrized study. I'IIIIB 56 pililnll with nansagmlrllll Wilgo. IIIIMIIIilu: PINA or NS.lNB Mi:e per week

111rfaca areatliatwas

11111 cooornwlch COJiljlled111

attliund

Infections
Bacterial Infections
often involve the epidermis, dermis, hair follicles or periungual region systemic
SUPERFICIAL SKIN (EPIDERMAL)

IP<D.001 ). Alter48 -ions BSAmavwas Gre111er in the NB-IJIIB grrAip 11'=.007) dis benefit -mlirlllillldat12111DIIIIIs.

cithCRP'f, ni11112111C1111hs. ReiIIIII: NS.lNB il..,arior mPUYA.64\ ci 25 patients in the NS.lNB group sbled gleller tlwl m imp!DYIIIlllllt in BSA campllld 1D 36\ rl 25 pllicm1J in tha PINA!JOUP. Colu mlll:h WIS Qrelller in the NB-IJIIB grrAip 1hm the PUYA group

Tabla , &. Comparison of Impetigo Vulgaris and Bullouslmpatigo


Impetigo Vulpris
Clinical Pnentation

Bullmalmpetiga

Acute purulent infaction which app1111rs V8Sicular; Scattered, thil-walled bullae containing dear yellow progresses to golden yellow or slightly turbid fluid with no surrounding erythema lesions surrounded by erythema trunk, intertriginous areas, face Sites: commonly face, anns, legs and buttocks

Etiology
Epidllliolagy

S. aunws, or both

Group A beta-hemolytic Stn!ptococcus (GAS I,

S. 8llllliJS group II elabarating exfoliating toxin

Preschoolllld young allllts livilg in crowded Neonates and older chillhn, can be epidemic conditions, poor hygiene, neglected minor trauma Infected eczema, HSV, varicella virus Bullous drug eruption, perqngus wlgaris, bLJious insect bites, thermal bums Same as impetigo wlgaris Cloxacillin for 7-1 0 days Topical antibacterial5 such a5 fu5idic acid or mupirocin; continue for 7-10 days after 01111 antibiotic is CQI11llication: hill! levels of toxin in irrmmocompromised or young children may lead to genaralillld skin pealing or staphyloccocal scalded skin syndrome (SSSSI

lnndgations Mln11111ment

Gram stain and culture of lesion fluid or biopsy Remove crusts, use saline compresses and topical antiseptic &aalai bid Topical antibacterials such as 2% mupirocin or fusidic acid 110; continue lor 7-10 days after resolution Systamic antibiotics such as cloxacillin or caphalaxin for 7-1 D days

D26 Denoatology

Heritable Disonlenllnfections

Toronto Notes 2011

DEEPER SKIN (DERMAL)


Table17. Comparison of Erysipel11 and Cellulitis
Elysipells
Clilic:al Presanllltian Involves upper dennis Confluent, erythematous. raised, warm well demarutad Very painU (once called St. Anthony's fire) Sites: lace and legs Systemic symptoms: fever, chills, headache, weakness (if prunnt. siiJl of mora &erious infuction)

Cellulitis
Involves lower derrnil/subcubmeaus fat Unilatenll erythematous flat lesion, Dften vasicl111 poor1y dellllltiiiBd. nDt Wliformy raised Tender Sites: commort( on legs Sysll!mic symptoms (Wlcornnon): fever, leukDcytosis, lyrrflhadenopathy

Etiology
Compli.:n-

GAS
Scar181 fever, ilnlptococcaiiJillgrune, 1at necrosis, coaguloplllhy Spreads via lymphatics

GAS, S. ameus (1.-ge sized wounds), H. Blfluenzae (p&riorbital), Pastsur&lle muJtocidl (doQI'cat billl)
Uncommon

Diffli...UI DiiiiRDiil

M (less red. less hat. smoother). superficial phlebitis, contact dennatitis, photosensitivity reaction. stasis dennatitis,

Same as erysipelas

IIIVBitiglliona

Same as erysipelas Clirical diagnosis: rarely do skin/blood culture If suspect necratimg do immsdiatu biopsy and frozen section, histopathology
1st line: panicillin, ciCXBcillin or cllfllmlin Znd lile: clindamycin or cephalexin If allergic to penicillin use erythromycin 1st line: cloxacillin or cehizclinlcephalaxin Znd line: erythromycin or clindamycin Chldren: ceflnxime If diabetes (folll infections): trimelhoprimsulfamethoxazole (lMP/SMX) and mlllronidazole

COMMON HAIR FOLLICLE INFECTIONS


Table 11. Comparison of Superficial Folliculitis, Furuncl11 and Carbuncles

Superficial Folkulitis
Clinical Preselltltion
Superficial infection of the hair follicle (wraus pseudofolliculitis: inllammlllion of follicle due 1D friction, irritation, or occlusion) Al:utelesion consists of a dome-shaped pustule Ill the mouth of hair follicle Pustule ruptures 1D form asmal crust Sites: primarily scalp, shoulders, arterior chest. upper back, other hairbearing !1"8118 Normal non-pathogenic bact&ria [Stuphytococcus - most common;

Furunc:la (Boila)
Red, hot. tender, inflnmatory nodules central 'f'llllowish point. which forms over summit and ruptures Involves subcutaneous tissue that arises from ahair follicle Sites: heir-bearing skin (thigh, neck. face, axillae. perineum. buttocks)

C..rbuncllll
Deep-saatud abscess formed by coalescing luruncles Usually in areas of thicker skin Occasionally ulcerates L111ions chin through multiple openings to the surfece Systemic symptoms may be associated

Etiology

Pseudanool3- hot tub)


Pityrosporom
M-g-11: Antiseptic Topicalllltibacterial (lusidic ecid. mupirocin, or erytiYornycin) Oral ciCXBcillin for 71 0 days Incise and dran large carbuncles to Same as for luruncles relieve pressure and pain Hafebrile: hot wet pack.s, topical antibiotic Hfebrll1/celulitis: culture blood and aspirate pustules (Gram stain and C&S) Cloxaciln for 1-2 weeks (especially for lesions near BXtemal auditory canal/ nose, with suiTOWiding cellulitis, and nDt responsive to topical therapy)

Dermatophytoses
Clinical Presentation infection of skin, hair and nails caused by dermatophytes (fungi that live within the epidermal keratin and do not penetrate deeper structures)

Pathophysiology digestion of keratin by dermatophytes results in scaly skin, broken hairs, crumbling nails Etiology

Trichophyton, Microsporum, Epidermophyton species (Pityrosporum is a superficial yeast)

Toronto Notes 2011

Infections

Dermatology D27

Investigations skin scrapings, hair, and/or nail clippings analyzed with potassium hydroxide (KOH) prep to
look fur hyphae and mycelia

Management
topicals as first line agents for tinea corporis/cruris and tinea pedis (interdigital type): e.g. clotrimazole or terbin.afine cream applied OD or BID, until one week after complete resolution oflesions oral therapy is indicated for onychomycosis or tinea capitis: e.g. terbinafine (Lamisil -liver toxicity; CYP 206 inhibitor) or itraconazole (Sporanox heart failure reported, CYP 3A4 inhibitor)

Tabla , 9. Diffarant Manir.statiDnl af DarmatDphyta lnfaetiDn


Clnic:al Praentlltilln TinA Ci!pitis

Diflnntial Diagnolil

Inlitigations Wood's light axarrination of hair. IJ!I!n llucrescence ort, for Micmsporum infl!ction Cullure Ill scaie&tlai' shaft MiC105CDpic IIXilllination of KOH preparation of scales or hair shafts

M1111g11111nt Griseofulvin x 8weeks or terbi!Bina (Lamisil 411 2-4 weeks x NB: oral agents are required to penetrate 1he hair root Adjunctiw antifungal shampoos or lotions may be helpful {e.g. selenium sulfide, ketllconOZDie, ciclopilllX)

Round, scaly petchBI Ill alopecia, Alopecia al'lllllll, psoriasis, possibly broken Dfl hain; pruritic seborrheic dermatitis. Sites: scalp, eyelashes, and eyebrows; 1richotillomania involving hair shafts and follicles Kerion {boggy, elevated. purulent inflamed nodui!Vplaquel may form secondary to infection by bacteria and result in scarring May hiMI occipilllllymphadanopathy Affects children (mainly black). inmmocompromised adult! 'Wf contagious and may be transmitted from barber, hats, theatre seats, pet& Pruritic, scaly, round/oval pi8Cf.!e with Granuloma annulzn, pityriasis actiw erythematous margin and cantral rosaa. psoriasis, seborrheic clearing dermatitis Site: trurt, limbs, face Scaly patc!Vplaque with a curved border and central clearing Pruritic, arylhematnus, dry/macaratad medialthigh Pruritic scaling and/or macaration of the web spaces and powdery scaling of soles Acute infection: inlllrdigillll (esp. 4th web spacal rvd/white &ealas, wsicles. bulae. often d maceration Secondary bacterial i'lection is common Clmic: non-pnritic, pink. scalilg laraiDsis on soles aoo sides of feet May present as lin-up of chronic tinea pedis Pllldi5p0sing factors: heat. occlusive footwell' Candidiasis (involvement of scrotum and satale lesionsI. contact dermatitis, arylhrasma

Tin Corporis (RilgwDnnl

Microscopic examinations of KOH prep of scales shows hyphaa Culture of scales Same as for tinea corporis

Topicals: 1% clotrimazole or 2% miconamla BID for 2-4 waaks

Tin Cruris ("Jock ltch1

Topicals: 1% ciDirimazole or 2% miconamle BID for 2-4 weeks

TinR Pldis
(Atllletl's FDGI)

Atopic darrnatitis, contact Sarna as for tinaa corporis dermatitis. dyshidrotic dermatitis. erythrasma, intl!rbigo (interdigital), psoriasis

Topicals: 1% ciDtrimazola or 2% miconamle BID for 2-4 weeks

Manuwn

Primary fungal infection of the hand is Atopic darrnatitis, contact rare; usually associa1ed with tinea pedis dermatitis, granuloma annulare, Acute: blisbn at edge of red arBBI on psoriasis hands Clmic: single dry scaly patch Crumbling. dirtally dystrophic nails; yallowish, opaque with subW'CjuBI hyperkeratotic debris Toenail infections usually precede fingernail infections T.lllbrum (90% of 1111 to-il irnctionsl Psoriasis, lichen planus, contact dermatitis, 1nlumstic onychodystrnphies, bacterial infections

