Pathophysiology: Skin

The Dermatologic Vocabulary ................................................................................................................................................. 2 Histopathology of the Skin ...................................................................................................................................................... 4 Acne & Rosacea....................................................................................................................................................................... 6 Cutaneous Autoimmune Bullous Diseases: Pemphigus & Bullous Pemphigoid ..................................................................... 9 Psoriasis & Atopic Dermatitis ................................................................................................................................................ 11 Pigmented Lesions & Melanoma .......................................................................................................................................... 14 Non-Melanoma Skin Cancer ................................................................................................................................................. 17 Dermatology of Pigmented Skin ........................................................................................................................................... 19 Birthmarks in Babies ............................................................................................................................................................. 20 Drug Eruptions ...................................................................................................................................................................... 22 Cutaneous Manifestations of Internal Diseases ................................................................................................................... 25 Common Infections of the Skin ............................................................................................................................................. 27

The Dermatologic Vocabulary

Lesion morphology: shape and relative size of the lesion(s)
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. MACULE PAPULE PLAQUE NODULE TUMOR VESICLE BULLA PUSTULE CYST WHEAL COMEDONE BURROW non-palpable, circumscribed, color change <1 cm; (macular or patch are used to describe larger areas of the color change) palpable, circumscribed lesion, < 1 cm palpable, circumscribed, relatively flat topped lesion, greater in surface area than in thickness, > 1 cm; palpable, circumscribed lesion, 1 cm and < 2 cm; large nodular lesion, 2 cm clear fluid filled lesion (blister), < 0.5 cm clear fluid-filled lesion (blister), > 0.5 cm turbid fluid-filled lesion nodule filled with a semisolid or liquid substance transient palpable lesion (hive) caused by an interstitial serous fluid accumulation in the upper dermis plugged pilosebaceous opening short, linear, thread-like lesion caused by the scabies mite tracking through the stratum corneum
junctional nevus molluscum contagiosum, intradermal nevus psoriasis, lichen simplex chronicus melanoma, squamous cell carcinoma squamous cell carcinoma, basal cell carcinoma herpes simplex and zoster infections, vesicular foot dermatitis bullous impetigo, toxic epidermal necrolysis, bullous pemphigoid folliculitis, acne epidermal inclusion cyst

acne comedone, solar elastosis with cysts and comedones (FavreRacouchot syndrome)

Secondary Changes in lesions are frequently seen and may result from the primary disease process, normal skin
repair, external manipulation, or infection. 1. SCALE accumulation of adherent stratum corneum 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. CRUST LICHENIFICATION EROSION EXCORIATION ULCER FISSURE SCAR ATROPHY HYPERKERATOTIC VERRUCCOUS accumulation of serous, cellular, squamous, and bacterial debris over a damaged epidermis accentuated skin markings due to thickening of the epidermis tissue loss confined to the epidermis erosion clearly caused by external factors tissue loss extending into the dermis crack in the epidermis extending into the dermis fibrous tissue replacing usual dermal tissue space loss of substance of the epidermis and/or dermis lesion with excessive heaped-up scale vegetating, wart-like surface
psoriasis, tinea corporis impetigo, secondarily infected eczema lichen simplex chronicus candidiasis neurotic excoriations venous stasis ulcer, ulcerated basal cell carcinoma perleche scarring alopecia steroid induced atrophy, lupus erythematosus hypertrophic actinic keratosis, squamous cell carcinoma verruca vulgaris

Further description:
COLOR 1. 2. 3. 4. ERYTHEMATOUS Reddened skin VIOLACEOUS PURPURIC PIGMENTATION Violet Related to purpura (small hemorrhage in skin) Hyperpigmented, hypopigmented, depigmented Well-defined, Poorly defined Shaped like / forming a ring (is there a difference between edge & center?) Like an arc (annular, but not complete With a central depression (like umbilicus) Symmetric, asymmetric Growing outward Growing inward Hardness Epidermis peeling off

Primary Lesion
1. Macule / patch 2. Papule / plaque / nodule 3. Vesicle / bulla 4. Pustule

DEFINITION SHAPE 1. 2. 3. 4. 5. 6. ANNULAR ARCUATE UMBILICATED SYMMETRY EXOPHYTIC ENDOPHYTIC

DEFINITION
1. Well-defined 2. Ill-defined

OTHER
(color, shape, distribution, etc.)

1. Scaly? Crusted?

INDURATION DESQUAMATION DISTRIBUTION 1. 2. 3. LINEAR CONFLUENT ZOSTERIFORM

TELANGIECTASIA

Lesions merge / run together Band-like distribution along dermatome (usually unilateral) Visible small blood vessels near surface of skin

Excoriated? 2. Linear? Annular? Umbilicated? 3. Erythematous? Hyperpigmented? Hypopigmented? Purpuric? 4. Atrophic?

Histopathology of the Skin

Overview (Superficialdeep) 1. Epidermis 2. Dermis (papillary rete) 3. Subcutaneous tissue

Epidermis
Layers: 1) Stratum corneum: anucleate; basket weave appearance, thickness changes with anatomic site 2) Granular cell layer (stratum granulosum): thickness varies with SC thickness; basophilic keratohyaline granules present 3) Stratum spinosum (spinous layer): 5-10 layers; flatter towards the top, connected by desmosomes (site of blistering problems in some conditions) 4) Basal layer: single layer ovoid cells; perpendicular to basement membrane zone, more basophilic, variable amounts of melanin 5) Basement membrane zone: bonds epidermis/dermis; PAS+; site of blistering disorder problems (structural abnormalities / inflammatory disruption) Cell types: 1) Keratinocytes: most cells; mature as you go up 2) Melanocytes: about 1 out of 10 cells; in basal layer, synthesize melanin, transfer to keratinocytes via dendritic processes 3) Langerhans cells (dendritic cells, antigenpresenting, have tennis-racquet-shaped Birbeck granules) 4) Merkel cells (sensory receptors)

Dermis

Papillary dermis (pegs) Reticular dermis (underneath) Thicknesses depend on anatomical site Contains: collagen, elastic fibers; GAGs vessels/nerves Mast cells (inflammation, etc.) adnexal structures: o Hair follicles: note that hair shaft itself is multi-layered Terminal anagen hairs: skin scalp (what we think of as hair) Vellus hair: nose, forehead (cant really see). Male pattern baldness = transition from terminal antigen to vellus hair on scalp o Smooth muscle (arrector pili goosebumps) o Eccrine units: dermal sweat glands, dump into ducts, merocrine secretion (exocytosed) o Apocrine glands: from hair/epidermial germ; 4

SKIN COLOR Skin color depends NOT on the NUMBER of melanocytes you have but instead the amount of pigment they produce.

