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Biopsy Techniques SHELLIE D. HILL DNP, RN, FNP-BC

Biopsy Techniques

Incisional biopsy - skin is removed using scalpel incision. This may involve taking part of the skin or removing a complete skin lesion

(excision biopsy).

Punch biopsy, which involves taking a small disc of full thickness skin

using a special punch biopsy instrument.

Shave biopsy, which involves removal of protruding, superficial skin

lesions.

Biopsy Techniques

Incisional biopsy

If the lesion is large and malignancy is not suspected it is acceptable to

perform an incomplete excision. This is often called an incision or

incisional biopsy. It is usually recommended that the specimen include

an area of normal skin.

An excisional biopsy should aim to remove the whole lesion, especially

if malignancy is suspected, with an edge or margin of normal skin

included around the lesion.

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Excisional Biopsy

Ellipse of skin has to be removed to obtain satisfactory closure. The long

axis of the ellipse should be in the direction to produce the best scar.

Langer's lines are a useful guide but wrinkle and contour lines (relaxed

skin tension lines) are also important.

Remember that lesions have three dimensions and it is important to

biopsy deeply enough, usually including some subcutaneous fat.

Close with a few neat Vicryl (nylon) sutures.

Be careful not to crush the specimen.

Rutowski, P., Zdzienicki, M., Zbigniew, N., & Van Akkooi, A. (2010). Surgery of Primary Melanomas. Cancers, 2(2), 824-841. doi: 10.3390/cancers2020824

3 to 1 length-to-width ratio

anesthetized with 1% lidocaine with or

without epinephrine.

30-gauge needle for patient comfort.

#15 scalpel blade held vertical to the skin. Don’t inward bevel. The first pass of the

scalpel on each wound edge should be smooth and continuous to prevent notching of the skin. A second pass of the blade may

be needed to extend these incisions down to the level of the fat.

Lift central island of skin with forceps and cut with scalpel.

Biopsy Techniques

Punch biopsy

punch biopsy is used when a full thickness biopsy is needed – usually

used for benign rashes and skin disorders to assist diagnosis.

Come in various sizes

A 4 mm punch is sufficient for non-facial lesions.

In granulomatous conditions or conditions with atypical features, 5

mm biopsies are preferred.

Biopsies of less than 3 mm may be difficult to process for histology.

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Punch biopsy

1. local anesthesia

2. stretch the skin at 90° to the tension lines

3. Rotate the skin punch into the dermis, being sure to obtain an

adequately deep specimen. Remove the punch when it enters the

subcutaneous fat

4. Raise the specimen above the incision. A 21 gauge needle is

advised rather than forceps that may crush the specimen

5. Cut the specimen free with iris scissors.

6. Close the wound if needed - A punch of 3 mm does not require a

suture but a larger one will need 1 or 2 sutures

Punch biopsy

Punch biopsy

Zuber, T. J. (2002). Punch Biopsy of the

Skin. American Family Physician, 65(6), 1155-1158.

Biopsy Techniques

Shave Biopsy

This is used with protruding skin lesions such as:

Skin tags

Actinic kertoses

Seborrhoeic keratoses

This type of biopsy is not appropriate for suspicious pigmented

lesions.

It usually requires local anesthetic.

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Shave biopsy

No suturing needed

Hemostasis is usually obtained with

aluminum chloride 20% solution or silver nitrate

Don’t crush specimen

(Pickett, 2011)

Anesthetic

Anesthetic Maximum Onset duration

Lidocaine 1% 4.5mg/kg (2 mg/lb.)

5-10 min 45-60 min

Lidocaine 1% with epinephrine

Do Not use on distal extremities, nose or penis.

7 mg/kg (3.5 mg/lb.)

5-7 min 1-2 hours

Suture Types

Suture type description Use for

Ethilon (nylon) Black, non-absorbable Good for wounds with tension – also good for

face if going non-absorbable

Prolene Like Ethilon but blue in color

Good for thick, dark eyebrows or hairy areas

Absorbable –natural (fast absorbing gut)

Absorbs 3-5 days, may cause reaction

Fine skin areas with low tension (lips/vermilion

border, mucous mem.