Sarna as for tinaa corporis

Topicals: 1% ciDirimazola or 2% miconamle BID for 2-4 weeks

Tinea un.,.ium (Cinyc.omycolill

Microscopic examinations of KOH prep of scales from subungual scraping shows hyphae Culture of subungual scraping or nail clippings on Sabouraud's agar

Tarbinalina (lmlisil 41) (6 waaks for fingernails. 12 waaks for to-is) ltraconazole (Sporanox) 7 days on, 3 weeks Dfl (2 pulses for fingernails, 3 pulses for toenails) Topical: ciclopilllX (Penlac411; naillaquar

Parasitic Infections
SCABIES
Clinical Presentation
a transmissible parasitic skin infection due to Sarcoptes scabiei, a mite, characterized by superficial burrows, intense pruritus (especially nocturnal), and secondary infection primary lesion: superficial linear burrows secondary lesion: small urticarial crusted papules, eczematous plaques, excoriations sites: axillae, groin, buttocks, hands/feet (especially web spaces), sparing of head and neck (except in infants)

D28 Denoatology

Infections

Toronto Notes 2011

Pathogenesis scabies mite remains alive 2-3 days on clothing/sheets incubation of 1 month, then pruritus begins re-infection followed by hypersensitivity in 24 hours Etiology

Sarcoptes scabiei, a mite


risk factors: sexual promiscuity, crowding, poverty, nosocomial, immunocompromised

Differential Diagnosis asteatotic eczema, dermatitis herpetiformis (vesicles, urticaria, eosinophilia, no burrows), lichen simplex chronicus (neurodermatitis) Investigations microscopic examination of root and content of burrow with KOH fur mite, eggs, feces Management bathe, then apply permethrin 5% cream (i.e. from neck down to soles of feet (must be left on fur 8-14 hours and requires second treatment 7 days after first treatment) o change underwear and linens; wash with detergent in hot water cycle then machine dry o antihistamine o treat family and contacts o pruritus may persist fur 2-3 weeks due to prolonged hypersensitivity reaction LICE (PEDICULOSIS) Clinical Presentation o intensely pruritic red excoriations, morbilliform rash, caused by louse (a parasite) o scalp lice: nits (Le.louse eggs) on hairs red excoriated skin with secondary bacterial infection, lymphadenopathy o pubic lice: nits on hairs excoriations o body lice: nits and lice in seams of clothing excoriations and secondary infection mainly on shoulders, belt-line and buttocks Differential Diagnosis o bacterial infection of scalp, seborrheic dermatitis Management o permethrin 1% cream rinse) (ovicidal) or permethrin 1% (RC & Cor-, Kwellada-pe shampoo) comb hair with fine-toothed comb using dilute vinegar solution to remove nits repeat in 7 days after first treatment change clothing and linens; wash with detergent in hot water cycle then machine dry

Viral Infections
HERPES SIMPLEX
Clinical Presentation herpetiform (Le. grouped) vesicles on an erythematous base on skin or mucous membranes transmitted via contact with erupted vesicles or via asymptomatic viral shedding

primary
children and young adults usually asymptomatic; may have high fever, regional lymphadenopathy, malaise followed by antibody formation and latency of virus in nerve root ganglion

secondary
recurrent form seen in adults; much more common than primary prodrome: tingling, pruritus, pain triggers for recurrence: fever, sunburn, physical trauma, menstruation, emotional stress, upper respiratory tract infection (URTI) potential complications dendritic corneal ulcer erythema multiforme (EM) herpes simplex encephalitis HSV infection on atopic dermatitis causing Kaposi's varicelliform eruption (eczema herpeticum) 2 biologically and immunologically different subtypes: HSV-1 and HSV-2

Toronto Notes 2011

Infections

Dermatology D29

HSV-1 typically "cold sores" (grouped vesicles at the mucocutaneous junction which quickly burst) recurrent on face, lips but NOT on mucous membranes (unlike aphthous ulcers)
Management

...

Bllth HSV-1 and HS\1-2 can DCCII' on

fllce or genitalia.

treat during prodrome to prevent vesicle formation topical antiviral (Zovirax) cream, apply 5-6x/day,4-7 days forfacial/genitallesions oral antivirals are far more effective and have an easier dosing schedule

HSV-2 sexually transmitted; incubation 2-20 days gingivostomatitis: entire buccal mucosa involved with erythema and edema of gingiva vulvovaginitis: edematous, erythematous, extremely tender, profuse vaginal discharge urethritis: watery discharge in males recurrent on vulva, vagina, penis for 5-7 days diagnosis negative darldield. negative serology for syphilis, negative bacterial cultures Tzanck smear with Giemsa stain shows multinucleated giant epithelial cells tissue culture and electron microscopy of vesicular fluid skin biopsy antibody titres increase one week after primary infection only (no increase with recurrent lesions) DDx of genital ulcers: Ccmdida balanitis, chancroid. multiple syphilitic chancres
Management

rupture vesicle with sterile needle wet dressing with aluminum subacetate solution, Burow's compression, or betadine solution 1st episode: acyclovir 200 mg PO 5times a dayx 10 days maintenance: acyclovir 400 m.g PO BID famciclovir and valacyclovir may be substituted and have better enteric absorption in case ofherpes genitalis, look for and treat any other sexually-transmitted infections

HERPES ZOSTER (SHINGLES)


Clinical Presentation

unilateral dermatomal eruption occurring 3-5 days after pain and paresthesia of that dermatome vesicles, bullae, and pustules on an erythematous, edematous base lesions may become eroded/ulcerated and last days - weeks pain is pre-herpetic, synchronous with rash, or post-herpetic severe post-herpetic neuralgia often occurs in elderly Hutchinson's sign: involvement of tip of nose suggests eye involvement distribution: thoracic (50%), trigeminal (10-20%), cervical (10-20%); disseminated in HIV

... , ,
Herpes Zoster typically involves a single darmatoma; lesions randy Cf1lll the midline.

Etiology

caused by varicella zoster in a person who has already had the primary infection (chicken pox) risk factors: immunosuppression, old age. occasionally associated with hematologic malignancy
Differential Diagnosis before thoracic skin lesions occur, must consider other causes of chest pain

contact dermatitis, localized bacterial infection, zosteriform herpes simplex virus (more pathogenic for the eyes than varicella zoster)
Management

compress with normal saline, burrow's, or betadine solution analgesics (NSAIDs, amitriptyline) for patients over 50 years old. with severe acute pain or ophthalmic involvement: famciclovir or valacyclovir for 7 days or acyclovir for 7 days ifimmunocompromised; must initiate within 72 hours to be ofbenefit gabapentin 300-600 mg PO TID for post-herpetic neuralgia

D30 Denoatology

Infections

Toronto Notes 2011

MOLLUSCUM CONTAGIOSUM Clinical Presentation

discrete dome-shaped and umbilicated pearly, white papules caused by DNA pox virus (Molluscum contagiosum virus (MCV)) sites: eyelids, beard (likely spread by shaving), neck, axillae, trunk. perineum. buttocks
Etiology

Molluscum contagiosum is spread via direct contact, auto-inoculation, sexual contact


common in children and AIDS patients

Management topical cantharidin (a keratolytic) liquid nitrogen cryotherapy curettage Aldara (imiquimod): immune modulator that produces a cytokine inflammation WARTS (VERRUCA VULGARIS) (HUMAN PAPILLOMA VIRUS (HPV) INFECTIONS) Table 28. Different Manifestations ol HPV Infection
lleliniliDn and Cli1icll Fllllures

lliffaranlill
Molluscum contagiosum. sebollheic keratosis

Venue: Vulgaris

(Common Wlrtl)

Hyperkeratotic. elevated discrete epithelial growths with papilill8d surface caused by HPV - at least 80 types 818 known Located at1nluma sites: fingn, hands, knees of c:hillhn and teens Paring of surface reveals punctill8, red-brown spscks {dili118d capilaries) Hyperbratatic. &hiny, sharply rnarginill8d growtiJ& HPV 1,2, 4, 1D Located at pressure sites: heads of mellllarsal, heels. toes Paring of surface reveals r&d-brown spscks (capileries). inllrruptian of epidermal ridges Muftiple discndB, skin colourad, flat topped papules grouped or in linear configuration Common in children HPV 3, 10 Sites: fees, dorsa of hands, shin&, knees

Venuc:a Pllllflris
(Plantar Wvll)

Need to scrape ("para") lesions to differentiate wart from callus end com {see side bar DB)

llld

Venue: Palmaris (Pal011r W..rta) Venuc:a PIIIIIG IFiiltWarta)

Syringoma, seborrheic keratosis, molluscum contagiosum. lichen planus

Candylama ACIIninata (Genilllll Wart.)

Skirt-coloured pmead papules to soft cauliflower Condyloma Iiiii! (secondary le&ion. darkfiald like masses i1 clusters strongly +vel, Molluscum contagiosum HPV 6 and 11 HPV 16, 18, 31, 33 cause cervical dysplasia. squamous call cancer and invasive cancer Sites: genitalia end parianaleraas Oftsn occurs in young adults, infants, children Can be asymptomatic, lasting months to years Highly contagious, tla\Siritled sexually and nor.sexually {e.g. Koebner phenomenon viii scratching. shavilg), end can spread without clinically apparent lesions Investigations: acetowhitening (subclinical lesions S81111 with 5% ecatic acid x 5 minutes and hand lens) Complications: fairy-ring werts {satellite warts at pl!f1lhery of treated area of original warts)

Toronto Notes 2011 Table 21. Management of Warts


Mln1111m111t
Dasbuc:livll Li(Jlid nitrogenfeleclrodesiccation Surgery

Infections

Dermatology D31

Type of Wart
All Resistant Resistant Small, CQI!lmon Cornnon Genital

Nates Dyschromia, pain, 11h!O seconds Scar, recurrence and Nd: Vag lasers Klnlolytic irritation, blistErs, hyperpigmentation Irritation, blisters, scar Erythema, erosions, ulcers, pain Pain, 111illo8Wdyslrophy, Reynaud' ph1111omanon CauSBI an Erythema, I'IIIICtion erosion

.....