duct enters at infundibulum; similar to eccrine duct but gland has apocrine secretion (secretion via budding of PM). Mostly in axilla/anogenital region but also external ear canal (ceruminous), eyelids, breast (mamillary): few non-functional on face, scalp, abdomen; more prominent in acral skin

Acral: extremities of peripheral body parts

Anatomic variation
Acral sites: hyperkaratotic stratum corneum nerve-end organs: o Pacini corpuscles (onion/shaped; palms/soles + some on nipples/anogenital, sense pressure) o Meissners corpuscles (ventral hands/feet; mediate sense of touch) No hair follicles Mucosal sites: no granular cell layer or stratum corneum Scalp: increased anagen hair follicles Nipple/scrotum: increased smooth muscle bundles Periorbital/perioral/perinasal/neck: skeletal muscle (neck, orbicularis oculi, etc.) Nail unit: nail bed under nail plate; cuticle. Note that things under cuticle can leave marks as nail grows (diagnostic help)

Dermatopathology
Pathologic conditions affecting skin and mucosal tissue benign/malignant tumors, inflammatory conditions, deposition disorders, infections Diagnosis: clinical history is key! Exam + demographics + history, etc. Inflammatory skin conditions: Diagnosis 1. Look for epidermal alteration a. Thickening (acanthosis = diffuse epidermal hyperplasia; rete hyperplasia) b. Atrophy c. Spongiosis (fluid): typically due to eczema; white space between keratinocytes, serum in SC d. Dyskeratosis/lichenoid tissue reaction (being eaten away?) e. Blistering (separation of layers) i. Fluid separation within/beneath epidermis ii. Can be from spongiosis, cytolysis of keratinocytes, acantholysis (loss of cell/cell contact); BMZ destruction, liquefactive necrosis iii. Can be tense (subepidermal separation) or flaccid (transepidermic usually) f. Stratum corneum alteration (hyperkeratosis, neutrophils in cornea) g. Cellular atypia (lymphoma, leukemia, breast cancer, melanoma, nevi) 2. Look for infiltrates a. Where is it? Dermal/epidermal junction, around vessels, interstitial, etc. b. What is it? Lymphocytes +/- eosinophils, granulomatous, etc. i. Urticaria (hives): PMNs & eosinophils ii. Arthropod bite: lymphocytes & eosinophils in wedge shape iii. Drug hypersensivity: spared epidermis; mostly perivascular lymphocytes in dermis 3. Miscellaneous findings a. Fat alteration (paniculitis) i. erythema induratum = thickened septae; erythema nodosum: whole lobule + septae involved b. Amyloid deposition (yellowish, can pinch & produce purpura) c. Cysts d. Cancer/precancerous: i. Actinic keratosis: precancerous, basal layers abnormal ii. Squamous cell carcinoma (in situ / invasive) basal cell carcinoma) 5

Acne & Rosacea

Things in bold, caps, underlined = things she said we should know

Acne Vulgaris: Pathogenesis

Self-limited condition of the pilosebaceous unit (hair follicle + associated sebaceous gland) Sebaceous gland: all skin with hair follicles (all but palms/soles) Sebocytes mature, accumulating more lipid secrete by holocrine (decapitation: cell dies & releases contents) Sebum is secreted product o KEY: SQUALENE AND WAX ESTERS DISTINGUISH SEBUM FROM LIPID IN INTERNAL ORGANS Activity fluctuates with age (and men>women) o high at birth, quiescent 2-6yo, increases @ 7yo o peak in 20s, gradual decline with age (decrease per decade: men < women) Androgens explain fluctuation: o sebum production corresponds to adrenarche, not puberty o DHEAS (weak androgen) is locally converted to testosterone & DHT (stronger) to stimulate sebum production (DHEAS in adrenarche although systemic T & DHT not til puberty) Comedogenesis (comedon = acne lesion) Keratinization pattern altered inside hair follicle Normal: loose organization; many lamellar granules, few keratohyaline granules) Changes: density, structure, keratinocyte turnover & apoptosis
o Etiology unclear: linoleic acid, IL-1, androgens?

Keratin shed, forms whorls, plugs follicle

Resident flora: Proprionibacterium acnes P. acnes is GRAM NEGATIVE, NON-MOTILE, MOSTLY ANAEROBIC No formal link between P. acnes & acne o Probably normal flora, protective role usually (but in acne pts) Possible mechanism of pathogenesis: 1. P. acnes has lipases that break down sebum (+ proteases, hyaluronidases too) 2. Production of FFA + other molecules inflammation 3. cytokine (IL-1, TNF, IL-8 ) release by kera tinocytes & local inflammatory cells 4. chemotaxis of T-lymphocytes & neutrophils damage follicular epithelium 5. Hair follicle keeps dilating; sebaceous gland atrophies scarring

Acne vulgaris
Comedo/comedone = initial lesion Closed comedone: slightly elevated, 1-4mm papule, mostly face (whitehead)
o Has lamellated/whorled keratin; not inflammatory grossly but infiltrate on path

Open comedone: similar but communicates with surface of skin (blackhead)

o Color from melanin deposition

Papulopustle: after progression; more inflammatory (erythema + tenderness + induration) Overlying pustule (pus blocks follicle) Nodulocystic acne: inflammation persists, becomes deeper; keratin shedding blocked (scarring imminent)

Acne Fulminans (acute febrile ulcerative acne)

Severe form of nodulocystic acne accompanied by systemic symptoms & signs Sudden onset, mainly in teenage boys o massive inflammatory, tender lesions on back + chest; rapidly ulcerate; heal with scarring o Febrile, leukocytotic (10-30k WBC/mm3) o Polyarthralgias, myalgias, other systemic complaints; +/- lytic bone lesions in tender bones o Often require hospitalization: can be a derm emergency!

Neonatal acne
20% newborns; 2-3 mo; spontaneous remission without scarring Infection with Malassezia furfur (yeast) Presentation: inflamed papules on cheek, across nose/forehead

Infantile acne
3-6mo, improves by 1yo but can persist for yrs Hormonal imbalances are key o boys: LH/Testosterone; DHEAS in both from immature adrenal gland

Occupational acne

A.k.a. chloracne; from occupational exposure (chlorinated aromatic hydrocarbons)

o Cutting oils, petroleum products, coal tar derivatives, electrical conductors/insulators, insecti/fungi/herbicides, etc

Classic: big nodules behind ear, on cheek/scrotum

o E.g. Victor Yushchenko post-dioxin poisoning attempt

Drug-induced acne
Key clue: Monomorphic (all in same phase of evolution) TONS of meds can cause it (EGFR inhibitors are newest but also anabolic steroids, lots more)

Endocrine acne
Cystic acne in association with other signs of hyperandrogenism (hirsutism, irregular menses, infertility, obesity) Polycystic ovary syndrome: #1 endocrine abnormality in US (5% women) o Diagnosis of exclusion (oligomenorrhea + clinical/biochemical hyerandrogenism) High glycemic index of western diet might be involved in prevalence of acne in developed countries

Rosacea
Less well understood Cutaneous reaction that initially presents with flushing of skin o Flares with remissions Epidemiology Females > Males 30-50 yo usually N. Europeans > Asians > Others

Pathogenesis Vascular dysfunction (blood flow vs regular skin, vessels dilated, blood/inflammatory substances extravasate) Microorganisms (maybe?) Demodex folliculorum (mite)? Neurologic dysfunction: o Parkinsons patients often develop o Hot drinks / emotions / alcohol can trigger flares!

