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Dermatology. By Katrice L. Herndon, MD Internal Medicine/Pediatrics June 2, 2005. What is this?. Acne Vulgaris. Acne is a self-limited disorder primarily of teenagers & young adults. Acne is a disease of pilosebaceous follicles. 4 factors are involved: Retention hyperkeratosis

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Katrice L. Herndon, MD

Internal Medicine/Pediatrics

June 2, 2005

Acne vulgaris
Acne Vulgaris

  • Acne is a self-limited disorder primarily of teenagers & young adults.

  • Acne is a disease of pilosebaceous follicles.

  • 4 factors are involved:

    • Retention hyperkeratosis

    • Increased Sebum production

    • Propionbacterium acnes within the follicle

    • Inflammation

Acne vulgaris1
Acne Vulgaris

  • External Factors that contribute to Acne

    • Oils, greases, dyes in hair products

    • Detergents, soaps, astringents

    • Occlusive clothing: turtlenecks, bra straps

    • Environmental Factors: Humidity & Heavy exercise.

    • Psychological stress

    • Diet is controversial

Acne vulgaris2
Acne Vulgaris

  • Acne vulgaris typically affects those areas of the body that have the greatest number of sebaceous glands:

    • the face, neck, chest, upper back, and upper arms.

  • In addition to the typical lesions of acne vulgaris, scarring and hyperpigmentation can also occur.

  • Hyperpigmentation is most common in patients with dark complexions

Acne vulgaris3
Acne Vulgaris

  • Classification of Acne

    • Type 1 — Mainly comedones with an occasional small inflamed papule or pustule; no scarring presentType 2 — Comedones and more numerous papules and pustules (mainly facial); mild scarringType 3 — Numerous comedones, papules, and pustules, spreading to the back, chest, and shoulders, with an occasional cyst or nodule; moderate scarringType 4 — Numerous large cysts on the face, neck, and upper trunk; severe scarring

Acne rosacea
Acne Rosacea

  • Rosacea is an acneiform disorder of middle-aged and older adults.

  • Characterized by vascular dilation of the central face, including the nose, cheek, eyelids, and forehead.

  • The cause of vascular dilatation in rosacea is unknown.

  • The disease is chronic.

Acne rosacea1
Acne Rosacea

  • rosacea is a chronic disorder characterized by periods of exacerbation and remission.

  • Increased susceptibility to recurrent flushing reactions that may be provoked by a variety of stimuli including hot or spicy foods, drinking alcohol, temperature extremes, and emotional reactions.

  • The earliest stage of rosacea is characterized by facial erythema and telangiectasias.

Acne rosacea2
Acne Rosacea

  • Patients with rosacea may develop severe sebaceous gland growth that is accompanied by papules, pustules, cysts, and nodules.

  • The diagnosis of rosacea is based upon clinical findings(1 or more of the following):

    • Flushing (transient erythema)

    • Non-transient erythema

    • Papules and pustules

    • Telangiectasia

Acne rosacea3
Acne Rosacea

  • Topical antibiotics or benzoyl peroxide are the initial treatments of choice.

  • Tretinoin cream is used in patients with papular or pustular lesions that are unresponsive to other treatments.

  • The chronicity of rosacea requires that medical therapy be continued long-term, not just for flare-ups of the condition.

Allergic contact dermatitis
Allergic Contact Dermatitis

  • Contact dermatitis refers to any dermatitis arising from direct skin exposure to a substance. It can be allergic or irritant-induced.

  • An allergen induces an immune response, while an irritant directly damages the skin.

Allergic contact dermatitis1
Allergic Contact Dermatitis

  • The most common sensitizer in North America is the plant oleoresin urushiol found in poison ivy, poison oak, and poison sumac

  • Other common sensitizers in the US:

    • nickel (jewelry)

    • formaldehyde (clothing, nail polish),

    • fragrances (perfume, cosmetics),

    • preservatives (topical medications, cosmetics),

    • rubber

    • chemicals in shoes (both leather and synthetic)

Allergic contact dermatitis2
Allergic Contact Dermatitis

  • Treatment

    • Avoidance of exposure to the offending substance.

    • Use of corticosteroids topical or oral in the acute phase of the reaction maybe helpful.

    • Cooling of the skin by using calamine lotion or aluminum acetate


  • Psoriasis is a common chronic skin disorder typically characterized by erythematous papules and plaques with a silver scale.

  • Most of the clinical features of psoriasis develop as a secondary response triggered by T-lymphocytes in the skin.


  • Several clinical types of psoriasis have been described:

    • Plaque psoriasis - symmetrically distributed plaques involving the scalp, extensor elbows, knees, and back.

    • Guttate psoriasis - abrupt appearance of multiple small psoriatic lesions.