Vicryl absorbable - synthetic

Synthetic, can take up to 2 weeks for absorption

Deep sutures to get initial alignment and eliminate

surface tension

Staples Very strong Scalp

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Suture guide

Body Region Suture type Removal

Scalp 5-0 or 4-0 or staples 5-7 days

Face 6-0 3-5 days

Eyelid 6-0 or 7-0 3-5 days

Eyebrow 6-0 or 5-0 3-5 days

Trunk 5-0 or 4-0 5-7 days

Extremities 5-0 or 4-0 7 days

Joint surface 4-0 10-14 days

Hand 5-0 7 days

Foot/Sole 4-0 or 3-0 7-10 days

References:

Nischal, U., K., N., & Khopkar, U. (2008). Techniques of skin biopsy and practical considerations. Journal of Cutaneous Aesthetic Surgery, 1(2), 107-111.

Pickett, H. (2011). Shave and Punch Biopsies for Skin Lesions. American Family Physician, 84(9), 995-1002.

Rutowski, P., Zdzienicki, M., Zbigniew, N., & Van Akkooi, A. (2010). Surgery of Primary

Melanomas. Cancers, 2(2), 824-841. doi: 10.3390/cancers2020824

Semer, N. (2007). Practical Plastic Surgery for Nonsurgeons: Hanley and Belfus.

Zuber, T. J. (2002). Punch Biopsy of the Skin. American Family Physician, 65(6), 1155-

1158.

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Common

Dermatological

Issues in Primary

Care SHELLIE D. HILL DNP, RN, FNP-BC

General dermatology points

You must see the rash to diagnose the rash.

Be descriptive in documentation using proper definitions: macular,

bullae, confluent, diffuse, grouped etc.

Biopsy early if unsure of diagnosis especially if you think you will refer

the patient.

Be aware that all types of skin cancer are on the rise. There has

been an alarming increase of melanoma in people aged 18-39.

Acne

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Acne - pathogenesis

Follicular keratinization: keratin

becomes dense and blocks

secretion of sebum. These plugs

are called comedones (closed

and open)

Comedones interact with

androgens and bacteria (P.

acnes) leading to inflammation.

The distended follicle wall breaks

and the leaked contents into the

dermis lead to more inflammation

and foreign-body response

(papule, pustule, nodule)

Contributing factors:

Drugs (Lithium, glucocorticoids,

androgens)

Emotional stress

Occlusion and pressure on the skin

NOT caused by foods - ? milk

Acne - management

Mild acne:

Comedones are best treated with

topical retinoids (tretinoin,

adapalene)

Topical antibiotics (clindamycin and

erythromycin)

Benzoyl peroxide (good anti-

P.acnes)

Combination therapy is best (Benzoyl

peroxide + erythromycin gels PLUS

topical retinoids

Moderate acne:

Continue topical treatment and add

oral antibiotics (minocycline, doxy)

Consider oral contraception or

spironolactone

Acne - management

Severe acne - nodulocystic

Continue topical treatment and refer

to dermatologist for Isotretinoin.

