Exam (elaborations) NR511 MIDTERM STUDY GUIDE

Exam (elaborations) NR511 MIDTERM STUDY GUIDE Actinic keratosis most common precancerous skin lesion in light skinned patients, more common in patients 50 years or older (most common in Celtic, Irish, and Scottish descent) Found in sun exposed areas Caused by skin cells that accumulate from repeated sun exposure Pathophys: continued sun damage from UV radiation damages the DNA in epithelial cells Primary lesions: macules or plaques, poorly circumscribed Secondary lesion: erythematous and scaly (May feel like sandpaper when touched) Not an aggressive form of cancer if/when it changes to squamous cell unless on the lip Patient complaints subjective: irritated, rough or scaly rash, pruritus, tenderness or stinging sensation Objective findings: reddened, scaly, rough, or uneven surfaces. Hard or spiny lesion. Sandpaper like texture. Diagnostic tests: fluorescence using photosensitizing drug (methyl ester of 5-aminolevulinic acid) over area of concern will have a pink fluorescence with the wood’s lamp Treatment: no evidence to support removal of lesion as most will not turn cancerous however it is standard to REMOVE the lesion(s) Topical Therapy: 5-fluorouracil (5-FU) cream (Efudex, Carac) applied in a thin layer over the lesion BID for 3 weeks, avoid eyelids, lips, and folds of the nose. This treatment causes red, raw, and painful skin in the areas applied which may lead to noncompliance. Exposure to sunlight makes this worse Imiquimod 5% cream used for face and scalp lesions. Applied 3x weekly for 8 weeks. Diclofenac 3% in 2.5% hyaluranon gell (Solaraza) applied BIF for 60 to 90 days Adapalene 0.1%to 0.3% (topical retinoid)applied daily for 4 weeks and then increased to BID Side effects of these treatments include redness, itching, rash, and dry skin Topical chemotherapy combined with phototherapy with blue or red wavelength have better cosmetic results than cryosurgery. 2 day course Cryosurgery tissue is destroyed by freezing using liquid nitrogen. Hypopigmentation may occur at site of previous lesion NR511 MIDTERM STUDY GUIDE Surgical curettage or shave excision are not considered first line treatments for actinic keratosis Surgical biopsy is the only way to obtain an intact sample to be analyzed as a way to confirm diagnosis If treatment does not work no matter the choice always refer to dermatologist Education is centered around prevention, avoidance of excessive sun exposure, use of protective clothing, and use of sunscreen. Should teach patients ABCDE mnemonic A= asymmetry B= border irregularity C= color change D= Diameter larger than a pencil eraser E= elevation from a flat lesion to a raised or evolving lesion 2. Dermatitis DERMATITIS ATOPIC DERMATITIS • Atopic dermatitis (eczema) is not considered a distinct disease entity but is a descriptive term for a group of skin disorders characterized by pruritus and inflammation, whose distinct cause is unknown. • Eczemais a more general term that is often used collectively to describe skin of an erythematous and inflamed appearance, reflective of a superficial pathological process. Currently, the terms eczema and dermatitisare often used synonymously in the clinical arena in a nonspecific sense. • The use of the term eczematous rash, although also indistinct, may be helpful both diagnostically and therapeutically, because eczematous dermatitis may be classified into two major etiological categories—contact dermatitis and atopic dermatitis. • Early in its presentation, atopic dermatitis is erythematous in appearance, with papulovesicular lesions that ooze and crust. At its later stages, the rash becomes a red-purple color, dries, and develops scaling and lichenification, which is exacerbated by itching resulting from its highly pruritic nature. Epidemiology and Causes • Atopic dermatitis is a constitutional and inherited reaction, which usually begins in infancy. • Children born to older women are more likely to develop eczema than children born to younger women. • Prevalence of atopic disease is now estimated at 1 in 18 or 5.5%, which amounts to 15 million people in the United States. About 10% of the U.S. population will have atopic dermatitis at some point in their lifetime. • Atopic dermatitis presents more severely in childhood. Onset during the first year of life occurs in up to 50% of all patients; in 85%, onset is before age 5 years. Up to 5% of all children are affected by atopic dermatitis. Most cases (40%) resolve by adulthood, however. The remainder of patients with atopic dermatitis are affected with a chronic course of the disease that is characterized by acute exacerbation (often during times of stress) and intermittent remissions. • No ethnic predisposition has been found for atopic dermatitis, and it occurs equally in both sexes. • The cause of atopic dermatitis is unknown. • Family history is positive for atopy in two-thirds of all cases. Genetic predisposition may be the most important etiological factor in all-atopic conditions. A personal or family history of all or part of the “atopic triad”—asthma, allergic rhinitis, and eczema—is often present. • It has been proposed that individuals with any of these three conditions have preferential production of allergenspecific immunoglobulin E (IgE) and that the presence of such antibodies should be a mandatory criterion