Clinical manifestations (subtypes)

Vascular rosacea
Earliest stage: recurrent blush, start of telangiectasia (nasal ala cheeks) Degree: related to degree of sun damage Edema + burning/stinging (when applying products to face, for instance

Inflammatory rosacea
Small papules/pustules deep persistent nodules Deeper red than acne; no comedones or follicular keratinization defects

Sebaceous hyperplasia & phymatous rosacea

Overgrowth of sebaceous glands is prominent in some patients Rhinophyma = nasal sebaceous hyperplasia o Swelling/smoothening of nose enlarging pores / lumpy fibrosis later (permanent) o Path: too many sebaceous glands!

Ocular rosacea
> 50% of rosacea patients: dryness / tired eyes Edema / tearing / pain / blurry vision / styes / chalazia (other features too, can be pretty severe) Possibly due to meibomain impaction (glands that secrete lipids in tears) lipid in tear film

Steroid-induced rosacea
Prolonged use of topical steroids on face (or could be systemic) Clues: lesions on UPPER LIP, EYELIDS, AROUND NOSE Withdrawing steroid ANGRY FACE syndrome (initial flare, then recedes)

Cutaneous Autoimmune Bullous Diseases: Pemphigus & Bullous Pemphigoid

Pemphigus Vulgaris
Pemphigus (Greek: Blister) Painful blisters of mucous membranes / skin o stratified squamous epithelium only (not respiratory epithelium, etc.) o Large erosions, weeping, can recur explosively; flaccid vesicles o Intraepidermal blistering Peak: 30-50 yo; natural history = 50% mortality @ 2yrs, 100% @ 5yrs Oral lesions at first skin lesions later

Pathology: no inflammatory cells but tons of antibodies (IgG fluorescence everywhere) Genetics: MHC Class II genes DR4 (Ashkenazi Jews) or DQ1 (other populations) Everybody with pemphigus has the mutation, but only 1:10,000 with the mutation develop pemphigus Desmosomes are key cell-cell junctions in epidermis, keratin filaments in cell desmosomal plaque desmogleins/desmocollins hemophilic interactions with next cell Auto-antibodies against desmoglein proteins Presentation o Epitope expansion can occur over time (antibodies Pemphigus foliaceus against new desmoglein epitopes); corresponds Pemphigus vulgaris (oral only) with progression of disease
Paraneoplastic pemphigus As long as Ab bind, cell detachment happens (see slide: mouse models tried to block other points). Weird: cell adhesion is complex. Why would blocking just one component block adhesion? Nobody knows exactly why (complex cell signaling pathways)

Pemphigus vulgaris (oral + skin)

Auto-Ab against Desmoglein 1 Desmoglein 3 Desmogleins 3 + 1 Dsg 3,1 + plakin proteins + more

Treatment Implications: need drugs that reduce autoantibody synthesis doesnt help just to reduce inflammation remission is slow (12-24mo) Treatment options: Apherisis (too invasive) IvIG (give lots of Ab, body starts chewing them up including anti-Dsg autoAb) Usually start with prednisone in high doses Add purine synth inhibitors (azathioprine; block T/B cell synth), IvIG / Rituximab (anti-CD20 mAb), cyclophosphamide (alkylating agent), plasmapheresis, etc. as needed

Bullous pemphigoid
Elderly patients (60-80yo) Large, dramatic, pruritic blisters on skin (not painful) 9

o o

On base of large inflammatory process mucosal lesions uncommon

Hemidesmosome antigen is target of IgG + complement Antigen right near cell membrane (extracellular, in lamina lucida) Subepidermal blistering (IgGs found in basement membrane zone) Blocking steps of cascade blocks blister formation (PMNs are critical) Treatment implications Suppress inflammation & wait for remission Bigger menu of drugs to choose from Treatment: Anti-inflammatory Topical steroids sometimes; tetracycline / methotrexate/ niacinamide for mild cases; maybe dapsone for some Can use prednisone in lower doses (purine synth / cyclophos / etc rarely, in lower doses)

PEMPHIGUS VULGARIS
Rare COMMON FEATURES Antigen targets known

BULLOUS PEMPHIGOID

Auto-Ab are pathogenic (not just markers) AGE OF PATIENT BLISTERS: MUCOUS MEMBRANES TARGET LEVEL OF SEPARATION INFLAMMATORY
REACTION

Middle-aged (30-50 yo) Painful

Large erosions, weeping, can recur explosively; flaccid vesicles

Elderly patients (60-80 yo) Painless but pruritic

Large, dramatic blisters on skin

Involved (oral skin) Desmosome Intraepidermal None Blocking steps of cascade doesnt help: Ab binding sufficient to cause blistering Block Ab synthesis; slow remission High doses (immunosuppressive levels); few drugs available

Involvement uncommon Hemidesmosome Subepidermal Big PMNs are critical: if you block PMN activity, cascade stops (Ab binding insufficient by itself) Reduce inflammation; wait for spontaneous remission Lower doses (anti-inflammatory levels), more options

BLOCKING STEPS OF
DETACHMENT CASCADE

TREATMENT IDEA THERAPY OPTIONS

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Psoriasis & Atopic Dermatitis

Quick immunology review: Helper T-cells Th1: key for clearance of intracellular pathogens; important in pathogenesis of autoimmune diseases Th2: key for clearance of parasites & allergic reactions (IgE); important in pathogenesis of allergic diseases Dendritic cell / T-cell Signaling (immunological synapse) Dendritic / APC cell presents antigen on MHC MHC + antigen binds complementary T-cell receptor on matching T-cell Other costimulatory molecules are key: e.g. ICAM-1 (APC) / LFA-1 (T-cell), LFA-3 (APC) / CD2 (T-cell) Combination of signals leads to T-cell activation

Psoriasis
Chronic disorder; polygenic predisposition + triggering factors Epidemiology of psoriasis Males = females 30% develop dz < age 20 2% of general pop 10-30% pts psoriatic arthritis Certain HLA subtypes associated (HLA Cw6 = 13x RR) Other Most common form; Auspitzs sign= bleeding on removal of plaque. Younger patients (esp several weeks post strep infection) Pathogenesis: Th1 cells are key (cytokines: IFN, TNF, IL-2): autoantigen in skin probably triggers Th1 rxn Results: o Epithelial hyperproliferation, vascular proliferation o PMNs recruited + T-cell mediated immune reaction Type Photo Description Palpable plaques, silvery scale are classic Extensor surfaces (knee / elbow), sacral