'9t-----------------, '

r-tmllll tar Slcin wn

Fint Unllhlrpla
Salicylic acid preparations (patches, solutions, ointments] Silver nitnJte stick Topical c.rtharone

Laser
C.ullic Acids
Cantharidin (topical) Mono-, artri-chiOiliCelic acid Chemlllharapalllic Agants Podophyllotoxin*

Glutalaldet!yde
Occlulive methods (duct tape]

s-mt u.,. Thenlpia


Topical imiquimod

Bleomycin (inlrlllllliollll)*
Hypenensitivity Aglllls Dilitrochlorobenzene (DNCB) lmmu111 Response Modilin 5% imiquimod cream

Cornnon
Cornnon, planlll' Genital All Cornnon Cornnon, planlll' Flat Resistant Cornnon, planlll'

1binl U1111 Tbagpi CLRUage

Cautery
SLQerY Law Oral cnn.tidina (particularly chidran]
Topical Topical tretinoin (flat warts] Localized heat lllenpy lnlnllalional bleomycin (plllnlllr werts]

Mitcell1111111111 No treatment Salicylic acid 40% minimum Tnllinoin (topical)* Cimetidile (oral)* Duct tape occlusiorv'callous scrapinQI'parilg
'Awid in pragnuq

65-911'!1. resolve spontaneously over years Ovarthe counlar (DTC), use with occulsion Irritation Best in children C811tharidin + podophyllin + salicylic acid

.....

',.-----------------, '

Trallllllllnt far Anopaital W.rts

Fim 11111 thllfapies


lmiquimod 5% cra11111 PodophyDotoxin (solution, cream, or gel) PodophyDin rasin

Yeast Infections
CANDIDIASIS

Cryolharapy
Second IIIII tlllrapill Trichloroacetic acid Topica15-ftuo1111ncil
Eltctrodnsication Surgical excision (with cold steal or scissors]

Candida! Paronychia
painful red swellings of periungual skin management: topical agents not as effective; oral antifungals recommended macerated/eroded erythematous patches that may be covered with papules and pustules, located in intertriginous areas often under breast, groin, or interdigitally peripheral "satellite pustules predisposing factors: obesity, diabetes, systemic antibiotics, immunosuppression, malignancy starts as non-infectious maceration from heat, moisture and friction management: keep area dry, miconazole, ketoconazole/clotrimazole cream bid until rash clears
PITYRIASIS (TINEA) VERSICOLOUR

Candida! Intertrigo

chronic asymptomatic superficial fungal infection with brown/white scaling macules affected skin darker than surrounding skin in winter, lighter in summer (does not tan) sites: upper trunk most common

Clinical Presentation

Pathophysiology
microbe produces carboxylic acid --+ inflammatory reaction inhibiting melanin synthesis yielding variable pigmentation affinity fur sebaceous glands; require fatty acids to survive

Etiology Pityrosporum ovale (Malassezia furfur)

also associated with folliculitis and seborrheic dermatitis predisposing factors: summer, tropical climates, Cushing's syndrome, prolonged corticosteroid use

Investigations
microscopic examination KOH prep of scales for hyphae and spores

Management
scrub off scales with soap and water selenium sulfide body lotion ketoconazole cream or PO daily for 10 days if more extensive

.....

''

Oral Tl!binllfina (LimisiP'] is not ellective because nis nat secnrted by sebaceous glands.

D32 Denoatology

Infections

Toronto Notes 2011

Sexually Transmitted Infections


SYPHILIS

Clinical Presentation characterized initially by a painless ulcer (chancre) following inoculation, systemic infection with secondary and tertiary stages Etiology

Treponema pallidum
transmitted sexually, congenitally, or rarely by transfusion

,,

Tabla 22. Stages of Syphilis


Primary Syplilis Clinical Presantmion Silgle red, indurated, painless chnre, that develops into painless ulcer with raised border and scanty serous exudate Chancre at site of ilocullllion after 3 weeks of D:ubation and h1111ls in 4-6 weeks; chancre may also develop on lips or anus Regional non-tender lymphadenopathy appears < 1 week after onset of chancre DDx: chancroid (painful), HSV (multiple lesions) Secondary Syphilis

Nllural Hiltory of Untrlllted Syphilil Inoculation Primary syphilis (1 B-90 daftsr infaction) Sacondll'( syphilis (simultanaous to primary syphilis or up to 6 mo after healing of primiiY lesion) Latent syphilis Tartillry syphilis [2-20 y)

Tartilry Syphilis

....

Lmnt Syphllil The period between healing of clinical lesions and appearance of 111111 miiiiDutions. 711'11. of untnsllllld patienb; will remain in this stage fur the mt of thair livaa and 11n1 immuna to new primary infection.

Presents 2-6 months after primary Extremely rare infection (patient may not recall 31 years attar secondary Main skin lesion: 'Gumma'- a of primary chancre) Associated with generalized granulomatous non-tender lymphadenopathy, splenomegaly, nodule headache, chils, fever, arlhralgias, myalgies, malaise, phatophobill Lesions heal in 1-S weeks and may recur for 1 year 3 types of lesions: 1. Macul85 and papul85: flat top, sceling, nan-pruritic, sharply defined, circular/annular rash (DDx: pityriasis rosea, tinea corporis, drug eruptions, lichen planus) 2. Condyloma lata: moist papules around genitaV peria1111l region 3. Mucous patches: macerated patches mainly found in oral mucosa

lnvatigations

CANNOT be based on dinical VORL positive presentation alone FTA-ABS +ve; -w after 1 year VORL negative- rapeat weekly following appennce of chancre for 1month Darklield +ve in all secondary Auorescent treponanal antibody-syphilis (FTA-ABSI test has jJ8ilter and may detect disease earlier in course Darklield examination spirochete in chancre fluid or lymph node aspirate Panicilin G, 2.4 million unils IM, single dose

As in prinary syphilis, WRL can be falsely negative

Mlnlg-11:

As far primary syphilis

Traalment: panicillin G, 2.4 million units IM weekly

GONOCOCCEMIA Clinical Presentation disseminated gonococcal infection hemorrhagic, tender, pustules on a purpuric/petechial background sites: distal aspects of extremities associated with fever, arthritis, urethritis, proctitis, pharyngitis and tenosynovitis neonatal conjunctivitis if infected via birth canal Etiology

Neisseria gonorrheae
Management notify Public Health authorities screen for other sexually transmitted infections (STis) cefu:ime 400 mg PO (drug of choice) or ceftria.xone 125 mg 1M

Toronto Notes 2011

Pre-Malignant Skin Conditioll8/Malignant Skin Thmours

Dermatology D33

Pre-Malignant Skin Conditions


actinic keratosis: 1-10% become squamous cell carcinoma (SCC) dysplastic nevi: risk of malignant melanoma (see Table 5}

Leukoplakia
Clinical Presentation a morphologic term describing homogenous or speckled white plaques with sharply demarcated borders sites: oropharynx, most often floor of the mouth, soft palate, and ventraUlateral surfaces ofthe tongue Pathophysiology precancerous or premalignant condition oral form is strongly associated with tobacco use and alcohol consumption Epidemiology 1-5% prevalence in adult population after 30 years of age; peak at age 50 M>F, fair-skinned most common oral mucosal premalignant lesion Differential Diagnosis lichen planus, oral hairy leukoplakia Investigations biopsy is mandatory because it is premalignant Management low risk sites on buccaUlabial mucosal or hard palate: eliminate carcinogenic habits, follow-up moderate/dysplastic lesions: excision, cryotherapy

Malignant Skin Tumours


Basal Cell Carcinoma (BCC)
--------------------------......

Subtypes noduloulcerative (typical} skin-coloured papule/nodule with rolled, translucent ("pearly"} telangiectatic border and depressed/eroded/ulcerated centre pigmented variant flecks of pigment in translucent lesion with surface telangiectasia may mimic malignant melanoma superficial variant flat, tan to red-brown plaque, often with scaly, pearly border and fine telangiectasia at margin sclerosing variant flesh/yellowish-coloured, shiny papule/plaque with indistinct borders Pathophysiology malignant proliferation ofbasal cells ofthe epidermis low grade cutaneous malignancy, locally aggressive (primarily tangential growth}, rarely metastatic usually due to UVB light, therefore >80% on face may also be caused by scar formation, radiation, trauma, arsenic exposure, or genetic predisposition (Gorlin syndrome) Epidemiology most common malignancy in humans 75% of all malignant skin tumours >40 years, increased prevalence in the elderly M>F, skin phototypes I and II, chronic cumulative sun exposure Differential Diagnosis benign: sebaceous hyperplasia, intradermal melanocytic nevus, dermatofibroma malignant: nodular malignant melanoma, sec

,...-----------------, ,

Wol'll-ql of Non11111lanoma Skin Cancer (NMSCI

HistDry: duration, growth rata, family/ personal hx of skin cancer, prior thanpy to the particular lesion.
Phyaiclll: location, &izu, whsther circumscriled, tethering to deep structures, full skiliXIIIIl, lymph node

axam

if shallow lesion do shave biop&y; othurwi&e punch biop&y.

.....

,.. ,

Margi Smallar liana: alectrodesicclllion and curatblge with 2-3 mm margin of normal skin. DHp mtiltratin IHiana: surgical excision with 3-5 mm margins beyond visible and palpable tumour border; may require skin graft or flap.