Some ongoing studies on laser

treatments

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Rosacea

Chronic inflammation + increased

reactivity of capillaries

Preluded by episodic flushing and

blushing

Stage I – persistent erythema with

telangiectasia

Stage II – persistent erythema,

telangiectasia, papules and tiny

pustules

Stage III – persistent dark erythema,

dense telangiectasia, papules,

pustules, nodules

Rosacea

Acneiform but key differences in

rosacea vs. acne vulargis

May be associated with

rhinophyma from marked

sebaceous gland hyperplasia and

fibrosis

May be associated with red eye

as a result of chronic blepharitis

Rosacea

Traditional treatments

Topical metronidazole (first line for

most), Azelaic acid, pimecrolimus

cream, sulfacetamide cream

Oral antibiotics for papulopustular–

minocycline, doxy or tetracycline

Oral Isotretinoin in severe disease

Rhinophyma and telangiectasia

respond well to laser treatments

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Rosacea

New treatments

Many new are emerging

Pathogenesis now thought to be

bacterial produced from

Demodex mites

Topical Ivermectin

Brimonidine tartrate 0.33% gel – treats

erythema

Topical sodium sulfacetamide 10%

with sulfur 5% - good for inflammation

and erythema

Laser and IPL

Atopic dermatitis - Eczema

Atopic dermatitis

Pathogenesis:

Interaction of skin barrier, genetic,

environmental and immunologic

factors.

Dry skin = pruritus = scratch = rash

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Atopic Dermatitis

Presents differently with age

Infants – red skin, tiny vesicles on

“puffy” surface. Also scaling

exudation with crusts and cracks.

Atopic Dermatitis

Childhood – Lesions are more papular

with lichenification, erosions, and

crusts.

Common pattern antecubital,

popliteal fossae, neck and face

85% of eczema presents before age 5

Atopic Dermatitis

Adults – more lichenification and

excoriations.

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Atopic Dermatitis -Management

Acute phase

Control of pruritus – oral

antihistamines

Wet dressings

Topical glucocorticoids

Topical Calcineurin Inhibitors (TCI’s)–

Tacrolimus, Pimecrolimus

Topical Mupirocin if secondary

infection – mostly S. aureus

Watch out for MRSA

Subacute and chronic

Hydration of skin – oil in bath followed

by emollients

Control of pruritus – oral

antihistamines

Topical glucocorticoids – bid x 2

weeks only – systemic should be

avoided

Topical TCI’s

Avoid exacerbating factors –

emotional stress, dry air, wool

Probiotics may aid in prevention

Atopic Dermatitis - New evidence

Some evidence that mometason

furoate is more effective for AD with

fewer side effects.

Oils with positive effects on AD –

sunflower seed, coconut and mineral

Negative effect on AD – olive oil

Bleach baths - positive effect on AD

+ decreases colonization of S. aureus

Impetigo

Pathogenesis

Gram-positive bacterial infection of

the epidermis occurring near

Staph aureus colonization

Usually Staph aureus but can be

streptococci or combination of

both

Types

Nonbullous – most common, papules

that progress to vesicles

surrounded by erythema then

pustules that break and form thick,

honey-colored crust

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Impetigo

Bullous – seen in young children,

vesicles enlarge to form flaccid

bullae (2-5mm) with clear yellow fluid

that rupture leaving thin, brown crust

Ecthyma – ulcerative lesions extend

through the epidermis and deep into

dermis, “punched-out” ulcers

covered with yellow crust

Diagnosis

Usually by clinical presentation

Impetigo

Management

Topical antibiotics – use when limited

number of lesions without bullae

Mupirocin tid x 10 days

Retapamulin bid x 5 days (>9mo)

Oral antibiotics – use when bullous or

many lesions

Doxycycline, Cephalexin or

amoxicillin-clavulanate x 7 days

Macrolides do not cover S. aureus or

strep well

Dermatitis

Irritant contact dermatitis

chemical irritant – detergents,

cement, fiberglass, poinsettias

Usually sharply demarcated to

exposure area. Starts with burning

or stinging before objective

findings. Itching can be delayed

Treatment – avoid irritant, barriers

Acutely treat with wet dressings,

topical or oral glucocorticoids

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Dermatitis

Allergic contact dermatitis

antigen causes reaction – nickel,

neomycin, plants

Dermatitis - allergic

Typically well demarcated, superimposed vesicles and papules

Distribution at exposure site

Allergic phytodermatitis occurs when sensitized individuals are exposed to wide variety of plant allergens

First exposure (sensitization) – dermatitis typically occurs 7-12 days after exposure

Dermatitis in previously sensitized patients can be less than 12 hours after exposure

Dermatitis - allergic

Allergens from plants are resins

(oils)

Blister fluid does not contain resin

and cannot spread dermatitis.