Plaque psoriasis

Guttate psoriasis

Well-defined, smaller, discrete papules (still with silvery scale)

Pustular psoriasis

Generalized, lakes of coalescing pustles on background of erythema Palmoplantar surfaces Onycholysis (distal lifting of nail bed); oil spots on nail bed, nail pits Mono / asymmetric arthritis (DIPs mostly) Arthritis mutilans severe disability Spondylitis/sacroilitis possible too Can present like RA (symmetric polyarthritis) too

Nail psoriasis

Psoriatic arthritis

Other forms: Erythrodermic psoriasis (diffuse, all over the place), scalp psoriasis, inverse psoriasis (not classic with silvery scales but erythematous plaques instead)

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Treatment: 1. Address triggers (trauma, infections, drugs that are exacerbating) 2. Topical treatment (corticosteroids are mainstay; vit D/retinoids/tar too) 3. Phototherapy (unless post-sunburn) 4. Systemic immunosuppresives if severe 5. Newer: TNF antagonists, mABs, others

Atopic dermatitis
Relapsing, pruritic skin disease Pathogenesis: Th2 cells are key (cytokines: biphasic) o Acute atopic dermatitis: Th2-mediated (IL-4, IL-5, IL-13) o Chronic atopic dermatitis: Th2 and Th1 (IFN, IL-12) o T-cells, eosinophils, monocytes activated; IgE increased Skin barrier defective: cutaneous superinfections; fewer lipids/FA in AD pts Polygenic inheritance pattern (autosomal dominant)
o

AD IS NOT THE SAME AS ECZEMA Eczema is a reaction pattern Erythematous patches/plaques with epidermal changes (Scale/crust) Can result from many causes o atopic dermatitis, irritant dermatitis,
allergic contact dermatitis, venous stasis, etc.)

81% of kids with 2 AD parents will have AD; 60% adults with AD have kids with AD

Stronger correlation between siblings with AD (environmental factors too)

Atopy: from Gr. atopos, Strange or unusual Epidemiology of AD Prevalence doubled in last 30 yrs in industrialized countries o 15-30% children, 2-10% adults Females < Males (1.3:1)
Often begins in infancy, 85% before 5yo; 70% remit before adolescence; 50% recur in adulthood; can start in adulthood: late-onset AD

Atopic march: associated with other atopic disorders Food allergy (30% AD pts) Asthma (30-60%) Allergic rhinitis (60-80%) Diagnostic criteria: Must have: Pruritis + Eczema (typical morphology / age specific patterns,
chronic/relapsing)

Signs: Dennie-Morgan folds under eyes (secondary to edema) hyperlinear palms, keratosis pilaris (spiny papules) Ichthyosis (plate-like dark scales on skin) Progression Location Infancy

Most will have: Early age at onset + Atopy (personal/family Hx, IgE reactivity, xerosis = abnormal dryness of skin / mucous membranes) May have other features too

Quality Erythematous + exudative

Skin folds, face, scalp, cheeks Extensor surfaces (not diaper area) Flexor surfaces;
pityriasis alba (post-inflammatory hypopigmentation)

Childhood

Often generalized xerosis (dryness) More ill-defined Lichenification (thickened epidermis) more common

Adulthood

Hand dermatitis common

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Cutaneous infections are common with AD Impetigo (90% AD pts S. aureus colonized) Eczema herpeticum (superinfection with HSV) discrete, punched out ulcers on background of atopic derm Eczema vaccinatum (severe widespread eruptin post-smallpox vax or exposure to vaccinated people, 1:25k-30k) Treatment: 1. Avoid triggers (irritants/allergens/heat/stress/etc): especially food allergies in children, bacteria + environment 2. Moisturize! (ointment>cream>lotion) 3. Mild soaps (Dove) 4. Topical therapy: steroids for flare-up, calcineurin inhibitors 5. Antihistamines: sedating for sleep, nonsedating for day 6. Treat superinfections 7. Phototherapy 8. T-cell suppression (corticosteroids to sequester T-cells, induce apoptosis; macrolides to block early phase of activation,
immunosuppressive agents like methotrexate or purine synth inhibitors if recalcitrant)

Other random conditions (Ddx of AD)

Contact dermatitis: irritant or allergic; sudden onset; linear / geographic (outside job), very pruritic Lichen simplex chronicus: elephant skin or tree-bark-like with accentuation of normal skin markings; more common in adults; chronic itch-scratch cycle (can see in AD, contact dermatitis, psoriasis), hard to treat Nummular eczema: coin-shaped, 1 or several well-demarcated pink plaques, fall/winter, easy to tx Seborrheic dermatitis: infants: cradle cap (scalp + skin folds); adults: pruritis + greasy white-yellow scales + erythema on scalp/eyebrows/ears/central chest (where sebaceous glands are) Tinea Corporis: fungal; one or more annular & polycyclic plaques, use scrape + KOH to diagnose

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Pigmented Lesions & Melanoma

Melanocytes: from neural crest cells; found within basal layer of epidermis (1 melanocyte: 4-10 keratinocytes) dendritic processes with clear cytoplasm & small, dark nuclei (use special stain), solitary cells (no desmosomes) make melanin in melanosomes (organelles) keratinocytes via phagocytosis o makes UV-absorbing cap to absorb radiation

Benign pigmented lesions

Description Ephelide (freckle) small clusters of macules, tan-red to brown, well-circumscribed Irregular evenly pigmented macules, tend to coalesce Location Sun exposed areas: nose, cheeks, shoulders, dorsal hands, arm Patient Common in children Histology pigmenentation; transfer to keratinocytes (not increased local # melanocytes) Other direct relation to sun exposure; recur in summer & fade in winter

Solar lentigo (age spots / liver spots)

Sun-damaged skin (face, dorsal aspects of hands/arms)

Common, middle-aged & elderly

Elongate of rete; no increase in # melanocytes

Incidence increases with age

Nevocellular Nevi (melanocytic nevus / mole): benign melanocytic neoplasms Proliferation of melanocytes cohesive nests & aggregates o (do see # melanocytes) Transformation: lose dendritic processes, become round/oval, nuclei uniform Acquired nevi: Adolescence/early adulthood; enlarge stable involute (maximum in 20s, regress/disappear by 70s-80s) Progression: normally distributed on BMZ, proliferate on junction, descend to dermis, then lose melanocytes in junction 1. Junctional nevus (just at dermal/epidermal junction) a. symmetric, sharply circumscribed, flat, uniform medium/dark brown color
b. No melanocytes in dermis, no atypia, regular size/shape/spacing of nests @ tips of rete ridges