for the diagnosis of atopic dermatitis. Such a diagnostic test, however, only establishes the diagnosis of atopic syndrome, not atopic dermatitis. Any patient with a history of hives (urticaria), hay fever, or rashes should be considered to have an atopic history. • All atopic individuals seem to have itchier skin, yet what seems to be unique about the atopic patient's skin is its hypersensitivity. • Many factors that do not make non-atopic individuals itch will make the atopic person feel itchy. Atopic patients are known to itch seconds after experiencing a stressful event. This type of reaction is thought to be caused by neuropeptide-induced vasodilation, which produces a rise in skin temperature and erythema. • Symptoms are triggered or exacerbated through the interaction between genetic predisposition and environmental factors. Environmental factors that trigger atopic dermatitis include dust mites, animal dander, pollen, microbes, pollutants, climate, and emotional stress. • Excessively hot or cold climates or excessively dry or moist environments are particularly suitable for setting the stage for the atopic process. Anything that dries the skin can aggravate symptoms: • Common triggers include excessive bathing, hand washing, lip licking, sweating, or swimming. • Contact with irritants such as solvents, detergents, deodorants, tobacco, cosmetics, soap, and woolen and synthetic fabrics can precipitate an exacerbation of atopic dermatitis. Heat and sweat may also be aggravating factors for atopic dermatitis. • Factors that generate an increase in body temperature include hot showers or baths, overdressing, use of heating pads, and electric blankets. • Patients with atopy are intolerant of heat, have difficulty with thermal sweating, and are more likely to develop heat exhaustion. It is thought that perspiration retention might be a complicating factor in atopic patients. • Excessive humidity is, therefore, a problem, because it interferes with normal evaporation of sweat from the body. Improperly fitting clothes can create friction and irritate the skin, and contact with certain fabrics, most notably wool, can precipitate a flare-up. Other skin conditions or infections can also lead to an exacerbation of atopic dermatitis (eczema). Pathophysiology The inflammatory process in eczema causes erythema of the skin as a result of dilated blood vessels that are surrounded by inflammatory cells that migrate into the epidermis, resulting in edema both inside and in between the epidermal cells (spongiosis). The epidermal cells malfunction as a consequence, resulting in thickening of the epidermis (acanthosis), excess production of keratin, and scaling. The outer epidermal layer of the skin, the stratum corneum, normally forms an impermeable barrier that protects the living cells beneath from environmental irritants and toxins. In atopic dermatitis, this outer barrier is impaired. There is an increase in the water loss and a decrease in water binding, which leads to a brittle outer barrier. This condition is made worse by environmental factors such as physical trauma from scratching, cycles of wetting and drying, and the chemical erosion that is caused by detergents and solvents. In addition, superinfection of eczematous skin by bacterial (e.g., Staphylococcus aureus) or fungal (e.g., Malassezia furfur) species and irritation from dust mites and their dung is an important factor that worsens atopic dermatitis by potentiating the immune response. Superinfection is also much more likely in atopic dermatitis than in other forms of dermatitis such as psoriasis. Thus, infection may be thought of as both a trigger and a complication of atopic dermatitis. Immunological abnormalities are key to the pathophysiology of the atopic response. These abnormalities can include elevated serum IgE levels, which are seen in 85% of affected individuals; hypereosinophilia; reduced cellmediated immunity and antibody-dependent cellular cytotoxicity; slowed chemotaxis of neutrophils and monocytes; relative increase in the number of CD4-positive (CD4+) Th2 helper T cells that secrete interleukin-4 (IL4); and a decrease in CD4+ T helper cells that secrete interleukin-2 (IL-2). Interestingly, however, in later stages of the immune reaction, Th1 helper T-cell activity, which enhances cell-mediated immunity, appears to play an increasing role. Th17 cells and their associated cytokines have also been implicated in this disease process, including in the protection against infection/colonization with superficial skin fungi and bacteria (e.g., Staphylococcus) containing superantigens that are thought to trigger dysregulated immune responses, resulting in eczematous lesions. However, reports in the literature are conflicting and have implicated Th17 cells in both proinflammatory and anti-inflammatory roles. Impairment of essential fatty acid metabolism has also been implicated as a causative factor of atopy. Clinical Presentation Subjective • Atopic dermatitis is characterized by an extremely low threshold for pruritus and has been referred to as “the itch that rashes.” Almost always, the itch occurs before the rash appears, and scratching the rash only worsens it clinically. • The cardinal sign of atopic dermatitis is severe pruritus, which is often extremely distressing in both the acute and chronic stages. In