Smoke from burning plant does

not cause dermatitis but

particulate matter in the smoke

can

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Dermatitis - allergic

Treatment

Topical glucocorticoids are effective

for non-bullous lesions

Systemic glucocorticoids may be

necessary if severe or exudative

lesions

Systemic treatment should be 10-14

days and taper

My standard taper: Prednisone

10mg. 6 po daily for 2 days, 5 po daily

for 2 days, 4 po daily for 2 days, 3 po

daily for 2 days and 1 po daily for 2

days (#42)

Alternatively, Triamcinolone

acetonide (long-acting) can be

given IM

Dermatitis

Lichen simplex chronicus

Pathogenesis

A localized form of lichenification

occurring in circumscribed plaques

resulting from repetitive rubbing and

scratching. Can last for decades.

Sensitive skin – habitually itches

Difficult to treat – patients must stop

scratching

Occlusive dressings with

glucocorticoids

Oral antihistamines

Psoriasis

Pathogenesis

Psoriasis a complex, chronic,

multifactorial, inflammatory

disease that involves

hyperproliferation of the

keratinocytes in the epidermis,

with an increase in the epidermal

cell turnover rate

It is the most common autoimmune

disease in U.S.

Writer John Updike wrote “ The name

of the disease, spiritually speaking,

is Humiliation”

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Psoriasis

Several different variants

Plaque psoriasis is the most common – 80-90%

Lesions present as sharply demarcated, erythematous plaques with a silvery, micaceous scale. Removal of these scales can cause pinpoint bleeding, known as Auspitz's sign.

plaques are commonly found on the elbows , knuckles, and knees. Can also be on the scalp, the lower back, the periumbilical region, and the intergluteal cleft.

Psoriasis

Guttate – type

Petite, mildly scaled, salmon-pink

papules, predominately on the

trunk, occurring 2-3 weeks after

acute episode of group-A

streptococci

Can spontaneously resolve in a

few weeks with no treatment but

more often evolves to chronic

plaque psoriasis

Psoriasis

Psoriatic arthritis

Can affect up to 30% of those with

cutaneous disease

Peripheral joint pain, stiffness and

damage – hands and feet

may be present without any visible

psoriasis (10%)

often involves fingertips, periungual

skin and nails

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Psoriasis - management

Daily topical emollients

Nonprescription tar preparations –

useful in combination with topical

corticosteroids

Topical corticosteroids (potent to

very potent)

Vitamin D analog or a retinoid –

more effective in combination with a

topical corticosteroid

Psoriasis

Treatment

Methotrexate may be used for as

long as it remains effective and well-

tolerated.

Cyclosporine is generally used

intermittently

Systemic retinoids

Combination therapy may be

helpful

Biologics

PUVA

Ichthyoses

Pathogenesis

Genetic, abnormal stratum

corneum formation and abnormal

keratins

Vulgaris type – Xerosis (dry skin) with

fine scaling, also larger adherent

tacked-down scales in fish scale

pattern

More than 50% of patients also have

atopic dermatitis

Xerosis and pruritus worse in winter

months

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Ichthyosis – KP

Keratosis pilaris

Common, genetic but etiology

unknown

Small, follicular, horny spines most

commonly found on shoulders,

upper arms and thighs

Incidence peaks at adolescence –

usually improves with age

Ichthyosis - KP

Treatment

Hydration of stratum corneum –

creams with urea bind water in the

stratum corneum

keratolytic agents – propylene glycol-

glycerin-lactic acid mixtures, 6%

salicylic acid in propylene glycol

and alcohol or alpha hydroxy

acids

topical corticosteroids or topical

retinoid – short courses

Rare, severe cases – oral retinoid

Pityriasis rosea

Pathogenesis

Herpes virus type 7 is suspected

Rare in infants and elderly

Pruritus – absent (25%), mild (50%),

or severe (25%)