2. Compound nevus (junctional & dermal nests) a. Raised/dome shape (involvement of dermis); uniform light/medium brown color, can be hairy
b. Dermal melanocytes mature with descent (deeper cells smaller/less pigmented/less nested); no atypia

Clinical features of benign acquired nevi Symmetrical Regular borders Uniform color Small (<5mm)
(Compare to melanoma, which inexorably progress)

3. Intradermal nevus (now in dermis) a. Raised lesions, light brown / flesh colored, can be hairy
b. Dermal melanocytes maturing with descent like above but in nests/cords/sheets, pushing upwards

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Congenital nevocellular nevi Present at birth, big variation in size (few mm bathing trunk) Varied appearance (can be asymmetrical, geographic borders but with uniform pigmentation, +/- hair growth) Increased risk of melanoma in affected areas Singular melanocites with dendritic morphology in lower 2/3 dermis

Other acquired melanocytic lesions 1. Dermal melanocytosis (Mongolian spot) o ill-defined patches, blue, Asian infants, birthfade by early childhood 2. Blue nevus o Well-circumscribed, dome-shaped papules, small (<1cm), gray-blue/blue-black, o On dorsal hands/feet/face); present @ birth or any age o M chewing up melanin on path Atypical (dysplasitic) nevi Acquired, pigmented lesion on skin but with different clinical/histological features than nevi o Usually > 5 mm in diameter, symmetrical, regular but fuzzy borders, variations of pigmentation o Architecture: disordered (elongated/bridged rete east-west architecture) o Hyperplasia, cellular atypia (large nuclei, irregular nuclear membrane, etc) but not clonal Some overlap with malignant melanoma o Abnormal ABCDE but clinically stable o Not necessarily precursor lesion but marker of risk 50-100 dysplastic nevi = atypical mole syndrome Puberty can keep developing throughout life Management: most dont progress; follow with photos, biopsy for atypia; re-excise for severe atypia on biopsy

Melanoma
Malignant growth of melanocytes Location: skin/sun-exposed areas; can happen on mucosal too; can be de novo or from existing nevi Epidemiology
8,400+deaths/yr, 60k cases/yr 5% skin cancers but >80% skin cancer deaths 1/75 lifetime risk in US (increasing) 53yo median age at dx nd Most common cancer in women 25-29, 2 to breast cancer in 30-34yo women

Pathophysiology: genetics, immune system (host); radiation, etc (environment)

Histology: nests dont mature; still make pigment as they go down; scattered throughout epidermis, diffuse atypia Risk factors Increased episodic exposure of fair skin to sun (especially in childhood) PMH or FHx melanoma; > 50 or irregular nevi, immunosuppressed pts too Familial atypical mole/melanoma syndrome(FAMM) Melanoma in 1+ 1st/2nd degree relative, >50 moles, autosomal dominant condition Develop melanomas at younger age, lifetime risk approaches 100% ABCDEs of Melanoma Asymmetry: compare one half to another Border: is it ragged/notched/blurred/irregular? Color: is it uneven? (reflects histology) Diameter: is it > 5mm? Evolution: is it changing or evolving in size, shape, color, symptomatology? (use photos) 15

Progression / growth phases Growth phases: radial (epidermis only) vertical (dives down) Stratifying by subtype does not improve prognostic information 1. In situ: no potential to metastasize, confined by basement membrane, no access to lymph / vasculature, can cure with excisional surgery 2. Invasive lesions
Type Superficial spreading Frequency Most common (70%) Location Upper back (+ legs in women) Growth pattern Variable radial phase vertical phase No radial, immediately vertical & aggressive Long radial phase vertical phase Cumulative instead of intermittent sun exposure, Most common subtype in darkly pigmented pts Other Sometimes changes in pre-existing mole

Nodular

20% 5% older (mean age = 65 yo) 5%

Legs + trunk Sun-exposed skin (head/neck) Acral sites (palms/soles/nail beds)

Lentigo maligna

Acral lentinginous

Diagnosis/Prognosis Biopsy is key for both (depth of invasion, # mitoses, ulceration, vacular invasion, sparse lymphocytic response?) Breslows tumor thickness: MOST IMPORTANT histologic determinant of prognosis o top of granular cell layer to base of ulcer @ deepest point of invasion, 90 to epidermis Staging: T1-4 by Breslow depth, N by LNs, M by metastasis o 0: in situ I: small, N0M0 II: larger, N0M0 III: N 1 IV: M 1 Treatment: surgery (need to Dx early) o bigger excision doesnt mean better survival (current guidelines: about 1cm margin per mm tumor) immune system might be key; no single systemic therapy proven to extend life; combo therapy maybe?

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Non-Melanoma Skin Cancer

Basal cell carcinoma and squamous cell carcinoma are most common (also Merkel cell carcinoma, others) Random facts:
SPF only tells you how good a sunscreen is against UVB radiation ABCDE doesnt help so much with these cancers (more for melanoma)

Pathophysiology Host: genetics (skin type, mutations in repair pathways, etc), immune system Environment: solar radiation, viruses, ionizing radiation, chemicals/trauma Triggers UV light is big one (90% cancers have signature UV mutations; on sun-exposed areas) Immunosuppression (100x risk increase for transplant patients); viruses like HPV Genetic mutations: p53 in SCC, Sonic Hedgehog pathway in BCC

Basal Cell Carcinoma

Clinical features: Waxy, pearly, translucent, persistent Friable (bleeds easily), ulcerated, pink scaling plaques 90% on sun exposed areas (head neck, other areas depending on culture) Locally aggressive: usually doesnt spread/metastasize (instead infiltrates surrounding area & destroys tissue) Epidemiology: #1 skin cancer (incidence)
o 80% new skin cancer cases o Annual incidence 0.1-0.5%

High cure rate but 20-40% chance of developing another case Pathophysiology: mutations in SONIC HEDGEHOG PATHWAYS Genes encoding patched homolog (PTCH1), smoothened homolog (SMO)
o

4:1 BCC:SCC in clinic

Usually hedgehog stimulates patched, which inhibits smoothed, which sends a signal for growth if not inhibited

Results in unrestrained growth

Squamous Cell Carcinoma

Clinical features Keratotic/scaly plaques on erythematous base Ulcerated / crater-like / friable 75% on head / neck / hands Invades more than BCC (LN, lungs, etc): risk of metastasis 0.5-5% Epidemiology: #2 skin cancer in gen pop 300k/yr in US #1 cancer in transplant pts

Pathophysiology: mutations in P53 Often 2 hits: one leads to dysplasia, second leads to invasiveness Progression: 1. Actinic keratosis (precursor lesion, can be detected & cured) a. Rough scaly spot on red, irritated base; can shed & recur b. Sandpaper texture (sometimes more easily felt than seen), can have more than 1 c. 90% go away on their own (immune system: transplant patients cant clear) 2. SCC in situ 3. Invasive metastatic SCC 17