turn, the diagnosis of atopic dermatitis cannot be made without a history of pruritus, and if pruritus is absent, alternate diagnoses should be sought. • The patient may report a personal or family history of other atopic conditions (asthma, allergic rhinitis). • The patient usually reports a history of episodic exacerbation of similar symptoms or of a childhood rash or eczema. • The clinician should inquire about any exposure to known or unknown common antigens and irritants, regardless of the history. Individuals with atopic dermatitis are not immune to contact dermatitis; in fact, they are more susceptible to irritant reactions because of their impaired epidermal barrier layer. Often, the rash is reported as better in the warmer months and worse in the fall and winter. Objective • Atopic dermatitis usually begins as infantile eczema, with lesions affecting the cheeks, face, and upper extremities. Erythema is often seen before pruritus. • The acute lesions are often excoriated, maculopapular, and inflamed. In infancy and early childhood, oozing and crusting usually characterize the erythema. As the child becomes older, the disease can go into remission or change to a flexural distribution (antecubital fossae and neck area). Flexural eczema usually lasts until about age 4 to 10 years but may continue into adulthood. • In adults, eczema presents with symmetrical lesions that are crusting and excoriated. I • n the early stages, lesions may be erythematous, papulovesicular, edematous, and weeping. Later the rash becomes crusted, scaly, thickened, and lichenified. Intergluteal involvement is uncommon and should raise suspicion of another diagnosis. • The classic locations for lesions are noted to correspond to areas that are most accessible to rubbing and scratching. In addition, the typical flexural sites are more susceptible because they are areas that are more likely to be hot and moist. Diagnostic Tests • Laboratory tests are usually not useful in the diagnosis of atopic dermatitis, but they can be helpful in ruling out other disorders or to confirm that a patient is prone to atopy (allergic reactions). • If a viral etiology (e.g., HSV) is suspected, a viral culture should be done on the exudate and moist parts of the rash. • If atopy (allergy) is suspected, a radioallergosorbent test (RAST) may be done on serum to quantify levels of allergen-specific IgE. The RAST test is usually available to primary-care clinicians, whereas the scratch (skin prick) tests are typically done only by trained allergists. However, interpretation of RAST test results requires specialized knowledge of the specificity and sensitivity of the assay, because false-positive results are not uncommon. Thus, RAST tests should not be ordered arbitrarily or as a general atopic screening tool; instead, they should be directed by a detailed patient history. RAST panels often include not only antigen-specific IgE levels but also antigen-specific IgG and IgM levels, which are not helpful in the diagnosis of atopic disease (hypersensitivity) and are, therefore, prone to misinterpretation. Distribution • Infants: Trunk, face, extensor surfaces, scalp • Children: Antecubital fossae, popliteal fossae • Adults: Face, neck, upper chest, genital area, hands Stages Acute • Erosions with serous exudate • Intense pruritus • Papules and vesicles on an erythematous base • Pain, heat, tenderness Subacute • Scaly, excoriated • Pruritus (may be intense) • Papules or plaques over an erythematous base • Secondary infection possible Chronic • Lichenification, pigmentary changes (increased or decreased) • Pruritus • Excoriated papules and nodules • Dryness, fissuring Other Clinical Manifestations • Keratosis pilaris (“chicken skin”): Asymptomatic follicular papules, particularly on the posterolateral aspects of the upper arms and lateral thighs • Lichenification of the skin: predilection for flexural creases • Ichthyosis vulgaris: Hyperlinear palms and soles and fishlike scales, especially on the lower legs • Dennie's sign/Morgan line: Infraorbital fold • Excessive fissuring under the earlobes, palms, soles, and fingers • Pityriasis alba: Hypopigmented asymptomatic areas on the face and shoulders • Allergic “shiners”: Facial pallor and infraorbital darkening • Anterior capsular cataracts • Keratoconus: A cone-shaped cornea may develop in the second or third decade of life (in severe cases) • Facial erythema, dry skin, history of wool intolerance, nonspecific hand dermatitis, and a tendency for skin infection (commonly impetiginization of excoriated skin CONTACT DERMATITIS • Contact dermatitis is a common condition categorized as either irritant dermatitis or allergic dermatitis. Although both of these conditions can have similar presentations, the etiology of each disease is what differentiates the two dermatitides. • Allergic contact dermatitis is immunologically mediated, whereas irritant contact dermatitis is the result of repeated “insults” to atopic skin from caustic, irritant, or detergent-type substances. Epidemiology and Causes • Almost any substance may induce a cutaneous reaction depending on its concentration, the duration of contact, and the condition of the contacted skin. • The etiology of allergic contact dermatitis may be from antimicrobials such as neomycin, antihistamines, anesthetics such as benzocaine, hair