A single herald patch (50-90% of

cases) precedes the exanthem

which develops over 1-2 weeks

Herald patch – oval, slightly raises,

salmon-red with fine collarette

scale at the periphery

Exanthem – fine scaling papules/

plaques, dull pink, oval, scattered

in “Christmas tree” pattern – rarely

on face

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Pityriasis Rosea

Management - symptomatic

oral antihistamines

topical antipruritic or

glucocorticoids

Self-limiting usually in 6-12 weeks,

can be up to 6 months

Recurrences are uncommon

Reassure PR is benign and not

contagious

Refer pregnant women who have

PR in first trimester

Dermatophytoses - tinea

Pathogenesis

Dermatophytes make keratinases that digest keratin and sustain existence of fungi in keratinized structures.

Transmitted by fomites from one person to another (less common by direct skin contact), animals and rarely soil

Predisposing factors: immunosuppression (including topical), atopy, ichthyosis, sweating, occlusion, geographical location, high humidity

Tinea

Clinical presentation varies by site of infection, immunologic response of the host and species of fungus

Can be dry scaling, macerated, moccasin-type, inflammatory, bullous or ulcerative

Tinea pedis (athlete’s foot)

Tinea manuum (hand)

Tinea cruris (jock-itch)

Tinea corporis (ringworm - trunk, legs & arms)

Tinea capitis (scalp)

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Tinea

Tinea

Management

Topical antifungal preparations:

applied bid to involved area for 4

weeks including at least one week

after lesions have cleared. Apply

3 cm beyond advancing margin

of lesion/s.

Imidazole (Lotrimin, Nizoral)

Allylamines (Lamisil, Naftin)

Naphthionates (Tinactin)

Substituted pyridone (Loprox)

Tinea

Systemic therapy:

Extensive corporis infection,

immunosuppression, failed topical

treatment, tinea capitis, tinea

barbae or tinea unguium

Griseofulvin 10mg/kg/day for 4

weeks

Itraconazole 200mg/day x 1 week

or 100mg/day x 2 weeks

Terbinafine 250mg/day x 2 weeks

Fluconazole 50-100mg/day or

150mg/weekly x 2-4 weeks

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Tinea (pityriasis) Versicolor

Pathogenesis

Not a dermatophyte infection but rather a yeast fungal infection (M. furfur)

Predisposing factors

Hot, humid climates, oily skin, hyperhidrosis, hereditary

Symptoms

Usually patients present for cosmetic reasons; occasionally mildly pruritic

Typically on trunk, back, abdomen and upper extremities; color varies; thin scale

Tinea Versicolor

Management

Ketoconazole shampoo- apply to affected area daily, leave on 10-15 minutes and rinse, use for 1 week

Selenium sulfide lotion or shampoo

Azole creams – qd or bid x 2 weeks

Terbinafine solution – bid x 7 days

Systemic therapy with ketoconazole, itraconazole and fluconazole are reserved for severe or resistant infections. Terbinafine and griseofulvin are not effective for tinea versicolor

Candidiasis

Candida is a genus of yeast that is

currently the most common cause

of fungal infections

Intertrigo – body folds

Interdigital – web spaces

Diaper dermatitis

Oral (thrush)

Genital (vaginitis or balanitis)

Characteristic features: multiple,

small erythematous “satellite”

lesions scattered along the edges

of larger erythematous macules

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Candidiasis

Management

Prevention – keep areas dry, washing

with benzoyl peroxide bar,

miconazole powder

Topical antifungal creams applied

twice daily until clear (10 days)

Topical glucocorticoids short term

only

Candidiasis

Intertrigo & Interdigital- topical

nystatin powder, clotrimazole, or

miconazole twice daily

Diaper dermatitis - nystatin,

amphotericin B, miconazole, or

clotrimazole twice daily

Oral – Infants - nystatin oral

suspension. 1ml to each side of

mouth 4 x daily for 10-14 days.