D34 Denoatology

Malignant Skin Tumours/Malignant Skin Tumours

Toronto Notes 2011

Management imiquimod 5% cream (Aldara) or cryotherapy is indicated for superficial BCCs on the trunk shave excision +electrodesiccation and curettage for all other types ofBCCs microscopically controlled, minimally invasive, stepwise exicison (Mohs surgery) or radiotherapy for lesions on the face or in areas that are difficult to reconstruct life-long follow-up 95% cure rate if lesion <2 em in diameter

Cutaneous T-Cell Lymphoma


Clinical Presentation Mycosis fungoides (limited superficial type) characterized by: erythematous patches/plaques/nodules/tumours, which may be pruritic and poikilodermic (atrophy, telagiectasia, hyperpigmentation) common sites include: trunk, buttocks, proximal limbs mildly symptomatic. usually excellent prognosis for early disease Sezary syndrome (widespread systemic type) rare variant characterized by: universal erythroderma ("redman syndromeD), lymphadenopathy, WBC >20 x 109/L with Sezarycells associated with intense pruritus, alopecia, palmoplantar hyperkeratosis, and systemic symptoms (fatigue, fever) often fatal Pathophysiology clonal proliferation of skin-homing CD4 T cells Epidemiology >50 years old, M:F 2:1 Differential Diagnosis tinea corporis, nummular dermatitis, psoriasis, discoid lupus erythematosus, Bowen's disease Investigations skin biopsy (histology, "lymphocyte antigen cella markers, TcR gene arrangement) blood smear looking for Sezarycells or flow cytometry(e.g. CD4:CD8 >10 is Sezary) imaging (for systemic involvement) Management Mycosis fungoides treatment is dependent on stage of disease topical steroids and/or PUVA, narrow band (311-313 mm), UVB (NBUVB) Sezary syndrome oral retinoids and interferon extra-corporeal photophoresis may need radiotherapy for total skin electron beam radiation may maintain on UV therapy

Malignant Melanoma (MM)

-----------------------------------------

Clinical Presentation malignant characteristics of a mole: see mnemonic "ABCDED sites: skin, mucous membranes, eyes, CNS
D-1his PaMnt h1011a Mu.. ur

Mal111011111?
.lAMA 1998; 279!91: 696-701

ABCDE c:hac:lclilt
Asymmlltry

Border {irragularl

Diameter (increasing or >6 mml Enlargement, elevation, evolution Sensitivity 92% (CI 82-96%1 Specificity 100% [CI 54-1 OO'lf.l

Colour !Vllriudl

Subtypes of Malignant Melanoma lentigo mallgoa malignant melanoma in situ (normal and malignant melanocytes confined to the epidermis) 2-6 em, tan/brown/black uniformly flat macule or patch with irregular borders lesion grows radially and produces complex colours sites: face, sun exposed areas 1/3 evolve into lentigo maligna melanoma lentigo maligoa melanoma ( 15% of all melanomas) malignant melanocytes invading into the dermis associated with pre-existing solar lentigo, not pre-existing nevi flat, brown, stain-like, gradually enlarging with loss of skin surface markings with time, colour changes from uniform brown to dark brown with black and blue found on all skin surfaces, especially those often exposed to sun

Toronto Notes 2011

Malignant Skin Tumours

Dermatology D35

superficial spreading melanoma (60-70% of all melanomas) atypical melanocytes initially spread laterally in epidermis then invade the dermis irregular, indurated, enlarging plaques with red/white/blue discolouration, focal papules or nodules ulcerate and bleed with growth nodular melanoma (30% of all melanomas) atypical melanocytes that initially grow vertically with little lateral spread uniformly ulcerated, blue-black, and sharply delineated plaque or nodule rapidly fatal acrolentiginous melanoma (5% of all melanomas) ill-defined dark brown, blue-black macule palmar, plantar, subungual skin melanomas on mucous membranes have poor prognosis Pathophysiology malignant neoplasm of pigment forming cells (melanocytes and nevus cells) Epidemiology incidence 1:100 risk factors: numerous moles, fair skin, red hair, positive personal/family history, large congenital nevi, familial dysplastic nevus syndrome most common sites: back (males), calves (females) worse prognosis if: male, on scalp, hands, feet. late lesion, no pre-existing nevus present Differential Diagnosis benign: nevi, solar lentigo, seborrheic keratosis malignant: pigmented BCC Management excisional biopsy preferable, otherwise incisional biopsy remove full depth of dermis and extend beyond edges oflesion only after histologic diagnosis beware oflesions that regress - tumour is usually deeper than anticipated lymph node dissection shows survival advantage if nodes uninvolved chemotherapy (cis-platinum, BCG), high dose interferon for stage II (regional) and stage III (distant) disease radiotherapy may be used as adjunctive treatment
Table 23. American Joint Committee on Cancer Staging System Based on Breslow's Thickness of Invasion
T1 <1.0mm T2. 1.01-2.0 mm T3 2.01-4.0 mm T4 >4.0mm Stage I T1a- T2a Stage II T2b -T4b Stage Ill any nodes Stage IV any melll 5-year survival 911% 5-year survival 711% 5-year survival 45% 5-year survival 1ll%
11:1

Risk Factors fer Mellnom no SPF in SIN Sun exposure Pigment hits {blue eyes, fllir/red hl.ir, pale complaxion) Fraclding Skin reaction to sunligtrt {increuad incidence of sunburn) lmm111osuppressive states {e.g. renal 1nnsplantation) Nevi (dysplastic nevi; increased number of benign malanocytic nevi)

... , ,

Node Dissllction lor LlsioM > 10 mm Assess sentinel nodes If macroscopically or microscopically positive, a lymph node dissection should be prefonned prior to wide excision of 111e primarv melanoma to ensure accurate lymphatic mapping.

.-----------------,

a = no ulceration; b = ulceration

Squamous Cell Carcinoma (SCC)

----------------------

Clinical Presentation indurated erythematous nodule/plaque with surface scale/crust. and eventual ulceration more rapid enlargement than BCC sites: face, ears, scalp, forearms, dorsum of hands Pathophysiology malignant neoplasm ofkeratinocytes (primarily vertical growth) predisposing factors include: UV radiation, PUVA, ionizing radiation therapy/exposure, chemical carcinogens (such as arsenic, tar and nitrogen mustards), HPV 16, 18, immunosuppression Epidemiology second most common type primarily on sun-exposed skin in the elderly, M>F, skin phototypes I and II, chronic sun exposure in organ transplant recipients sec is most common cutaneous malignancy, with increased mortality Differential Diagnosis benign: nummular eczema. psoriasis, irritated seborrheic keratosis malignant: keratoacanthoma, Bowen's disease, BCC

D36 Denoatology

Malignant Skin 1\unours/Alopecla (Hair Lou)

Toronto Notes 2011

Management surgical excision with primary closure, skin flaps or grafting lifelong follow-up (more aggressive treatment than Bee) Prognosis good prognostic factors: immediate treatment, negative margins, and small size of lesion sees that arise from actinic keratosis metastasize less frequently (-1 %) than other sees (e.g. arising de novo in old burns) (2-S% of cases) overall control is 7S% over 5 years, 5-10% metastasize
BOWEN'S DISEASE (SQUAMOUS CELL CARCINOMA IN SITU)

Clinical Presentation erythematous plaque with a sharply demarcated red and scaly border often 1-3 em in diameter and found on the skin and mucous membranes evolves to sec in 10-20% of cutaneous lesions and >20% of mucosal lesions Management same as for Bee biopsy required for diagnosis topicalS-tluorouracil (Efu.dex) or imiquimod (Aldara) used if extensive and as a tool to identify margins of poorly defined tumours shave excision with electrodesiccation and curettage

Alopecia (Hair Loss)


Hair Growth
It'

lllirl.nl TOP HAT Telogen ElflwiLm, tilea capitis Out of Fe,ln Physical"com-row" bnliding Hormonal- hypothyroidism, androgenic Autoimmune- Slf, Tmcins- huvy mltll1, anticoeguillnts, chemothanpy, V"lt A, SSRI1

hair grows in a cyclic pattern that is defined in 3 stages 1. growth stage = anagen phase

2. resting stage = telogen phase 3. degenerative stage = catagen phase total duration of the growth stage reflects the type and location of hair: eyebrow, eyelash, and axillary hairs have a short growth stage in relation to the resting stage growth of the hair follicles is also based on the hormonal response to testosterone and dihydrotestosterone (DIIT): this response is genetically controlled

Non-Scarring (Non-Cicatricial) Alopecia


PHYSIOLOGICAL

Clinical Presentation male-pattern alopecia (androgenic alopecia) fronto-temporal areas progressing to vertex, entire scalp may be bald Pathophysiology action of testosterone on hair follicles Epidemiology early 20's-30's (female androgenic alopecia is diffuse and occurs in 40's and SO's) Management minoxidil (Rogame) lotion to reduce rate ofloss/partial restoration spironolactone in women (anti-androgenic effects), cyproterone acetate (Diane-3s) finasteride (Propecta) (S-a-reductase inhibitor) 1 mgld in men hair transplant
PHYSICAL

trichotillomania: impulse-control disorder characterized by compulsive hair pulling with irregular patches of hair loss, and with remaining hairs broken at varying lengths traumatic (e.g. tight "com-row" braiding of hair)

Toronto Notes 2011

Alopecia (Hair Loss)

Dermatology D37

TELOGEN EFFLUVIUM
Clinical Presentation
uniform decrease in hair density secondary to an increased number of hairs in resting stage (telogen stage)

......

'

follicl1111 on IIXIIm -+ biopsy not requillld. Scring lllupecill: llbsent hair follicles on IIXIIm -+ biopsy raquinld.

Non--rma ICIIIICia: intact hair

Pathophysiology precipitated by: malnutrition, Fe deficiency, thyroid dysfunction, post-partum/miscarriage,


scalp diseases (seborrheic dermatitis, allergic contact dermatitis), medications (e.g. OCP), physical!mental stress, Fe deficiency hair loss typically occurs 2-4 month after exposure to precipitant regrowth occurs within a few months but may not be complete

......

