Protection

Thermoregulation

Immunologic Response

Barrier to water loss

Secretion of Wastes

Sensation

History

Examination

Identify the primary lesion

The size in millimeters

Secondary changes

Color

Arrangement and distribution of the lesion

Approach to the case

(Dermatology)

Color change in the skin that is flat to the surface of the skin and not palpable, <1cm

OR

If > 1cm in size

Macule

Patch

Intradermal

Subcutaneous

Types of Birthmarks

Vascular

Epidermal

Other:

Lymph vessel birthmarks

Pigmented cell birthmarks

Hypopigmentation

Nevus simplex

Port wine stains

Hemangiomas

Epidermal nevus

Nevus sebaceous

Stork bite on the nap of the neck

Angel eyes when on the upper eyes and facial area

Present at birth

Persists through life

Port Wine Stain (Naevus Flammeus)

Relatively uncommon (0.3%)

Present at birth as sharply demarcated red macules or patches

Port Wine Stain (Naevus Flammeus)

Port Wine Stain (Naevus Flammeus)

Although initially macular, they become irregular, thickened and nodular over time

Port Wine Stain (Naevus Flammeus)

Can occur anywhere on the body, but most common on the face

Unilateral and segmental

Port Wine Stain (Naevus Flammeus)

Port Wine Stain (Naevus Flammeus)

Common 44%

Patches are scarlet to pink and flat, can be totally blanched and deepen in color with vigorous activity or changes in temperature

Resolve or significantly regress with time

Most commonly found on nape followed by the glabella and eyelids

Nevus Simplex (Salmon Patch)

Nevus Simplex (Salmon Patch)

Appear in form of circumscribe oval or round, soft domed swelling of intense scarlet-red color

Usually stabilize within 9-12 months

Incidence: 10% of infants by 12 months of age

-Increased in low-birth weight infants

Risk Factors:

Caucasian

Female

Multiple gestations

Advanced maternal age

Family Hx

Maternal Hx of miscarriage

Physical Exam:

Neonate: Flat pale lesion, superficial telangiectasia with halo border, pinkish eccymotic lesion

Physical Exam:

Infant: Raised red rubbery non-tender lesion with well-demarcated borders. Overlying skin is usually intact.

Physical Exam:

Deep layer lesion: Raised soft mass with bluish-purplish discoloration with smooth, intact, overlying skin

Physical Exam:

Complex/combined: lesions will have both cutaneous and deep layer features

Physical Exam:

Involuting lesions: Flat, atrophic pale or gray center with surrounding raised reddish border with stippled texture

Diagnostics:

Imaging occasionally helpful to distinguish ____ from vascular malformations

Diagnostics:

May be necessary to determine the extent of internal or visceral lesions

Consider Tx of lesions interfering with critical organ function such as vision or breathing or leasion significantly affecting the appearance

Sugical removal

Intralesional or systemic steroids

Propranolol either systemically or topically as an alternative to steroid therapy

Pathophysiology: ____ arise from pluripotential germinative cells of the basal layer of the embryonic epidermis

Incidence: female to male ratio 4:1

Epidermal Nevi

Majority present in first year of life

Range in color from skin-colored to dirty yellow to brown

Epidermal Nevus

Epidermal Nevus

QD or BID treatment with topical calcipotriene may flatten lesions.

Surgical excision only definitive cure.

Nevus Sebaceous

Pathophysiology:

Abnormality results from a defect in the ectoderm

Nevus Sebaceous

Pathophysiology:

Thought to be due to a mosaic genetics abnormality

Nevus Sebaceous

Pathophysiology:

An over abundance of sebaceous glands without hair follicles

Nevus Sebaceous

Physical Exam:

Infancy or young child: presents as a solitary smooth, yellow-orange hairless patch, often oval or linear in shape

Adolescence: Become more pronounced appearing bumpy, warty or scaly

Nevus Sebaceous

Nevus Sebaceous

Diagnosis

Monitor

Full skin thickness excision may also be arranged for cosmetic reasons but a scar is inevitable

Excision at puberty

Laser treatment

Nevus Sebaceous

Complications

Sebaceous Naevus Syndrome

Approx 15% will develop secondary epithelial tumors including basal cell carcinoma and trichoblastoma

Ichtyosis

Epidermolysis bullosa

Ichthyosis

Ichthyosis

May be classified according to clinical manifestations, genetic presentation, and histologic findings.