Treatment

BIOPSY BIOPSY BIOPSY BIOPSY BIOPSY BIOPSY BIOPSY BIOPSY Lots of treatment options
One cool new treatment is Mohs micrographic surgery: can check 100% of margin while pt waiting & take out more

Consider: tumor type, age, cosmetic results, #/size lesions, distinctness of borders, 1 vs recurrent, location

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Dermatology of Pigmented Skin

People have different colors of skin. A majority of Baltimore & soon the US will be people with skin of color. Non-white ethnic groups tend to have poorer health care outcomes Know the answers to these questions below

What determines skin pigmentation? AMOUNT OF MELANIN PRODUCED BY MELANOCYTES (melanosome activity)
Number of melanocytes generally constant Pigmentation differences from melanosome activity (#/size/composition/distribution) Melanosomes: dendritic cells; produce/distribute melanin to keratinocytes, functions for photoprotection o Pheomelanin (red/yellow melanin): light/dark skin, especially red-heads, women>men Can become carcinogenic when exposed to UV light o Eumelanin (brown/black): abundant in dark-skinned people Epidermal-melanin unit: melanocyte + its 30-40 keratinocytes

What is the rate-limiting enzyme in melanin biosynthesis? TYROSINASE

Melanosomes: organelles that contain melanin; exported to surrounding cells. Matrix proteins + enzymes o 4 stages of development (1=no melanin, type 4 = lots of melanin) o Different skin types have different predominant melanosomal stages (dark skinned = has more stage IV) Tyrosinase is rate-limiting (part of DOPA/etc pathway) deficient in some albinism pts Darker skin: more melanized melanosomes (later stages); bigger, more melanosomes/cell, slower degradation

Differences in epidermal structure: Melanosomes in black skin are larger, individually dispersed in keratinocytes
Stratum corneum Stratum lucidum Water barrier Lipids in SC Melanosomes WHITE Thicker, fewer layers Swells with sun exposure Higher Fewer Smaller, grouped in KC, more numberous in SC than basal layer High Big changes BLACK Thinner, more layers No change with sun exposure Lower More Larger, individually dispersed in KC, more numerous in basal layer Low Less changes ASIAN

Grouped but individually dispersed in sun-exposed areas

Vitamin D production Photodamage

Big changes

Differences in dermal structure: More dilated blood/lymphatic vessels in Black skin (nobody knows why)
Dermis = collagen + elastic fibers + interfibrillar matrix (GAGs & water) Also: less solar elastosis, thicker/more compact than white skin WHITE BLACK Dermis Thinner / less compact Thick / compact Paipillary/reticular layers More distinct Less distinct Collagen fiber bundles Bigger Smaller, closely stacked Lymphatic vessels Moderate/dilated Many, dilated, empty Fibroblasts Fewer, some binucleate cells Many, many binucleated cells Elastic fibers More, more evidence of solar Less, little evidence of solar elastosis (photodamage) elastosis Superficial blood vessels Sparse / moderate More numerous, mostly dilated

Most derm diseases have WORSE PROGNOSES IN BLACK PATIENTS than in white patients
Vitiligo (depigmented patches) Sarcoidosis Pseudofolliculitis barbae (Razor bumps) Keloidosis (more common in AA/Asian pop, can lead to scarring / disability) Traction alopecia from braids, etc.

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Birthmarks in Babies
Neurofibromatosis Type I (BROWN)
Autosomal dominant, 50/50 spontaneous mutations & inherited, multisystem disorder, 1/3500 people, variable expression, nearly 100% penetrance by age 20

Diagnostic Criteria: NEED 2 OF 7 Color-Coded Birthmarks 6+ caf au lait macules (>5mm pre-puberty, >15mm post-puberty) Brown Neurofibromatosis type I 2+ neurofibromas of any type, or 1+ plexiform neurofibroma White Tuberous Sclerosis Freckling in axillae / groin (Crowe sign) Red Infantile Hemangiomas Optic glioma Yellow Nevus sebaceus 2+ Lisch nodules Dysplasia of sphenoid; dysplasia or thinning of long bone cortex 1st degree relative with NF1 Comprehensive screening finds mutations in >95% individuals only indicated if theyre at risk Clinical findings Finding Caf au lait macules

Picture

Description Need 6+ (2 SD from mean)

Age Increase in number throughout childhood

Skin fold freckling ( Crowe sign)

Most specific, nearly pathognomonic finding Hallmark sign; dome-shaped,

90% adults have freckling

Neurofibromas

soft, fleshy, skin-colored to slightly hyperpigmented / firm / nodular;

major source of morbidity (not painful though) Plexiform neurofibromas Feels like bag of worms; disfiguring, can threaten function of area, 8-12% develop malignant tumor

Onset at puberty Increase in size/# throughout adulthood Grow most in puberty & pregnancy

Usually congenital

Tuberous Sclerosis (WHITE)

1/6k-10k, autosomal dominant Can include seizures / multisystem hamartomas / brain/skin/heart/lungs/kidney, along with derm abnormalities Findings around infancy: Cardiac rhabdomyomas (often detected on prenatal U/S) o 50-70% infants with TS have one; 96% infants with one will have TS! Often have several o Often Asx; in ventricular wall, can cause complications Hypopigmented macules (ash leaf spots or more subtle confetti macules) at birth Later findings Seizures before age 1 (70-80%) Angiofibromas (facial in adults, periungual, fibrous forehead plaques in ~20% kids) Retinal (44% pts, call opthamology!) / pulmonary (bad prognosis) hamartomas 20

Renal angiomyolipomas: 70-90% of adults, spontaneous hemorrhage is #1 complication o RENAL PROBLEMS ARE #1 CAUSE OF DEATH IN TS

Infantile Hemangiomas (RED)

Vascular tumor, not malformation; COMMON (4-10% white infants) Nearly all double in size in first 2 months, reach 80% size in 3-5 months, then regress 10%/yr (50% regress @ 5yr, etc) Can complicate: big size, on face, segmental morphology is bad Risk factors: KNOW THESE Females (2-3:1) White, non-Hispanic Premature LOW BIRTH WEIGHT is #1
(40% / 500g in weight)

PHACE(S) Syndrome: need 2 of these Posterior fossa malformation Hemangiomas Arterial anomalies Coarctation of aorta Eye anomalies (S)ternal clefting +/- supraumbilical raphe 9:1 females:males, 20% of pts with facial segmental hemangioma are PHACE(S) Means a more complicated presentation: associated with structural brain & CV anomalies, 50% have neuro sequelae

New therapy for severe hemangiomas: Propranolol (-blocker) nobody knows how it works

Nevus Sebaceous (YELLOW)