Adults – nystatin oral

suspension. 5 ml swish and

swallow or clotrimazole troches 5

x daily for 14 days.

Candidiasis

Genital

Vaginal - Topical miconazole

nitrate, clotrimazole OR One-time

oral therapy with fluconazole (150

mg) or itraconazole (600 mg)

Balanitis - Topical therapy is

sufficient in most patients.

Evaluate sexual partners and treat

if needed.

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Molluscum Contagiosum

Pathogenesis

Molluscum Contagiosum Virus (MCV

types 1-4) closely related to

poxvirus

Transmission – skin to skin contact

Typical features – papules or small

nodules, pearly white or skin

colored, round, oval, umbilicated.

Inflammatory “halo”

Distribution – isolated single lesion,

multiple, scattered discrete lesions

or clustered. Can occur

anywhere.

MCV

Autoinoculation is common

Usually asymptomatic but can be pruritic

Benign and self-limiting within 6 months

Treatment

prevention of spread (auto or to others), resolution of pruritus, prevention of scarring from trauma or secondary infection

Curettage or cryosurgery

Topical imiquimod, cantharidin tretinoin, lactic acid, salicylic acid, silver nitrate

Erythema infectiosum (Fifth

disease)

Pathogenesis

Parvovirus – DNA virus

Most common in young – 60%

young adults are seropositive

Transmitted by aerosol droplet

Symptoms

Prodrome of fever, malaise,

headache, coryza - 2 days before

rash

Edematous erythematous plaques on

the cheeks and erythematous lacy

rash on trunk and extremities

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Erythema infectiosum

Headache, sore throat, fever,

myalgia, nausea, cough,

conjunctivitis may coincide with

rash

Infected adults likely to have

arthralgia

Management

Symptomatic

Self limiting – 3 weeks

Hand-foot-mouth disease

Pathogenesis

Coxsackievirus

Typically occurs < 10 years of age

Highly contagious – transmitted by

oral-oral and fecal-oral

5-10 painful oral ulcers, cutaneous

lesions (palms, soles, buttocks) can

be asymptomatic or painful

Hand-foot-mouth disease

Low grade fever, malaise, less

commonly arthralgia, diarrhea

Management

Symptomatic

Course 7-10 days

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Herpes (HSV-1 & HSV-2)

Pathogenesis

DNA virus. Once an individual is infected, HSV persists in sensory ganglia proximal to site of infection, recurring when immunity is lessened

Labialis (oropharyngeal): HSV-1 (80-90%), HSV-2 (10-20%)

Urogenital: HSV-1 (10-30%), HSV-2 (70-90%)

Transmission

Infected person sheds virus at peripheral site, mucosal surface or secretion and inoculates close contacts at susceptible mucosal surface or break in skin

HSV1 & HSV2

Worldwide, 90% are seropositive

for HSV-1 by 4th decade of life

HSV-1 infections can be severe

and cause encephalitis especially

immunocompromised hosts

Typical features: prodrome -

vesicles in groups on a

erythematous base-pustules-ulcers

Diagnosis: viral culture, serology,

immunofluorescence, Tzanck

HSV-1 & HSV-2

Treatment

HSV-1: topical acyclovir cream

Acyclovir 200-400mg 5 x daily

Famciclovir 1500mg as single dose

Valacyclovir 2 gram bid x 1 day

HSV-2: initial outbreak: acyclovir 400mg tid x 7-10 days

Famciclovir 250mg tid x 7-10 days

Valacyclovir 1 gram bid x 7-10 days

Recurrent outbreaks: acyclovir 800mg tid for 2 days

Famciclovir 1000mg bid x 1 day

Valacyclovir 1 gm daily for 5 days

Suppressive therapy for HSV-2

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Herpetic whitlow

< 20 years of age usually HSV-1, >

20 years of age usually HSV-2

HSV infection of fingers that can

occur as a complication of

primary HSV-1 or HSV-2 by

inoculation of the virus through a

break in skin barrier (commonly a

torn cuticle)

painful

Herpes Zoster

Pathogenesis

Viral infection caused by reactivation

of varicella-zoster virus (VZV)

Primary infection (varicella) resolves

and the viral particles remain

dormant in the dorsal root or

sensory ganglia. When hosts

immune systems fails to suppress

replication of VZV, reactivation

occurs.