Acquired or inherited

Ichthyosis

Ichthyosis vulgaris

Lamellar ichthyosis

Epidermolytic hyperkeratosis

Congenital ichthyosiform erythroderma

X-linked ichthyosis

Ichthyosis

Ichthyosis vulgaris (95% of all ichthyosis cases) FLG (filaggrin is a structural protein)

Recessive X-linked ichthyosis STS

Harlequin ichthyosis ABCA12

Lamellar ichthyosis TGM1 (transglutaminiase 1 is an enzyme) and others

Congenital ichthyosiform erythroderma ALOXE3 and others

Diagnostics:

Routine histopathology

Electron microscopy

Skin biopsy specimens may be required to determine the specific classification of disease

Ichthyosis

Ichthyosis Management

Controlling scaling with ammonium lactate 12% or urea cream 10-40% QD or BID

Oral retinoids- antikeratinizing

Daily lubrication and good skin care regimen

Reduce risk for infection

Epidermolysis Bullosa

Epidermolysis Bullosa

Diagnostics

Genetic testing

Biopsy

Epidermolysis Bullosa

Prevent Blisters:

-Avoiding overheating by keeping rooms at an even temperature.

-Applying lubricants to the skin to reduce friction and keep the skin moist.

-Using simple, soft clothing that requires minimal handling when dressing a child.

-Waring mittens at bedtime to help prevent scratching

Care for blistered skin

Treat infections- with antibiotic ointments

Treat nutritional problems

Genetic Counseling

Affects 85% of adolescents

Onset between 7 and 10 years

Early lesions are usually limited to the face and are primary closed comedones

Risk Factors:

Genetics

Pathophysiology:

Increased sebum production

Hyperkeratinization

Proliferation of Propionibacterium acnes

Inflammation

Etiology:

Environmental factors

Friction

History: age of onset, medications, menstrual history, androgens excess, psychological impact

Diagnostics: Consider lab work up if early or late onset, signs of androgen excess, or __ unresponsive to traditional therapy

Topical Keratolytic Agents

Topical Antibiotics

Systemic Antibiotics

Oral Retinoids

Hormonal Therapy

Retinoids

Benzoyl Peroxide

Side Effects:

Erythema

Dryness

Irritation

Initial acne flares

Hypo or Hyperpigmentation

Photosensitivity

Retinoids:

1st line for most pts

Tretinoin

Adapalene

Tazarotene

Salicylic acid

Azelaic acid

Use for mild inflammatory and comedonal acne or as adjunct with oral or topical antibiotic to prevent antibiotic resistance

Available as a lotion, cream, wash, and gel in 2.5-10%; 5% concentration up to twice daily

Benzoyl Peroxide

Side effects include

Drying

Erythema

Burning

Peeling

 Stinging

Rarely contact dermatitis

Benzoyl Peroxide

Benzoyl Peroxide

Topical Antibiotics

Systemic Anitbiotics

Oral Retinoids

Oral Contraceptives

Topical Antibiotics

(Management of Acne)

Topical Antibiotics

(Management of Acne)

Topical Antibiotics

(Management of Acne)

Management of Acne

Topical Antibiotics: ___ is the most effective

Systemic Antibiotics

(Management of Acne)

Management of Acne

Systemic Antibiotics

Minocycline or doxycycline 50-100mg BID (with food) or Tetracycline >8yrs 0.5-1g divided BID (on empty stomach).