1/300 newborns; Definition: small immature sebaceous glands with abortive hair follicules Raised at birth (moms hormones) less warty with time flare up again in puberty May need surgical intervention (scalp / central face) Risk of malignant change: Formerly thought it was around 31% but most of these were benign growths BCC in 0.8%, NO malignant tumors in children, (4 benign tumors) Nevus sebaceous syndrome: EXCEEDINGLY RARE; large nevus sebaceous + mental retardation / neuro signs. NOT IN NORMAL NS

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Drug Eruptions
Background: 2.2% - 13.6% inpts have drug rash, 75% from antibiotics, 94% exanthematous/morbiliform Drug-induced Reaction Patterns: think of pattern for diagnosis! 2. Erythema 4. Blistering
Red man syndrome

1. Exanthemous / Morbilliform
Exanthemous drug eruption Drug hypersensitivity syndrome

5. Pustular
Drug-induced acne AGEP

3. Urticarial
Urticaria Serum-sickness-like reaction

Fixed drug reaction Drug-induced pemphigus, pemphigoid, linear IgA Stevens-Johnson Toxic epidermal necrolysis

Exanthemous / Morbilliform
PICTURE Exanthemous drug eruption exanthem: bursting out DESCRIPTION Morbilliform (maculopapular) Pink / red / salmon Macules/papules, can be confluent Can spread symmetrically (headtrunk) OTHER #1 drug eruption (94%) Starts within 1wk of exposure (semi-synthetic PCNs > 1wk) Resolve 1-2wk post cessation Antibiotics are #1 cause (anti-convulsants too) Management: stop offending agent, antihistamines, topical corticosteroids +/- systemic steroids as needed Occurs after first exposure, 2-6wks afterwards 1 in 1k-10k taking anticonvulsants, sulfonamide abx Allopurinol too Mortality ~10%! Management: MUST STOP offending agent; +/- corticosteroids, topical steroids & antihistamines for Sx

Drug-induced hypersensitivity

Similar to exanthemous drug eruption + systemic

DRESS syndrome: Drug Rash with Eosinophilia and Systemic Sx Fever/malaise / cervical LAD / eosinophilia Skin eruption (exanthema / exfoliative dermatitis) Internal organ involvement (Liver: hepatitis + jaundice, 50% elevated LFTs, renal, CNS, pulmonary)

Erythema
PICTURE Red Man Syndrome DESCRIPTION OTHER Related to Vancomycin exposure (rapid infusion; dont see much anymore), others too Within 10m initiation or completion of infusion Histamine release involved Management: antihistamines (incl. pretreatment); discontinue infusion

Pruritis Erythema: face, neck torso

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Urticarial
PICTURE DESCRIPTION Red, erythematous, pruritic papules / plaques (wheals) with pale halo OTHER nd 2 most common drug eruption (5%) Benign, transient Type I / IgE-mediated hypersensitivity (think about anaphylaxis, watch BP if extensive rash) PCN & derivatives #1 cause, also ACE inhibitors Angioedema: subcutaneous fat / deep dermal tissue rxn Management: discontinue drug, antihistamines, corticosteroids

Urticaria

Serum-sicknesslike reaction (SSLR)

Urticaria & angioedema Fever & arthralgias Serpiginous / erythematous / purpuric eruption at lines of transgradiens on hands/feet (where plantar/palmar surfaces meet

Serum sickness: injection of protein that induces immune response, deposition of immune complexes in vessels, etc. SSLR: from non-protein drugs, NOT associated with circulating immune complexes nd rd 1-3wks post exposure, after 2 -3 exposure, F>M Cefaclor / buproprion are top 2 drugs

Blistering
PICTURE DESCRIPTION Sharply demarcated, round, dusky, erythematous/edematous plaques Happens at same anatomic site each time exposed (weird!) Genetalia / lips / hands / feet OTHER Resolves over 2-3wks, post-inflammatory hyperpigmentation Tetracyclines & sulfonamides often, anticonvulsants too Mortality 5% - EMERGENCY! Histology: full thickness epidermial necrosis & blistering, no SC involvement (FAST) Management(TEN too): ID/stop drug, IVF & supportive care, get to BURN UNIT

Fixed drug eruption (FDE)

Stevens-Johnson Syndrome

Fever, cough, malaise Macula exanthema (can blister) Mucous membrane erosions at 2+ sites < 10% body surface area

Toxic epidermal necrolysis (TEN)

Think of it like more severe SJS Fever, pruritis, conjunctivitis (non-specific) Painful skin (plaques, target lesions, erythema, sheet-like loss of epidermis,
blisters spread with lateral pressure = nikolskys sign)

Mortality 30-50%: BIG EMERGENCY! Histology, management like SJS GET TO BURN UNIT

>30% body surface area

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Pustular
PICTURE Acute generalized exanthematous pustulosis (AGEP) DESCRIPTION OTHER

Acute pustular eruption but sterile (no bacteria) Facial edema, fever + leuckocytosis, 100s of sterile pustules

Resolves 1-2 wks Allopurinol, macrolides + PCN/derivatives (Abx + anticonvulsants)

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Cutaneous Manifestations of Internal Diseases

Oncology
PICTURE DESCRIPTION Firm papules/nodules that are often bound down (rubbery & connected) ulceration Side lighting can help OTHER 10% all metastasis, 75% skin metastasis is first sign of extranodal spread Metastasis spreading upwards, invading dermis, chewing up everything, full of atypia ASSOCIATED DISEASES

Cutaneous Metastasis

Breast / lung / GI / skin cancers

Leukemia Cutis

Small (2-5mm) pinkish, non-tender papules

Localized / diffuse skin infiltration by leukemic cells Can be sign of leukemic cells in peripheral circulation In dermis: epithelial structures /markings still intact Overlap with both pemphigus vulgaris & bullous pemphigoid Intraepidermal split (like pemphigus) Direct/indirect immunofluorescence like pemphigus immunoprecipitation (+) on transitional epithelium of bladder: like bullous pemphigoid) TONS of types of auto-AB very polymorphic very poor prognosis (doesnt get better)

Leukemia

Paraneoplastic Pemphigus (PNP)

Severe mucosal ulceration and polymorphic eruptions associated with neoplasia Erythema multifome-type lesions Friable Vermillion border involvement

CLL/large cell lymphoma/NHL, Waldenstroms macroglobuline mia

Bullous Neutrophilic Dermatosis

Rapidly expanding, very painful, ulcerative lesions Pus: sea of PMNs Looks like bad infection but is aseptic process (can be superinfected though) Violaceous hemorrhagic border

DEBRIDING BAD (if you traumatize lesion, it grows) No antibiotics: want to immunosupress (prednisone, CSA)