Persons who have had previous

varicella infections or vaccination

may develop herpes zoster.

Herpes zoster

Rash and pain: erythematous

papules-vesicles-pustules-crust

Course in healthy people = 7-10

days

Usually affects one dermatome

but 2-3 neighboring dermatomes

may be affected.

Post herpetic neuralgia (PHN)

Diagnosis: history and clinical

examination – lab not beneficial

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Herpes zoster

Treatment

Antivirals: acyclovir 800mg 5 x daily for 7-10 days

Valacyclovir 1000mg tid x 7 days

Famciclovir 500mg tid x 7 days

Mixed data for using oral steroids to prevent PHN

Pain control: gabapentin, opioids

Referral needed

Ophthalmicus

Oticus – triad of facial paralysis, ear pain and vesicles in auditory canal

Measles

Vaccine became available in

1963

Travelers with measles continue to

bring the disease into the U.S.

Highly contagious – transmitted by

aerosol droplet, can live up to two

hours on a surface or airspace.

90% of close contacts of infected

persons that are not immune will

become infected

Infected people are contagious from

four days before to four days after

the rash appears

Measles

Can be very serious – especially

age <5 or >20. 1-2/1000 mortality

2014: 644 cases from 27 states

From January 1 to February 6,

2015, 121 cases from 17 states -

most of these part of a large,

ongoing outbreak in Disneyland

The majority of the people who

got measles were unvaccinated,

under vaccinated or status was

unknown

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Measles

Symptoms: 7-14 days after

exposure

high fever, cough, coryza and

conjunctivitis

2-3 days later - Koplik spots

3-5 days – maculopapular erythema

that appear on the face at the

hairline and spread downward to

the neck, trunk, arms, legs, and

feet. Some papular and confluent

– fever may spike when rash

appears

Measles

If measles is suspected, report to local health

department and obtain serum and throat

swab for testing

Close follow up

Seborrheic keratosis

Most common benign epithelial

tumors

Hereditary, start after age 30

Evolve over months to years

Early lesions small, slightly elevated

papule, later – larger plaque

Late lesions – plaque with warty

surface “stuck on” appearance

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Seborrheic keratosis

Management

Rule out malignancy first – punch

biopsy

Cryosurgery with liquid nitrogen – only

effective on flat lesions

Curettage is best followed by light

cautery to prevent recurrence

Careful application of trichloroacetic

acid

Ammonium lactate and alpha

hydroxy acids have been reported

to reduce the height of lesions

Actinic keratosis

Precancerous - actual

percentage that progress to

squamous cell carcinoma remains

unknown, estimates vary from as

low as 0.1% to as high as 10%

Biopsy – initial or treatment

resistant

Single or multiple, discrete, dry,

rough, adherent scaly lesions

Occur on sun-exposed skin

Gently abrading lesions usually

causes pain – helpful diagnostic

finding

Actinic keratosis

Therapy is generally well tolerated

and simple; therefore, treatment

of all actinic keratosis is warranted.

Medical management

Prevention - sunscreen

5-Fluorouracil – bid for 1 month

Imiquimod – 2-3 x weekly for 1 month

Ingenol mebutate – 2-3 consec. days

Topical diclofenac sodium 3% gel –

bid for 3 months

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Actinic keratosis

Surgical management

Photodynamic therapy - painful

Cryosurgery

Curettage or excision – scarring

Laser

Combination topical with cryosurgery

Pyogenic granuloma

Rapidly developing vascular lesion

usually following minor trauma.