DDx of No1HC8rring Alopeci

Aulnimmune Alopacill arealll Endocrine

ANAGEN EFFLUVIUM
Clinical Presentation
hair loss due to insult to hair follicle impairing its mitotic activity (growth stage)

Hypotllynoidism
Androgens Micronutrient deficienci1111

Iron
Zinc Toxins Heavy rnebU Anticoagullllll Chemo1herapy VrtaminA

Pathophysiology precipated by chemotherapeutic agents (most common}, other meds (bismuth.levodopa,


colchicine, cyclosporine}, exposure to chemicals (thallium, boron, arsenic) dose-dependent effect hair loss 7-14 days after single pulse of chemotherapy; most clinically apparent after 1-2 months reversible effect; follicles resume normal mitotic activity few weeks after agent stopped

Trauma to 1he hair follicle


Trichotllomanill 'Com-row' bniding Other Severe illn8SS

Childbirth

ALOPECIA AREATA
Clinical Presentation
autoimmune disorder characterized by patches of complete hair loss localized to scalp, eyebrows, beard, eyelashes alopecia totalis -loss of all scalp hair and eyebrows alopecia universalis -loss of all body hair associated with dystrophic nail changes - fine stippling "exclamation mark" pattern (hairs fractured and have tapered shafts, i.e. looks like "!") may be associated with pernicious anemia, vitiligo, thyroid disease, Addison's disease spontaneous regrowth may occur within months of first attack (worse prognosis if young at age of onset and extensive loss) frequent recurrence often precipitated by emotional distress

Management
generally unsatisfactory intralesional triamcinolone acetonide (corticosteroids) can be used for isolated patches UV or PUVA therapy imm.unomodulatory (diphencyprone)

......_._______________ '
DDx of Sallmlg (aianlcill Alopellill

Scarring (Cicatricial) Alopecia


Clinical Presentation
irreversible loss ofhair follicles with fibrosis

Developmenmi/Heredilary Disorders
Aplasia cutis conganila Epidennal nevi Romberg's ryndr011111 Genlnllized follicLJar hamartoma Primary caus1111

Etiology
physical: radiation, bums infections: fungal, bacterial, TB, leprosy; viral (herpes zoster) inflammatory lichen planus (lichen planopilaris} discoid lupus erythematosus (DLE} (note that SLE can cause an alopecia unrelated to discoid lupus lesions which are non-scarring) morphea: "coup de sabre" with involvement of centre of scalp

Group 1: Lymphocytic
Lupus urythematosus Lict.n plllnopillris

Clllnic Pseudopalllde Group 2: Neutrophilic


FoUiculitis declllvans

Group 3: Mixlld
Acne k!loidalis nuchae Secondary C8USIIS Infectious agents Bacturial (i.e. post-callulitis) Fungal (i.e. tinea capitis) Neopla&ma (i.e. BCC, SCC, Lymphomas, and metastatic Physiallagants Mechanical tnuma Bums

Investigations
biopsy from active border

Management
infections: treat underlying infection inflammatory: DLE treated topical/intralesional steroid or antimalarial

Radiotherapy C-uatic chemicals

D38 Denoatology

Nails and Disorders of the Nail Apparatus

Toronto Notes 2011

Nails and Disorders of the Nail Apparatus


Table 24. Nail Changes in Systemic and Dennatological Conditions
Nil Abna11111lity
Dafinition/EtioiiJIW

Associltld DiISI
Cyanotic heart disease. bacterial endocarditis. pulmonll'( disorders, Gl disorders, etc.

NAIL PLATE CHANGES


Clubbing Kaiiiiii'{Chia Onycholysis Onychogryphosis Onychohemia Onychomycosis Onychocryptosis (III!J1IWII toenail Proximal nail plate has greal!!r 1han 180 degree to nail fold, watch"{llass nails, bLJbous digils Spoon shaped nails Sepanrtion of nail plate from nail bed Hypertrophy of 1he nail plate and subungal hypertenrtosis SubuiiiJIIII hematoma Fungal iriaction of nail (e.g. dermatophyte, yeast. mould) Often hallux with congenital malalignment. painfij inflammation. granulation tissue Distal margn has v-shaped indentation Distal nail plate does not sapanrte from nai bed Punctate depressions 1hat migrate distally with growth

11111 deficiency, malnutrition, dillbsllls


Psoriasis, dermatophytes, thyroid disease Poor circLJation, chronic irlllmnation, tinea Trauma to nail bed HIV, diabetes, piii1Jheral arterial disease light fittilll shoes, excessive nail clipping

SURFACE CHANGES
Wedge shaped Darier's disease (follicular dyskeratosis) Scleroderma Psoriasis, alopecia areata. eczema

Pterygium inversus unguium


l'itlilg

Transverse ridging Transvene white lines

of nail plate
COLOUR CHANGES
Yellow Green Black Brown Splirter hemorrhages

Transverse depressions often more in central portion Serious acute illness slows nail growth (Beau's Iiles), eczuma, chronic paronychia. trauma Poisons, hypoelbuminemia (Muhetb's lines) linea, jaundice, telracycline, pityriasis rubra pilaris, yellow nail synome

Bands of white discalouration

Pseudomonas
Melanoma, hematoma Nicotine use, psoriasis, poisons Extravasetion of blood from longitudinal vessels of nai bed Blood attaches to nail plate and moves distally as it grows Brown-yellow discolouralian HSV infection of dstal phalanx Local inflammation of 1he nail fold around the nail bed Cuticular hemorrhages, roughness, capillary chang as Trauma, bacterial endocarditis, blood dyscrasias, psoriasis

Oil spots

Psoriasis Gerital herpes infection

NAIL FOLD CHANGES


Herpetic whitlow Paronychia

Acute: painful infection


Chronic: constant wetting {e.g. dishwashing, thumbsuckilll) Scleroderma, SLE

Nail fold telangiectasias

Toronto Notes 2011

Skin Manifestations of Systemic Disease

Dermatology D39

Skin Manifestations of Systemic Disease


Tabla 25. Skin Manifllltationa of Internal Conditions
Dilell8

Rallllld D1111111Du1
Painful apthous ulcers in oral cavity genital mucous membrales, erythema nodosum Superficial migratory thnontophlebitis. cyanosis, gqrene, ulcerations
It'

AUTOIMMUNE DISORDERS
Behs disease Buerger's disease Dermatomyositis

Periorbital and perioral violaceous erythema, heliotrope with edema. Gottron's papules (violaceous ftat-topped papules with atrophy), periungual erythema, telangiectasia, calcinosis cutis Polyarbritic noll.IIB5, &t&llirte purpura, urytherna, gangrena, 5plirt11r hamanhages, liwdo raticula'is Petechiae, urticaria, erythema nodosum, rheumatic noWies Raynaud's, nonpitting edema, waxy/shiny/tense atrophic skin (morphea), ulcers, cutaneous calcification. periungual telangiectasia, acrosclerosis Malar erythema, discoid rash (erythematous papules or plaques with keratotic scale, follicular plugging, atrophic scarrilg on face, hillds, and anns), hemonhagic bulae, palpable purpura, urticarial purpura, patchy/diffuse alopecia, mucosal ulcers, photosensitivity Pyudlll'rll8 gangrano&UIIl, erythBillB nodosum Genaralized hyperpigmentation or limitad to skin folds, buccal mucosa and scars Moon facies, purple sbiae, acne, hyperpigmentation, hirsutism, atrophic skin with telangiectasia Infections (boils, carbuncles. Cllldidiasis, S. aureus, dermatophytoses. tilea pedis 111d cruris, ilfectious eczematoid dermatitis), pruritus. eruptive xanthomas, necrobiosis lipoidica diabaticorum, granuloma annulare, diabatic foot. diabBtic bulaa, acanthosis nigricans, calciphylaxis Moist warm skin, seborrhea, acne, nail atrophy, hyperpigmentation, toxic alopecia, pretibial myxedema, acropachy, onycholysis Cool, dry, scaly, thiclrBned, hyplll'pigmented skin; toxic alopecia with dry, coarse hair, brittle nails, myxedema, loss of lateral1/3 eyebrows

Rayu.ud's Phllno11111nan DDx


COlD HAND Cryoglobulini;/Cryofibrinogans ObstructioWOccupationll Lupus arythamatasus, other connective tiuue disease Diabstes mallitulllllrugs Hematologic problams (polycythamia, leukemia, ell:) Arterial problems (alherosclerosis) Neurologic problems (vascular tone) DiseiUIII of unknown origin !idiopathic)

Polyarteriti& nodO&a
Rheumatic fever Scleroderma Systemic lupus etylhematosus

Ulclllllliw colitis (UC)

ENDOCRINE DISORDERS
Addison's disease Cushing's syndrome Diabetes mellitus
...._' I

9,.-----------------,

Acantholis Nigrit:An asymptamatic dar1t thickened velvety hyparpigmantation of fiBXIIral skin most commonly around the neck. Associated

Hyperthyroidism Hypothyroidism HIV-RELA'IED Infections

with diabstes, obesity and other

endocrine disorders and malignancy. It is a cutanaous marbr of tissue insulin resismnce.

Viral (HSV. HZV, HPY. cytomegalovirus, molluscum contagiosum, oral hairy leukoplakia), bacterial (impetigo, acneiform folliculitis. denllll caries, cellulitis, bacillary epithelioid angiomatosis, syphilis), ather (candidiasis)
Seboi'Thea, psoriasis. pityriasis rosea, vasculitis

lnftammatory dermatoses Malignancies

Kaposi's sarcoma, i'r'n1Jhoma, BCC, SCC, malignant melanoma

MAUGNANCY
Adenocarcinoma Gastrointestinal (Gil Cervix/anus/rectum Cancinoma Breast Gl Thyroid BrearVGU/IunQ/DVllry Peutz-Jeghars: pigrnanted maculas on lipli/oral mucosa Paget's Disease: eroding scaling pla!Jies of perineum Paget's Disease: eczematous and crusting lesions of breast Palmoplantar keratoderma: thickened ski1 of palmli/soles Sipple's SyncRma: multiple mucosal neuromas Dlll'llllltomytJ8itis: heliatropa of ayalids and purplish plaquas DVllr knucldas Ataxia Telangiectesia: telangiectasia on pinna, bulbar conjunctiva Ichthyosis: generalized scaling especially on extremities Bloom's syndrome: butterfly etylhema on face, associated with short stature Amyloidosis: la11Je, smoath tongue with waxy papules on syelids, nasolabii111olds illd lips, as well as facial petechiae

Acute Leukemia

Multiple Myaloma

DTIIERS
Liver disease

Pruritus, hyperpigmentation. spider lle'Ji, palmar erythema, while nails (Terry's nails), porphyria cutanea tarda, xanthomas, hair loss Pruritus, pigmentation, half and half nails
Erythematous papules or urticarial plaques in distribution of striae distensae: buttocks, thighs, upper inner arms and lower backs Palpable purpura in cold-exposed areas. Reynaud's, cold urticaria, acral hemorrhagic necrosis, bleeding disordars, associated with hepatitis Cinfection

Renal disease
Pruritic urticaria papules and of pregnancy Cryoglobulinemia

D40 Denoatology

Pecliatrlc: E:unthems

Toronto Notes 2011

Pediatric Exanthems
It'