Lymphoreticular system malignancies

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Gastroenterology
PICTURE DESCRIPTION Early life: hyperpigmented macules (lips, buccal mucosa, palms/soles / periorifical) Macules fade except on buccal mucosa (stay til adolescence) OTHER Herditary polyposis (autosomal dominant, high penetrance) ASSOCIATED DISEASES GI: Hamatomatous polyps (mostly small bowel, low malignant potential, mostly recurrent pain) GI: Zinc absorption disorder From excessive glucagon production (-cell tumor of pancreas)

Peutz Jeghers

Acrodermatitis Enteropathica

Infancy: acral dermatitis, alopecia, diarrhea Dry, scaly, eczematous patches/plaques early, then evolve into vesiculobullous/erosive lesions

Autosomal recessive Can be acquired (dietary Zn

deficiency, failure of GI absorption, nephrotic syndrome, bypass surgery)

Lab: anemia, low serum/urine Zn Lab: serum glucagon + abdominal CT

Glucagonoma Syndrome (migratory necrolytic erythema)

Edge-active skin lesions (blisters, crusting, scales) Periorificial and intertriginous dermatitis / erythema Glossitis (red tongue) + angular cheilitis (cracks at corner of mouth)

Endocrine / Metabolic
PICTURE Necrobiosis Lipoidica Diabeticorum (NLD) DESCRIPTION Well-demarcated, atrophic plaques Yellow-brown color Anterior / lateral surfaces of lower legs Indurated (thick & firm) plaques/nodules Flesh-colored On pretibial areas of lower legs Can be tender OTHER Chronic, indolent, relatively asymptomatic W>M (3:1) 2/3 with overt diabetes, rest have abnormal glucose tolerance

Pretibial Myxedema

Hyperthyroidism of Graves disease / recovering from thyroid storm

Acanthosis Nigricans

Diffuse, velvety thickening & hyperpigmentation Axilla, other body folds, dorsum of hand

5 types Hereditary Endocrine (insulin resistance, acromegaly, Cushings, Addisons) Obesity Drug-induced Malignancy (usually GI adenocarc)

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Common Infections of the Skin

New techniques: instead of growing bacteria (only see what you grow!) deep sequencing of rRNA with universal primers Flora similar between people, different by site Skin is a defense organ Physical barrier (SC) + constantly shedding Chemical (low PH) Immunologic (skin-associated lymphoid tissue) Microbiological: normal skin flora occupy niche NORMAL SKIN FLORA Cornyeforms (diptheroids)
o cornyebacterium, brevibacterium, propionibacterium spp)

(GM+)

Staphylococci (coag neg) Micrococci Acinteobacter spp Proteus, pseudomonas,enterobacter M. furfur Demodex spp.

(GM+) (GM+) (GM-) (GM-) (yeast) (mite)

THE BIG PICTURE: SKIN INFECTIONS Bacterial: homogeneous, tense red skin, or individual areas + pus (exudates, suppuration),dried pus/serum (crust) Viral: can be diffuse immune rxn or localized with discrete areas of cytopathic damage Fungal: often has leading edge activity with central clearing; often has scale

Bacterial infections: Strep pyogenes and Staph aureus

Streptococcus pyogenes (group A, -hemolytic) Not part of normal skin flora Proteolytic enzymes: RAPID SPREAD through tissue planes; greater local invasion, lymph/vascular spread Edema with scarce exudation Impetigo, erysipelas, celulitis Strep pyogenes skin infections (examples)

Impetigo
Note golden crust (dried serum)

Erysipelas Involves upper dermis, superficial lymphatics

Celulitis Involves deeper dermis and subcutaneous fat

Staph aureus skin infections (examples) Staphylococcus aureus (coagulase positive) Frequently found transitorily on skin Coagulase abscess formation Well-circumscribed, walled-off Central fluctuation Folliculitis, furuncles, carbuncles

Folliculitis
Pilosebaceous unit Overlaps with acne

Furuncle (boil)
Tense, pus-filled, tender, drain eventually

Viral infections
DNA Viruses HPV (warts / cancers) Molluscum contagiosum HSV, VSV (note herpes zoster is VSV)

Papova viruses Poxviridae Herpes viruses

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HPV infection WARTS (STI & otherwise) Make sure to test for HIV & other STIs after Dx 100+ types, 30 infect anogenital mucosa, 12+ oncogenic o HPV-16 HPV-18,31,45 for oncogenicity Cervical (+ anal, oropharyngeal, penile) cancers Vaccine: gardasil (3 shots x 6 mo, 11-12 yo females)

HSV Epidemiology 75% population 15-49yo

Subclinical infection: 15% gen pop, 23% HIV- MSM, 93% HIV+ MSM

Most infections: Asx and undiagnosed Genital warts are just the tip of the iceberg HSV infections

Herpes simplex 2nd most common STD in US (after HPV) HSV-1 > HSV-2 Most asymptomatic Primary infection & recurrences (orolabial / genital) o can reactivate with stress, UV light, etc GROUPED ULCERS ON ERYTHEMATOUS BACKGROUND

Generic HSV
Grouped ulcers on erythematous background

Orolabial Herpes cold sore

HSV-1 > 2

Genital Herpes
HSV-2 > 1

Varicella Zoster Virus: Herpes Zoster (and chicken pox too) latency in sensory dorsal root ganglion outbreak with immunosuppression or age PAINFUL erythematous papules and plaques in a dermatomal distribution Vesicular / bullous within hours, neuralgia can persist for months

Molluscum contagiosum Pox-virus Patients: 1. Children (most common) 2. Sexually active adults 3. Immunosuppressed (HIV) 4. Atopic dermatitis Smooth-surfaced, dome-shaped papules with characteristic umbilication Custered around site of inoculation

Fungal infections
Superficial infections: dermatophytoses (tinea corporis, cruris; onychmycosis, etc.) & candidiases Deep fungal infections too Use KOH prep for diagnosis

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Lesions: edge-active, scale, central sparing

Fungal infections

Tinea Corporis
Microsporum canis, Trichophyton rubrum

Tinea Cruris
Mostly men, inner/upper thighs, jock itch

Tinea Capitis
Mostly schoolchildren T. rubrum, M. canis mostly (US)

Tinea Pedis / Manus

Athletes foot: most common T. rubrum mostly sandal distribution common

Onchyomycosis DSO, WSO, PSO

Tinea versicolor M. furfur

Other answers to test-type questions

Name the infection

Tinea Versicolor Intertrigo HPV

Mostly schoolchildren T. rubrum, M. canis mostly (US)

Tinea Capitis

Molluscum

Tinea

Perleche

Basal Cell Carcinoma

Which isnt a common strep pyogenes infection?: (erysipelas, cellulitis, intertrigo, necrotizing fasciitis, impetigo) Pox virus are DNA viruses
Infection Tinea versicolor Thrush Superficial onychomycosis Distal subungual onchyomycosis Bug Pityrosporum ovale (& M. furfur) Candida Albicans Trichophyton metagphraphes Trychophyton rubrum

29