Benign but send in for confirmation

and r/o malignancy

Solitary, smooth surface, red,

brown/black with or without

crusts/erosions

Bleeds easily

shave excision and cautery

surgical excision with primary closure

- if large

Cutaneous Carcinomas

Most common cancer in the U. S.

Each year, more new cases of skin

cancer than cancers of the

breast, prostate, lung and colon

combined (Skin Cancer

Foundation, 2011)

Melanoma is the deadliest form of

skin cancer, killing approximately

8,650 Americans in 2009 (Skin

Cancer Foundation, 2011)

Overall, the literature research

revealed evidence that PCPs

could reduce morbidity and

mortality of skin cancer if they

focus screening on patients at risk.

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Cutaneous Carcinomas

Major Risks:

a personal or 1st degree relative with

melanoma

immunosuppressive therapy after

transplant

more than 100 nevi or more than 4

dysplastic nevi

received 250 or more PUVA

treatments

radiation as a child for cancer,

Risks:

naturally red or blonde hair color

Freckles easily

50 to 100 nevi or dysplastic nevi

burns easily, tans poorly

history of many sunburns

age >50

Basal Cell Carcinoma (BCC)

The bad news – most common skin cancer in U.S. and many other countries

The good news – slow growing and usually do not metastasize

Characteristic features

Waxy papules with central depression

Pearly

Rolled border

Bleeding

Crusting

Erosion or ulceration

Basal Cell Carcinoma

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26

BCC

Treatment

Biopsy – Excise if can, shave may be

acceptable if large or in difficult

place

Refer

Squamous Cell Carcinoma (SCC)

Second most common skin cancer

and higher mortality than BCC

Twice as frequent in men as in

women and rarely appears before

age 50 (Nolen et al., 2011)

Some form grow slowly, some quickly

Common features

Raised, firm, skin-colored or pink

Keratotic papule or plaque

SCC

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27

SCC

Treatment

biopsy – shave biopsy can miss

well-differentiated SCC

refer

Malignant Melanoma

The good news – only about 5% of

skin cancers

The bad news – Three times as

many deaths each year

compared to nonmelanoma skin

cancer

Most often in skin but can be from

melanocytes in eyes, ears, GI

tract, genital or oral mucous

membranes (Habif, et al., 2011)

Melanoma

Common features

Can be found anywhere on body

Plaque – few mm-several cm

Irregular borders

Varied colors

Nodular

Nonpalpable tan or brown macule

– lentigo melanoma

ABCDE

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28

Melanoma

Melanoma

Treatment

Refer

References:

CDC. (2015a). Centers for Disease Control and Prevention: Measles. Retrieved February 2015 http://www.cdc.gov/measles/index.html

CDC. (2015b). Centers for Disease Control and Prevention: Public Health Image Library - measles. Retrieved February 2015 http://phil.cdc.gov/phil/home.asp

Dermnet Skin Disease Atlas. (2015). Retrieved January 6, 2015, from http://www.dermnet.com/

Dermquest Images. (2015). Retrieved January 7, 2015, from https://www.dermquest.com/image-library/ Lyons, F., & Ousley, L. (2015). Dermatology for the Advanced Practice Nurse. New York, New York: Springer.

Medscape. Retrieved January, 2015, from http://www.medscape.com/nurses

Nolen, M. E., Beebe, V. R., King, J. M., Bryn, N., & Limaye, K. M. (2011). Nonmelanoma skin cancer part 1. Journal of the Dermatology Nurses' Association, 3(5), 260-283.

Samuel Freire da Silva, M. D. (January 2015). Dermatology Atlas. Retrieved January, 2015, from

http://www.atlasdermatologico.com.br/index.jsf

Son D, H. A. (2014). Overview of Surgical Scar Prevention and Management. Journal of Korean Medical Science, 29(6),

751-757.

Wolff, K., Johnson, R. A., & Suurmond, D. (2005). Fitzpatrick's Color Atlas & Synopsis of Clinical Dermatology (fifth ed.).

New York: McGraw-Hill.