Itchy Eruptione il Childhood

Definitions exanthem: an eruption on the skin occuring as a symptom of a systemic disease typically with a fever enanthem: an eruption on a mucous membrane occuring in the context of an exanthem Table 26. Common Pediatric Exanthem
Eunthem Etiology
Human herpes virus (HIN)3 Incubation 10-2.1d, Communicable 1-Zd Pre-rash to Sd post-rash Clilicalllelcription Diffuse vesicular pustular beginning on thorax spreading to lmpoltant Co11plication Necrotizing fasciitis, er.:ephalitis, cerebellar ataxia, disseminated intravascular coagulation (DIC), hepatitis Supportive therapy, Acyclovir severe, Varicella Zoster immunoglobulin (within 96 hrs Dl contact), Varicela vaccine Supportive care mr majority Serious cases (irrmunosuppriiBSed) can be 1ntated pleconaril No 1reatnur1t: clildren oftan feel wall NSAIDs mr symptomatic arthropathy

UC-SCAB
Urticaria Canlllct dermatitis

Scabies Chicksn pox Atopic dennatitis


Bitn

New lesions wery Enanthems

Entarovhl

EnllrDviruses Polymorphous rash None Most conmon exanthem (macules, papules, vesicles, in summer and fall pBIBchiae, urticaria) Plrvavirus 819 Slapped cheeks (rad, Incubation 4-14d flushed cheaks)then Paaks in winter and sprilg 1-4 days IIIIer lacy/raticular maculo-papular rash Dl trunlr/axtremities STAR complex (Sore Tlroat, Artllilis, Rash) Fetal infection (anemia. fatal hydrops or death) Aplastic crisis in siclde cell patients None

Erythema

lnfectiolum

Gilnafti.Cnllti Epstein-Bill virus most Symmetric papular Synd111111 conmon, hepatitis B, of face, buttocks, cDXSaCkie, parvovirus and extremities Spring and early summer
Hand, Foot

Supportive treatment

and Malllll Disalltl


Kawasaki

Coxsackie A and Bviruses Vesicular eruption Dl Hijiy contagious virus palms and soles with an erosive stomatitis No proven viral etiology, but infllctious etiology suggested Superantigen toxin mediated bacterial process proposed Late wilter to spring l'lnnyxovirus Incubation 10-1 4d Communicable 4d before and after rash

Pulmomry, neurological death

Supportive treatment

Disa11t1

,.....

Fever> 5 days and 4/5: Most common cause of Aspirin, intravenous unilateral lymphadenopathy; vasculitis and acquired immunoglobulin, baseline pufty/red palms and soles; heart disease in clildren echo and repeat in 6 weaks red, cniCked lipt/strawberT'f CNS, Gllnlct, kidney, eyes tongue; skin rash; non purulent bilateral conjunctivitis Erythematous macular beginning on head and spreading downwards, deslJlllmeteS. no palm or sole involvement Enanthem: Koplik spots (grey/white papules on buccalll'lJcosa) Pink maculss and papulas on trur*. neck. pnlXimal extremities, and occasionally face Eruption aftEr high fever ends 1-5 daysmllowing mild prodrome /lever, headache, respiratory symptoms), a pink maculo-papular rash erupts on face Slfl!llding in a caphalocaudal direction Occipital and nrtroauricular nodas Otitis media. pnewnonia, er.:ephalitis, SJS, glomerular nephritis, Vitamin A. irrmunoglobulin, measles/ITIJII1ps/rubella (MMR) vaccine

RaiiiCIII

HHV6,HHV7 Incubation 9-1 Od

Neurological involvement Viral reactivation in immunosuppressed patients STAR complex Congenital rubella (cataract, glaucoma. thrombocytopenia, hepatitis, deafness. congenital heart disease)

Supportive treatment Antipyretics during 1he febrile pariod

Rubella

RNA virus Dlthe Togaviridae famly Incubation 16-1 8d

Supportive treatment MMR vaccine Serologic testing in rubellaexposed pregnant women

Scarlet Fever Group A beta-hemolytic


streptococci toxin types A, B,and C Late fall, winter, and

Generalized rash, red Mastoiditis, otitis, sinusitis, 10-1 4 day course of papules, sand-paper" pneumonia, meningitis, penicillin myocarditis, arthritis, textura, dasquamation. hepatitis, rheumatic fever, flexural accentuation, enanthem {strawbeny and gomerulonephmis tongue. petechiae on palate) Pastia's Iiles -linear petechial streaks i'1 axillary, and antecubital ereas

Toronto Notes 2011

Dermatology D41

Miscellaneous Lesions
Angioedema and Urticaria
Angioedema
deeper swelling of the skin involving subcutaneous tissues; often involves the eyes, lips, and tongue may or may not accompany urticaria hereditary or acquired forms hereditary angioedema (does not occur with urticaria) onset in childhood; 80% have positive family history recurrent attacks; 25% die from laryngeal edema triggers: minor trauma, emotional upset, temperature changes treatment prophylaxis with danazol or stanozolol epinephrine pen to temporize until patient reaches hospital in acute attack

......

.. ,

Whaal Typically arythamalllus flat-lllppad, palpable lesions wrying in size circumscribed dermal edema lndividlllllesion lasts < 24 hrs Associated with mast cell release of histamile May be pruritic

Urticaria
also known as "Hives"; see Table 27 for classification transient, red, pruritic well-demarcated wheals each individual lesion lasts less than 24 hours second most common type of drug reaction results from release of histamine from mast cells in dermis can also result after physical contact with allergen

Tabla 27. Classification of Urticaria

Acute Urticaria >2/3 of cases Attacks last <6 weeks Individual lesions last <24 In

Drugs - especially aspirin. NSAIDs Foods - nuts, shellfish, eggs, fruit Idiopathic Infection

IE'

DDx fur UrtiCllria

Insect stings
Percutanous absorption - cosmetics, wart exposures

Stress
Systemic disiiiiSes - systemic lupus erythBilllltosis {SL.E], endocrinapathy, neoplasm
Ch11111ic Ullicaril

<1/3 of cases

Attacks last >6 weeks Individual lesion lasts <24 In

lgE-dBP&ndent: trigger associated Idiopathic {90% of chronic urticeria patients! Aeroallergens Drugs {antibiotics, honnones,locellllestheticsl Foods and additives Insect stings (bees, wasps, homstsl Parasitic infections Physical contact (animal saliva, plant resins, latex, metals, lotions, soap) Direct mast cell release Opiates, muscle reiiiXllnts, radilt-contrast agents Corl1Jiement-mediated Senun sickness, transfusion reactions Infections. vira[lbacterial ( >110% of urticaria in pediatric patientsI Urticarial vasculitis Arachidonic acid metabolism ASA,NSAIDs Physical Dennatographism (friction, rubbilg skinl, cold (ice cube, cold waterl. cholilergic (hat shower, exerciseI. solar, pressure (shoulder strap, buttocks!. aquagenic (exposure to water), adrenergic (stress!, heat

DAM HIVES Drugs and loads Allergic Malignancy Hereditary Infection Vasculitis Emotions Stings

......

Approach to Urticaria 1. Thorough Hx and P,ll: 2. Acute: if individual lesions last < 24 hours, but IIIW:ks last <6 weeks; no immediate investigllions needed; consider for allegy te5ting 3. Chronic: if individual lesions last < 24 hours but attacks lui > 6 weeks; further invastigations roquirad: CBC+diff, urinaiY$il. ESR, LFTslll help identify underlying causa 4. Vuculitic: if individual lesions last > 24 hours; biopsy of lesion and dennatology

Other Mastocytosis, Llticllia pigmentosa


lndividuallesioll51ast >24 In nan.puritic Requires biopsy
lluculilic Urtic:aria

Idiopathic Infections Hepatitis


Autoirrrnme diseases

..... ,
M..tacytoU. (Urticaria PigmentlllaJ Rare dilene due tc IIXCenive infilbation of the skin by mast calls. It manifests as many reddiah-brown ellllllllad plaques and maculas. Applying prassu111 tc a lesion produces a whell surrounded by intansa erythema (Dariar's sign), due tc mast cell degranulation. This occtn within minute..

SLE Drug hypersensitivity cimetidine and

D42 Denoatology

Miscellaneous Lesions

Toronto Notes 2011

Erythema Nodosum
Clinical Presentation

----------------------------------------

acute or chronic inflammation of subcutaneous fat (panniculitis) round, red, tender, poorly demarcated nodules sites: asymmetrically arranged on lower legs, knees, arms associated with arthralgia, fever, malaise

Etiology
DDx of Erythema Nodoe1m
NDDDSUM No cause [idiopmhic) in 40% Drugs [sutfonamidas, OCP, ate.) Other inflctions [GAS+) Sarcoidosis Ulcerative colitis and Crolvl's Malignancy [leukemia, Hodgkin's lymphoma)

40% are idiopathic drugs: sulfonamides, oral contraceptives (also pregnancy), analgesics, trans retinoic acid infections: GAS, primary tuberculosis (TB), histoplasmosis, Yersinia inflammation: sarcoidosis, Crohn's > ulcerative colitis malignancy: acute leukemia, Hodgkin's lymphoma

Epidemiology 15-30 years old, F:M = 3:1


lesions last for days and spontaneously resolve in 6 weeks

Investigations
chest x-ray (to rule out chest infection and sarcoidosis) throat culture, antistreptolysin (ASO) titre, purified protein derivative (PPD) skin test

Management
symptomatic: bed rest, compressive bandages, wet dressings NSAIDs treat underlying cause

Pruritus
Clinical Presentation
a sensation provoking a desire to scratch pruritis can present with or without skin lesions lesions may arise from the underlying disease, or from excoriation causing crusts, lichenified plaques, or wheals
It'

Etiology
dermatologic - generalized asteatotic dermatitis ("winter itch) pruritus of senescent skin (may not have dry skin, any time of year) infestations: scabies, lice drug eruptions: ASA, antidepressants, opiates psychogenic states dermatologic -local atopic and contact dermatitis, lichen planus, urticaria, insect bites, dermatitis herpetiformis infection: varicella, candidiasis lichen simplex chronicus prurigo nodularis systemic disease - usually generalized hepatic: obstructive biliary disease, cholestatic liver disease of pregnancy renal: chronic renal failure, uremia secondary to hemodialysis hematologic: Hodgkin's lymphoma, multiple myeloma, leukemia, polycythemia vera, hemochromatosis, Fe deficiency anemia, cutaneous T-celllymphoma neoplastic: lung, breast, gastric (internal solid tumours) endocrine: carcinoid, DM, hypothyroid/thyrotoxicosis infectious: HIV, trichinosis, echinococcosis, hepatitis C psychiatric: depression, psychosis neurologic: post-herpetic neuralgia, multiple sclerosis