    • Pustular psoriasis - most severe form of psoriasis. Characterized by erythema, scaling, and sheets of superficial pustules with erosions.

    • Inverse psoriasis - refers to a presentation involving the intertriginous areas.


  • Nail psoriasis -the typical nail abnormality in psoriasis is pitting w/ color changes & crumbling of the nail.


  • Most patients w/ psoriasis tend to have the disease for life.

  • There is variability in the severity of the disease overtime w/ complete remission in 25% of cases.

  • The diagnosis of psoriasis is made by physical examination and in some cases skin biopsy.



  • Treatment modalities are chosen on the basis of disease severity.

    • Topical emmollients, topical Steroids, tar

    • Calcipotriene(Dovonex) affects the growth and differentiation of keratinocytes via its action at the level of vitamin D receptors in the epidermis.

    • Tazarotene, is a topical retinoid, systemic retinoids

    • Methotrexate, cyclosporine

    • Immunmodulator therapy (embrel, remicade)

    • Ultraviolet light.


  • Vitiligo is an acquired skin depigmentation that affects all races but is far more disfiguring in blacks.

  • The precise cause of vitiligo is unknown Genetic factors appear to play a role.

  • 20-30 percent of patients may have a family history of the disorder.

  • The pathogenesis is thought to involve an autoimmune process directed against melanocytes.


  • Peaks in the second and third decades.

  • The depigmentation has a predilection for acral areas and around body orifices (eg, mouth, eyes, nose, anus).

  • The course usually is slowly progressive.

  • The diagnosis of vitiligo is based upon the clinical presence of depigmented patches of skin


  • Repigmentation therapies include:

    • corticosteroids

    • calcineurin inhibitors

    • Ultraviolet light

  • Pseudocatalase cream

  • Surgery – minigrafting techiniques

  • Depigmentation therapy w/ hydroquinone

Pityriasis rosea
Pityriasis Rosea

  • Pityriasis rosea is an acute, self-limited, exanthematous skin disease characterized by the appearance of slightly inflammatory, oval, papulosquamous lesions on the trunk & proximal areas of the extremities.

  • The eruption commonly begins with a "herald" or "mother" patch, a single round or oval, rather sharply delimited pink or salmon-colored lesion on the chest, neck, or back.

  • 2 to 5 cm in diameter.

Pityriasis rosea2
Pityriasis Rosea

  • A few days later lesions similar in appearance to the herald patch, appear in crops on the trunk & proximal areas of the extremities.

  • The eruption spreads centrifugally or from the top down in just a few days.

  • The long axes of these oval lesions tend to be oriented along the lines of cleavage of the skin, like a christmas tree pattern.

  • Then the lesions fade without any residual scarring.

Pityriasis rosea3
Pityriasis Rosea

  • The presence of a herald patch by history or on examination.

  • The characteristic morphology and distribution of the lesions.

  • The absence of symptoms other than pruritus combine to make PR an easy diagnosis in most instances.

Pityriasis rosea4
Pityriasis Rosea

  • Differential Dx include: Psoriasis, secondary syphilis, tinea corporis, Lyme disease, & drug eruptions.

  • Treatment is usually reasurrance.

    • Topical Steroids

    • Antipruitic lotions (prax, pramagel)

    • Phototherapy

    • Erthyromycin in severe cases

    • Rash usually persists for 2-3 months


  • Cellulitis is an infection of the skin with some extension into the subcutaneous tissues.

  • An extremity is the most common location but any area of the body can be involved.


  • Five factors were identified as independent risk factors:

    • Lymphedema

    • Site of entry (leg ulcer, toe web intertriginous, and traumatic wound)

    • Venous insufficiency

    • Leg edema

    • Being overweight


  • Cellulitis is a recognizable clinical syndrome with both local & systemic features.

  • Systemic symptoms include:

    • Fever and chills

    • Myalgias

    • Increased WBC count


  • Local findings typical of cellulitis:

    • Macular erythema that is largely confluent

    • Generalized swelling of the involved area

    • Warmth to the touch of the involved skin

    • Tenderness in the affected area

    • Tender regional lymphadenopathy is common

    • Lymphangitis may be present

    • Abscess formation also may be present


  • Cellulitis in the majority of patients is caused by beta-hemolytic streptococci groups A, B, C, G, and Staphylococcus aureus.

  • Other less common pathogens include H.flu, P.aeruginosa, Aermonas hydrophilia, Pasturella multocida.


  • Diagnosis is clinical

  • Treatment: Anti-strep/Anti- staph

    • Cefazolin

    • Nafcillin

    • Clindamycin

    • Vancomycin

    • Fluoroquinolones (3rd & 4th generations)

    • Macrolides (erythromycin, azithromycin)

      Duration of treatment is usually 10-14 days


  • Erysipelas is a characteristic form of cellulitis that affects the superficial epidermis, producing marked swelling.