Use with retinoids; do not use alone

Isotretinoin

(Management of Acne: Oral Retinoid)

Isotretinoin

(Management of Acne: Oral Retinoid)

Side Effects:

Teratogenicity

Depression

Suicide

Isotretinoin

(Management of Acne: Oral Retinoid)

Oral Contraceptives

(Management of Acne)

Use caution in girls that smoke

Side Effects:

Nausea

Breast tenderness

Weight gain

Breakthrough menstrual bleeding

Oral Contraceptives

(Management of Acne)

Complications:

Scarrinig

Self esteem

Depression

Suicide

Impetigo

Ecthyma

Cellulitis

Folliculitis

Abscess

Scalded Skin Syndrome

Superficial skin infection characterized by the eruption of shallow pustules that rupture and form thick yellow crusts

Contagious

Non-bullous impetigo

Bullous impetigo

Ecthyma

Pathogens:

Group A beta-hemolytic strep

Staphylococcus aureus

Misc. gram-neg and anaerobic bacteria

Pathogens:

S. aureus

Pathogens:

Group A beta-hemolytic strep

Staphylococcus aureus

Misc. gram-neg and anaerobic bacteria (including Pseudomonas)

Physical Exam:

lesions first begin as thin-walled vesicles or pustules on an erythematous base. They promptly rupture, releasing their serum which dries forming a light brown, "honey-colored" crust.

As lesions resolve with treatment, the crusts slough from the affected areas and heal without scarring

Physical Exam:

lesions form on grossly normal or previously traumatized skin. The vesicles do not rupture as easily or quickly as non-bullous lesions, but they do enlarge into bullae that are usually 1-2cm in diameter. The bullae contain a clear yellow fluid that subsequently turns cloudy and dark yellow

After lesions rupture, a thin, light brown, crust remains

Physical Exam:

The lesion is a vesicle or pustule overlying an inflamed area of skin that deepens into a dermal ulceration with overlying crusts

Physical Exam:

The crust of the ___ lesions is gray-yellow and is thicker and harder than the crusts of impetigo.

A shallow, punched out ulceration is apparent when adherent crust is removed and the deep dermat ulcer has a raised indurated surrounding margin

Physical Exam:

___ heals slowly and commonly produces a scar

Regional lymphadenopathy is common

Topical therapy; preferred Tx with limited number of lesions without bullae

Mupirocin 2% ointment or cream TID x 5 days

Oral Therapy: used when lesions are bullous or large surface area

Amoxicillin-Clavulanic acid 40mg/kg/d divided intot 2 doses x 10 days

Cephalexin 25mg/kg/d in 4 divided doses x 10 days

Clindamycin 15-25mg/kg/d in 3 divided doses x 10 days

Complications:

Cellulitis

Lymphangitis

Scalded skin syndrome

Pathophysiology:

Usually occurs after local trauma that breaches in the integument; may develop to local invasion or infection

Etiology:

S. aureus

GABHS

S. pyogenes

History:

An expanding, red, painful area of swelling is most common presentation

History of local trauma

Physical Exam:

Erythema, edema, tenderness and warmth

Distinct demarcation of raised erythema

A red streak extending proximally

Diagnostics:

WBC normal or elevated

Wound Cx

Imaging

B-lactam oral antibiotics active against Staph and Strep (Amoxicillin-Clav or Cephalexin) 7-10 days

Cephalexin- most cost-effective

Clindamycin or Bactrim (when high suspicion of MRSA)

Abscess: I and D; treat against S. aureus with Clindamycin or Bactrim

May require IV antibiotics

Localized collection of pus in the skin, occurs deep in the skin, diagnosed as an erythematous, firm, acutely tender nodule with ill defined borders

Incision and drainage

May require adjunctive systemic antibiotics

Remove follicular obstruction

warm wet compression for 2h

Topical or oral antistaphylococcal antibiotics may be required

Caused by a circulating toxin

Staphylococci (S. aureus)

Diagnostics:

WBC

ESR

PCR serum test