DDx of Pruritu
SCRATCHED ScabiN Cholestasis Banal Autoimmune Tumours Crazies (psychiatric) Hematclogy [polycythemia. lymphoma)

Endocrine (thyroid. parathyroid, ..V Fe) Drugs, dry skin

Investigations
detailed history complete physical, including rectal and pelvic examination bloodwork: CBC, ESR, Cr/BUN, LFT, TSH, fasting blood sugar, stool culture and serology for parasites

Toronto Notes 2011

Miscellaneoua Lesions/Common Medications

Dermatology D43

Management
treat underlying cause cool water compresses to relieve pruritus bath oil and emollient ointment (espedally if xerosis is present) topical corticosteroid and antipruritics (e.g. menthol, camphor, phenol, mirtazapine, capsaicin) systemic antihistamines: Hl blockers are most effective, most useful for urticaria phototherapy with UVB or PUVA

Wounds and Ulcers


Tabla 28. Diffarant Typas of Ulcars and Traatmant

Ulcer Type
Arterial

Cliniclll'nlsemtion
Wlund ill lip& uf toB5, cold feet with claudication, gangll!lle, distsl hypenmia, decreased pedal pulses Doppler &tudy If ankle:brachialmtio <0.4, cCIISider amputation If gangrenous, paint with betadine Otherwise, dressings to promote moist inlerllc1ive wound healing

Uncommon Cau- of Ulcers

CHIP IN Cancar, chrom0101118.1


Hemoglobinopathy

Inflammatory
Pyoderma gangrenosum Infections Necrobiosis lipoidica diabeticorum

Wlund at malleolus, stasis change, edema, Local wound dressing: moist iniBllctive healing previous venous i!lury Compression: preferably four layers After wound heals, suwort stockings for lit& Nratropic and Diabetic llllculitic Wlund ill prassura point or secondary to unknown trauma. common at base uf 1st metatarsal phalangeal (MTP) Livedo reticularis, petechiae, extreme tenderness, delayed healing

Prassura downloading by usilg proper sho8f/s8ills Promote moist irrteractiva wound healing Appropriate broad-spectrum arrtibio'lic cDVerage
Biopsy to determine Serum screening for vasculitis Treat vasculitis Local moist irteractive healing

.....

.. ,
antimicrobials

Key to I Wound tlllt doll Nat Hill ...

llelenllaA dabridemant of biofilm and


8iopay lll1'f wound without siiJIII of healing altar 3 months to rule out

CIIICerl

Common Medications
Sunscreens and Preventative Therapy
Sunburn erythema 2-6 hours post UV exposure often associated with edema, pain and blistering with
subsequent desquamation of the dermis, and hyperpigmentation chronic UVB exposure leads to photoaging, immunosuppression, photocardnogenesis prevention: avoid peak UVR (10 am to 4 pm), wear appropriate clothing, wide-brimmed hat, sunglasses, and broad-spectrum sunscreen clothing with UV protection expressed as UV protection factor (UPV) is analogous to SPF of sunscreen

.....

,
UVBorWC

uv Radlltian
UVA (3Z0-4011 nmJ: Aging Penetrates skin more effectively 1han

Sunscreens
sun protection factor (SPF): under ideal conditions an SPF of 10 means that a person who normally burns in 20 minutes will burn in 200 minutes following the application of the sunscreen topical chemical: absorbs UV light requires application at least 15-60 minutes prior to exposure, should be reapplied every 2 hours (more often if sweating, swimming) UVB absorbers: PABA, salicylates, cinnamates, benzylidene camphor derivatives UVA absorbers: benzophenones, anthranilates, dibenzoylmethanes, benzylidene camphor derivatives topical physical: reflects and scatters UV light titanium dioxide, zinc oxide, kaolin, talc, ferric chloride and melanin all are effective against the UVA and UVB spectrum less risk of sensitization than chemical sunscreens and waterproof, but may cause folliculitis or miliaria some sunscreen ingredients may cause contact or photocontact allergic reactions, but are uncommon

Responsible for tanning, burning, wrinkling and pl8mllluru skin aging Penetnrtes clouds. gl- and is ruftac:l&d off Wlltar, 1110w lllld carnant

UVB (ZIW20 nmJ: laming Ablorbed by 111e out&r dermis Is mainly responsible for burning and p18mlllu18 skin aging tor BCC, sec Dan not p811111nrte gl11111 and is substantially absorbed by ozone
UVC (ZO&-ZIU nml Is fillll'ld by olllllellyar

Management sunburn: if significant blistering present, consider treatment in hospital; otherwise, symptomatic
treatment (cool wet compresses, oral anti-inflammatory, topical corticosteroids) antioxidants, both oral and topical are being studied for their abilities to protect the skin; topical agents are limited by their ability to penetrate the skin

D44 Denoatology

Common Medications

Toronto Notes 2011

..... '
....mv. Percutann .._,lllitln
Fornnn 1.0 1.7
3.7 6.0
13.0 42.0 Body Site:

Topical Steroids
Tabla 29. Potency Ranking of Topical Steroids
Ralllin Patency
Welk

Rallllive Strtlngth
x1
x3

G..ric Nm
hydrocortisone 1% hydrocortisone 2% 17-valeme- o.Z'l. dasonide mDI1IBtllsone furorata bstamsthasona - 0.1% 11-valeme - 0.1% ncinonide betamethasone dipropionate - 0.05% fluocinonide - 0.05% clobetasol propionate (mo&t potentl betamethasone dipropionate ontment halobetasol propionate

Tl'llla Na11111

UMgl
ntertriginous !l'eiiS, clildren. face, thiukin Arm, leg, tJUnk

Plantar fuat Palm BliCk Scalp Forehllld Cheeks Scrolum

0.14 0.83

Modanrlll

Tridesilon Bacornat Batnoval88 Celestodenn -vat Diprosonellt Lidex, Topsyn ger' Lydannat Body

Patent

x6

Calculation of strangth of staroid compared 1D hydrocortisone on fo1'811111: relative strength of staroid x ralllliva

pwcutaneousllbsO!p!ion

Very Patent
Extr.nely Potllnt

x9

Palms 111d soles

....

''
Steroid acne
ROMCII

x12.

Dennovate8
Diprol-at

Palms 111d soles

Side Efflcts of Topical Sttroldl 1. Local: A1rophy Plrionll dl!llllllitis


Contact Tachyphylaxis {tolanncaf 2. Sysmmic: of HPA axis

Dermatologic Therapies
Tabla 30. Topical Therapies that are Important in Dematology D11111 Nama Dosing Schala lndicllliC.lcipotriol (Dovan..-1
0.005% cream, ointment. scalp Psoriasis
solution, apply BID For maintenance DD
Cammants

Burning, itching, skin irritation, worsening of psoriasis Avoid face, rrucous mentranes, eyes; wa&h hand& after Maximum weekly dosage of cream by

2.-5 years - 2.5 !Vwk 6-10yaars- 50 WWk 11-14 years- 7511fwk >14 years-100 glwk
lmiquimod (Aiduall] Genital warts 5% cream applied 3llfwk at bedtime, leave on Cutaneous warts 6-10 hours, 1han wash off with Actinic keratosis mild soap and water Max. ckuation 16 weeks Superficial basal call carcinoma Avoid naturaVartificial sun exposure Local skin and application site reactions

age:

Erythema,

edema,

sympllms Works best for warts on mucosal surfaces May induce inllammation and erosion

(Kwelllda41 P Lotion and Dennal C1111m)

Parmatl11i1

....

,...----------------. ,
greasy

5% cream, applied once Scabies (Kwellada-P Lotion, DVIII11ight to all skin areas torn NiJ:8 Dermal Cream) neclkdown Padiculosis (ICwallad&-P Cnina Nix Crime Rinse411 1.0% cream BID
Usa for as long a& lesions pa1$ist and die upon resolution of symptoms Atopic dennatilis (mild to moderate)

Do not use in children <2 vrs old Hypersensitivity to drug, or known sensitivity to chrysanthemums Local reactions only (resolve rapKJvl; including burning, pruritis Low toxicity, excellent results Consider 2nd application after 7 days
Burning
May be used on all skin surfaces including head, neck, and intertriginous areas Expensive

VlbiciH

PiiiiiiCrOimUI (Bidalll]

Lack& adverse 8lf8cbi of &taroid&

Ointmarrt (watar in oiU: hydrate,

Cream {ail in waf: hydra... variable lotion (powder in watar]: drying,


cosmasis Solutions {water, alcohol, propylene
glycalf

TIICIIIIimUI topical
(PrDIDpic8}

Gil (.wtian 1hlrt lllllts an cantac1 with skin]: dryinq

0.03% (children) or 0.1% Atopic dermatitis (mild to (ackllts) ointment BID moderate) Conti111e for cklration of disaBSe PUJS x 1 week after clearing

Burning Lacks adverse effec1ll of steroids May be used on all skin aurfacas including head, neck, and intertriginous areas Expensive

Toronto Notes 2011

Common Medications

Dermatology D4S

T1ble 31. Or1l Ther1pies th1t 1re Important in Dermltalogy


DIUU Name

Dosig
25-50 mg PO OD; maximum 75 mgld

Indications

Comments

Acill'ltil (Sorimne8)

SIM!rll p&oria&i& Mcnitori'll stratagia&; Other disorders of hyperkntinillltion Mcnitor lipids. LFTs at baseline and q1-Zwkun1il stable Contnjndjcatjons: (ichthyosis, Dlliar's disBBSa) Women of childbearing potential unless strict contraceptive requirements are met Drug idnctions Olhar systanic llllinoids, mathoti'BXIIIII, tatracydinas, certain contraceptives May be combined with PINA phototherapy (known as re-PUVAI

famcydovir 250 mg PO no x 7-10 days (for 1&t episode of genital harpe&) 125 mg PO BID xSd (for recurrart gerital herpes) wlecydovir 1000 mg PO BID x7-10 d (for 1&tepisode of genital harpe&) 500 mg PO BID xSd (for recurrart gl!llital herpes) 2.5-4 mwlc!Vd PO div BID Max4mg.\Wd After 4weeks may increase by 0.5 mg.\Wd qZwb Ccn:omilllrt dose of may protect the kidneys