  • Bacterial Organisms:

    • Beta-hemolytic streptococci group A

    • Group C & G less commonly

    • Staph. Aureus

    • Streptococcus pneumoniae, enterococci, gram negative bacilli


  • The erysipelas skin lesion has a raised border which is sharply demarcated from normal skin.

  • This is its most unique feature and allows it to be distinguished from other types of cellulitis.

  • The demarcation is sometimes seen at bony prominences.

  • The affected skin is painful, edematous, intensely erythematous, and indurated (peau d'orange appearance).


  • The face historically was the most common area of involvement.

  • Erysipelas is diagnosed clinically

  • It can mimic other skin conditions:

    • Herpes zoster (5th cranial nerve)

    • Contact Dermatitis

    • Urticaria


  • Treatment:

    • Penicillin is the preferred treatment

    • Erythromycin

    • Clindamycin

    • Fluoroquinolones

  • Erysipelas does have the propensity of recur.


  • Ecthyma is an ulcerative pyoderma of the skin caused by group A beta-hemolytic streptococci.

  • Because ecthyma extends into the dermis, it is often referred to as a deeper form of impetigo.

  • Preexisting tissue damage (excoriations, insect bites, dermatitis) & immunocompromised states ( diabetes, neutropenia) predispose patients to the development of ecthyma.


  • Ecthyma begins as a vesicle or pustule overlying an inflamed area of skin that deepens into a dermal ulceration with overlying crust.

    • A shallow, punched-out ulceration is apparent when adherent crust is removed.

    • The deep dermal ulcer has a raised and indurated surrounding margin.

  • Ecthyma lesions can remain fixed in size or can progressively enlarge to 0.5-3 cm in diameter.

  • Ecthyma heals slowly and commonly produces a scar.

  • Regional lymphadenopathy is common.



  • Topical mupirocin ointment

  • Gentle surgical debridement

  • Oral/IV antibiotics

    • Penicillin

    • Clindamycin

    • Macrolides

    • Cefazolin

Tinea vesicolor
Tinea Vesicolor

  • Tinea versicolor is a common superficial infection caused by the organism Pityrosporum orbiculare.

  • Which is a saprophytic yeast that is part of the normal skin flora.

Tinea vesicolor1
Tinea Vesicolor

  • Lesions can be hypopigmented, light brown, or salmon colored macules.

  • A fine scale is often apparent, especially after scraping.

  • Individual lesions are typically small, but frequently coalesce.

  • Lesions are limited to the outermost layers of the skin.

Tinea vesicolor2
Tinea Vesicolor

  • Most commonly found on the upper trunk & extremities, & less often on the face and intertriginous areas.

  • While most patients are asymptomatic, some complain of mild pruritus

  • The diagnosis of tinea versicolor is confirmed by direct microscopic examination of scale with 10 % potassium hydroxide (KOH).

Tinea vesicolor3
Tinea Vesicolor

  • The differential diagnosis includes seborrhea, eczema, pityriasis rosea, and secondary syphilis.

  • Treatment includes topical antifungals. Oral antifungals can be used for more extensive disease: Ketocanozole 400mg x 1 dose. Fluconazole and itraconazole are also effective.

Cutaneous warts
Cutaneous Warts

  • Cutaneous warts AKA verrucae are caused by HPV which infects the epithelium of skin and mucus membranes.

  • Cutaneous warts occur most commonly in children and young adults.

  • Also more common among certain occupations such as handlers of meat, poultry, and fish.

  • Predisposing conditions include atopic dermatitis & any condition in which there is decreased cell-mediated immunity.

Cutaneous warts1
Cutaneous Warts

  • Infection with HPV occurs by skin-to-skin contact

  • Incubation period following exposure in 2-6 months.

  • Warts can have several different forms based upon location & morphology (flat, mosaic, and filiform warts)

  • Lesions may occur singly, in groups, or as coalescing lesions forming plaques.

Cutaneous warts2
Cutaneous Warts

  • The diagnosis of verrucae is based upon clinical appearance.

  • Scrape off any hyperkeratotic debris & reveal thrombosed capillaries (seeds).

  • The wart also will obscure normal skin markings

Cutaneous warts3
Cutaneous Warts

Differential Diagnosis:

  • Lichen Planus

  • Seborrheic Keratosis

  • Acrochordon or skin tag

  • Clavus or corn


  • Spontaneous regression in 2/3 over 2yrs

  • Salicylic acid, liquid nitrogen, cantharidin

  • Cyrotherapy, curettage, laser therapy

  • Immunotherapy, intralesional injections

Secondary syphilis
Secondary Syphilis

  • Syphilis is a chronic infection caused by the bacterium Treponema pallidum which is sexually transmitted.

  • Syphilis occurs in 3 stages:

    • 1st stage is characterized by the classic chancre, which is a 1-2cm ulcer with raised indurated borders, usually painless and occurs at site of innoculation. Heals spontaneously.

Secondary syphilis2
Secondary Syphilis

  • Secondary or systemic syphilis is characterized by a rash.

  • The rash is classically a symmetric papular eruption involving the entire trunk & extremities including the palms and soles.

  • Systemic symptoms include fever, headache, malaise, anorexia, sore throat, myalgias, & weight loss.

  • Lymphadenopathy (inquinal, axillary)

  • So-called "moth-eaten" alopecia

  • Condyloma lata, grayish white lesions involving the mucus membranes

Secondary syphilis4
Secondary Syphilis

  • Diagnosis at this stage is usually by serologic testing but darkfield microscopy can also be done for direct visualization of spirochete.

  • Non-treponemal testing:

    • Veneral disease research laboratory (VDRL)

    • Rapid plasma reagent (RPR)

  • Treponemal testing:

    • Fluorescent treponemal antibody absorption test

    • Microhemagglutination test for antibodies

Seconday syphilis
Seconday Syphilis


  • T.Pallidum remains very sensitive to PCN.

  • Long-acting benzathine penicillin G should be used.

  • If documented chancre or a NR serologic testing was done in the past 1 yr, one IM dose is appropriate.

  • If neither of the above applies this needs to treated as latent syphilis and 3 q week doses must be given.

  • Doxycycline, erythromycin or zithromycin in pen allergic patients x 14 days.

Herpes zoster
Herpes Zoster

  • Reactivation of endogenous latent VZV infection within the sensory ganglia results in herpes zoster or "shingles", a syndrome characterized by a painful, unilateral vesicular eruption in a restricted dermatomal distribution.

  • How the virus emerges from latency is not clearly understood.

  • Patients frequently experience a prodrome of fever, pain, malaise and headache which precedes the vesicular dermatomal eruption by several days.

Herpes zoster1
Herpes Zoster

  • The rash initially appears along the dermatome as grouped vesicles or bullae which evolve into pustular or occasionally hemorrhagic lesions within three to four days.

  • The thoracic and lumbar dermatomes are the most commonly involved sites of herpes zoster.

  • The complications of herpes zoster include ocular, neurologic, bacterial superinfection of the skin and postherpetic neuralgia

Herpes zoster2
Herpes Zoster


  • Antivirals:

    • Acyclovir

    • Famciclovir

    • Valacyclovir

  • Antivirals w/ corticosteroids

  • Analgesics: opioids/acetominophen

Actinic keratosis
Actinic Keratosis

  • Actinic keratoses (AKs) are premalignant lesions that develop only on sun-damaged skin.

  • AKs appear as patches of hyperkeratosis with some surrounding erythema on sun-exposed areas of the head and neck, forearms and hands, and upper back.

Actinic keratosis2
Actinic Keratosis

  • The differential diagnosis of AKs includes seborrheic keratoses, verruca vulgaris, SCC, and superficial BCC.

  • The treatment of AKs begins with prevention.

    • Avoiding sun exposure

    • sunscreens reduce the development of AKs,

    • Active treatment of AKs depends upon the size of the lesion and the number of lesions present.

    • Liquid Nitrogen

    • Surgical curettage

    • Chemotherapy (5-FU, diclofenac, imiquimod)

    • Dermabrasion

    • Photodynamic therapy


  • Basal Cell Carcinomas begins as small shiny nodules and grows slowly. It is the most common form of skin cancer.

  • Frequently, the central portion breaks down to form an ulcer with a reddish-purple scab. These tumors usually remain fairly localized and rarely spread elsewhere.


  • Squamous Cell Carcinoma is another common form of skin cancer. When these tumors first appear they are firm to the touch. They appear most often on sun-exposed areas of your body.

  • Squamous cell carcinoma evolves very slowly through a premalignant stage known as a solar or actinic keratosis.

  • Untreated, significant numbers of these lesions can metastasize to distant sites. Tumors on the lower lip and ears are at higher risk to spread.


  • Malignant Melanoma is the most dangerous form of skin cancer.

  • They arise from either pre-existing moles or normal skin.

  • Malignant melanoma, like basal and squamous carcinomas, is linked to overexposure to the sun.

  • But it can appear any place on your body.

  • When detected early & with proper treatment, the recovery rate from this form of skin cancer can be very high.


  • Harrison’s 15th Edition. Principles of Internal Medicine

  • Up to Date

  • Emedicine

  • Dermatology Pearls Adult and Pediatric