ChiCkeiliOX Herpes zoster Genital Herpa& Acute llld prophylactic to rerilce transmission in infected patients Herpes labialis

Side eflects: Headache, nausea. diarrhea, abdomilal pain Reduce dose impaired 1111allunction

Side eflects: Dizziness, depression, abdominal pail Rerilce dose n impairad 1111allunction Drug inhn!ctiops: cimetidine Monjtorim stgtegjes Blood pressure, renal function Contraindications: Abnonnal renal function, uncontrolled hyperterlsion, malignancy {axcapt nonillelanoma skin cancar), uncontrolled infection, immunodeficiency (excluding autoimmune diseaseI, hypersl!llsitivily to drug long tl!nn eflects preclude use of cyclosporin for >2 yea11; discontinue aartiar possille May consider rotating therapy with other drugs to minimize adverse eflects of each drug Monjtorina strategies: Obtain G6PD levels before initiating; in the initial two weeks obtain levels and follow the blood coun1s carefully lor the first few months Side eflects: Neuropathy Hemolysis (V'rlilmin Cand Esupplementation can help prevent this) Drug jnb!n!ctjops: Substrate of CYP2C8/9 (minor), ZC19 (milor), 2E1 {minor), 3A4(majorl Often adramatic response within hours Monitoring strategies: Baseline lipid profile and hepatic l!llzymes befure treatment, Contmjndjcatjons Teratogenic -in females, reliable contraception is necessll'{ Generally regarded as unsafe in lactation Sjdaeff!lcb: Night blindness. decreased tolerance to contact ll!llses, dry mucous membmnes May tmnsiently exacelbate acne, dry skin Depression. myalgia DNg jnb!n!ctjons Do not use at the same time as tetr8cycline or minocycline - both may cause pseudolumour cerebri Discontilua vililmin A Drug may be discootinued at 16-20 weeks when norille coun1 has dropped by >711%. A second course may be iritiated after 2 monthspm Refractory casas may require >3 coursas Contraindications: CHF Sjda ellec!i: Serious hepatotoxicity Drug Interactions: nhibits CYP 3A4. ncmases concantration of soma drugs matabolizad by this snzyme Give capsules with food, capsules must be swallowed whole

Psoriasis May also be eflective in: Lichen Planus Dermatitis herpetiformis Erythama multifonna Recalcitrant urticaria Recalcitrant atopic dermatitis

Dlp10n1

150 mg PO OD tapering to 25-50 mg PO OD to as low as 50mg Zxlwk

Dermatitis herpetiformis

llatnltinoin (Accmne*)

0.5-1 mg.\Wclay given OD, to achi8VII a IDIBI dose of 120 mwlcg (i.e. 16-20 weeks)

SIM!rll nodular and/or inflammatory acne Acne conglobala Recalcitrant acne

llrlconllilla (SporaiiiiX*I

100-400 mg PO 00, dapencing on Onychomycosis infliction 1r8Btad Tin1111 carpori1, cruris, pedis. wrsicolor, capitis Tin corpo!Wc:ruri&: 200 mg PO OD X 7days Tinea pedis: ZOO mg PO BID x 7days Tin wrsicolor: 200 mg PO OD x 7 days Toenails with or without fingamail involvement: 200 mg PO BID x 7 days once per month, repealed 3x Fingamail involwment only: 200 mg BID PO x 7 days once par month, repaated 2x

D46 Denoatology

Common MedicationsJR.eferenc:es

Toronto Notes 2011

Table 31. Oral Therapies that are Important in Dermatology (continued) Drug Nne
lvlrmllclin

Do.ilg SdJediH
2DIJ-250 !l9"kg PO qwkly x 2 Take once as directed; repeat one week later

lndil:alion
Onchocerciasis (USA only) Not licensed for use in Canada Also effective for: Scabies Psoriasis Atopic dennatitis Lymphomatoid papLJosis May also be elfective in: Cutaneous sarcoidosis

Cummem.
No significant serious side effects IJiicacious Mgnilorioo rtnrteqies: Baseline renal, liver, and hematological studies Contraildications: Prepncy, lactation, alcohol abuse, liver dysfunction, immunodeficiancy syndrome, blood dyscrasias, hypsrsansilivity to drug Resbicted to severe, recalcitrant or disabling psoriasis not responsive to other fonns Dl therapy May be combined with cyclosporile to allow lower doses of both drugs Contn!indi!:a!ions: Caution if impaillld ranal or liver function Drug interactigns: Do not use with isCJtrelinoin {Accutane8 1 Side ef!ects: fxbnivll; affect& multiple organ sy&!BIIIs including CNS, l88th, eyes, bones, renal, ll1d skin (photosensitivity, and bkle pigmentation) Attemative to tetracycline Contraindicatians Pregnancy, chronic or active liver disease Drug interactions: Potent inhibitor Dl CYP 206; use wilh caution whan also taking beta-blockers, certain anti-an1lyllrnic agants, MAOI type B, andfor antipsychotics Drug concentrates rapidly in skin, hair and nails at levels associated with fungicidal activity Cootraindications: Severe ranal or hepatic dysfunction Pregnancy/lactation

StromadDPI
MathlllniDill
(TIIIXIP)

(Meclizln,

1D-25 mg qwk. PO, IM, or IV Max: 30 mQIWk


To minimize side effects, consider fnlic acid supplementation: 1 mg to 5 mg 6 daytlweek

Minacyclne {Minocin)

5B-100 mg PO BID Tapsr to 50 mg PO DO as acne lessens

Acnewlgaris Rosacea

Terlli111ine {Lamilil"l

250 mg PO DO x 2 weeks Fingernails x 6 wks Toenails x 12 wk.s Conlinn diagnosis prior to treatment

Onychomycosis linea corporis, cruris, pedis, capitis

Tetncyclina

251J-5DO mg PO daily Acne wlgaris Taken 1 hour before or 2hours after a meal Rosacea Bullou1 pBIIIphigoid

References
Tllllbool:l Bolognia Jl., Jori1lD J. Rapini RP, edilurs. Textboot of Demwtnlogv. Vol. land 2. Toronto: Mosby, 2003. Filzpalrict JE and Aaling JL.IlernwiDiogy Semis. 2nd ed. Phil-ia: Hlrirt & Ballus, 2001. Godelrt II, Goodheuft Phologlide Ia Cormal Slin Dillllllel$: Dillgi1Diislllld management. 3nl Edition. Uppincotl, Wiiuns and Wilijns, 2008 John11111 RA. Swiii1DIId D. Willi(, adilars. Colcur adaslllld II clinical 5th ed. Naw Yark: McGraw Kill! J, Ng C. Bllllll:ci V.lllivarsily ri TD111111D Pharmacology H111cliool: Chllptw. Toranta: 111bliCI!im panding. L.elwlohl MG, Heymann WR, l!erlhJDIU16 J, Coullon aditoJS. T1811ment ri 5ijn di1ua: 1ha11pautic $11118gia11. 2nd ad. Plilldalphia: Mo$by, 2006. Pillar AS, Mancini AJ.!Uwilz clilical pediatric darmatalogy: A18idbook of skin disorders ri mldhDDd 111d lllolllsanct. 3nl ed. Cln: Elsevier, 2006. Slllny W, Plus W. BuiQIIDII Wedilorl. Thieme Clinical Compum: llermatalogy. s1l ed, Naw York: Thieme. 2005. Wall! I(, Uld Johnlion RA. Fibpalril:t's Cobrr Atlas Uld Symop!ii II Clinicalllunnatalagy. 61h Edition. Naw York: McGraw Hill2009
Alliclll

Currvnings SR et al. AIIPIDathesto tha prMTI!ion Uld allllrol of skin cancar. Cancer Matastatis Rav. 19!7;16:309. DeShiiZD RD alii. Alaf9ie 181CtiDill Ia biologic agantJ. JAMA. 1197;278:1895. Ellis C, at ILICeAD II FWly. lnlamllilllll Can11111u Comi11nce on llllmmiliiiiiiiXAD II): Clinical updlla IIlii current tr811trrumt i!ra11Qia11. Br J llarmataL 2003; 148 j1Uppl63):31 0. J, Baron R. ciricll and diagnlllis ri onydilll11ycDiis. Br J lllrrmi 2003; 149 j1Uppl65):1-4. Friednain PS. Aaessmenl II urticaria111d 11111io-ede1T1. Cln Exper Alle!vv. 1999;29 tsuppl31:109. Gordon ML at II. Cart of the skin ltrrdl: ri pigmenlad lesions. Geriatrict. 1997;52:5667. Kllift:hik. BR. T1811ment II damwlitil. J IAJt Med Surv 3. 1989; 3!wppl2):16-23. Mlll1nllanll!a A. Urbano FG. Sailiiani l. at al A1ypical molluscum CDII!IgiDIIIII in an HN-inflctad palilnt. tit J Darma!DI. 1998; Z7:37s.380. 19111;341:964. Roujeau JC. S!Mns-Jolmson S'jlldrame and lolic necrolysis are severe variants of tile same disease Mich dillels from erythema multifonne. J Denratal. 19JI;Z74.ZJ6. Walsh SRA and Stlll8l NH.I'saliasis and the naw biok9c11Q81111: lnlarruplilg 1 T-AP danCI. CMAJ. 2004;170[13):1 933-1941. Wli1Bd JD at II. D11111 thi& paliBill hiVII mala ora1111111111n1 JAMA. 1988;Z7t-676. Wlin J,lllhl M,llalmrir M,llllb l., Fainllllin A. Odam R. Puwlll F. Stlnd1rd clusifiCIItion of RJacea: illplll ri tha Nltionlllloacaa Society Elqiart Commitlaa 1111 IIIII Clusificltion lind Stlgilg of RDIIICliL JAmar Acid llarmatal2002;46{4):584-587. Canadilllllunnatalogy AAociltion 82nd AmuiConr...:u. Juna zt.luly 4, 2007. TD!Dn!D, Ontlrio, Coneda. Pope E. Peclatric Dnthems.l.ec11Jre presenmtion to 2009-2010 lliiveiSilyofTDnllla Year 3Medical Students. hl1pi/dlrmnaln!.org

Cribier Bet II. &ytheml nodosum and assocnd di-s. lnt J Dennatal 1998;637-667.

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