dyes, preservatives, latex, or adhesive tape. • The etiology of irritant contact dermatitis may be from soaps, detergents, or organic solvents. Irritant contact dermatitis accounts for about 80% of all cases of contact dermatitis. Delayed-type hypersensitivity reactions are immunological responses to contact allergens that occur in sensitized individuals. • One of the most frequent causes of allergic contact dermatitis is from plants in the Rhus genus, which includes poison ivy, poison oak, and poison sumac. • Other common topical sensitizers include ragweed pollen, dust mites, ethylenediamine (a stabilizer in many topical creams), potassium dichromate, paraphenylenediamine (dyes), nickel (10% of females are allergic to nickel found in jewelry), rubber compounds, and benzocaine (an OTC topical anesthetic for itching or pain). • It is estimated that there are more than 6 million chemicals in the environment and that approximately 3,000 of them are potential sensitizers. • Contact dermatitis accounts for 4% to 7% of all dermatology consults. • Hand dermatitis affects 2% of the population at any given time, and 20% of female patients will be affected at least once in their lifetime. • Contact dermatitis is more common in adults than in children, and effects are more extreme in elderly patients. • Women are twice as likely as men to develop dermatitis and are at highest risk after childbirth. • White Americans are affected more frequently, and fair-skinned redheads are the most vulnerable population. Pathophysiology Contact dermatitis is considered either allergic or irritant induced. A delayed-type hypersensitivity response (type IV immune reaction) elicits a non–IgE-mediated allergic response to specific antigens when applied to the skin, producing a local reaction characterized histologically by epidermal changes including intracellular edema, spongiosis, and vesiculation. • On initial contact with the offending agent, the antigen is taken up and processed by epidermal antigenpresenting cells known as Langerhans cells. These cells present antigens to naïve, antigen-specific CD4+ and CD8+ T lymphocytes, located in regional lymph nodes that drain the affected areas of skin. Over approximately 10 to 14 days, sensitized T cells migrate from the lymph nodes to sites of antigenic exposure, where subsequent reexposure to the same antigen results in an allergic reaction mediated by cytokine release. This response with notable skin surface changes typically occurs within 12 to 48 hours of reexposure to the antigen. • Irritant contact dermatitis is the result of a direct cytotoxic effect of an irritant to the cells of the epidermis, with a subsequent inflammatory response in the dermis. The main pathological feature of contact dermatitis is intracellular edema of the epidermis, which may result in intraepidermal vesicles and bullae formation in the acute phase. In chronic cases, papules, scaling, and lichenification occur. Irritants penetrate and disrupt the stratum corneum and injure the underlying epidermis and dermis as various immune cells congregate around dilated capillaries, contributing to the inflammatory process. • Rubber-glove dermatitis demonstrates the spectrum of pathophysiological mechanisms involved in contact dermatitis. • Chemical irritants used in the glove manufacturing process (e.g., thiram, mercapto derivatives) may cause an allergic dermatitis via a delayed-type T-cell–mediated hypersensitivity reaction. In addition, rubber glove components may result in a direct irritant effect on the moist skin of glove-wearers. • Finally, the natural rubber protein latex, once widely used in medical products, may elicit a profound IgEmediated immediate hypersensitivity response, leading to systemic anaphylaxis and even death. • Interestingly, people with venous stasis (i.e., impaired venous return with pooling of blood in distended veins, particularly in the lower extremities) are more susceptible to irritant contact dermatitis, particularly from wood alcohols such as lanolin, fragrances, topical antibiotics such as neomycin, and methylparaben preservatives. • Correctly diagnosing this condition is often difficult because contact dermatitis is often indistinguishable from stasis dermatitis. Clinical Presentation Subjective The cardinal symptom of contact dermatitis is a pruritic erythematous rash. • Often, the patient is not aware of a previous history, but there may have been periodic episodes of pruritic rash that resolved spontaneously. • The patient may or may not be able to describe the conditions or substances contributing to the dermatitis, but exposure history to known or unknown common antigens and irritants should be sought by the clinician. • In allergic contact dermatitis (in contrast to atopic dermatitis), the inflammatory reaction on the skin occurs much faster, typically within 6 to 12 hours of reexposure. • In contrast to allergic contact dermatitis, irritant reactions do not always occur immediately after contact with the offending substance. The response time between the initial contact with the irritant and the symptoms is variable, and the severity of the reaction depends on the concentration, amount, and length of exposure to the irritating substance. Objective Contact dermatitis presents with inflammation of the epidermis and is manifested by erythema (as in all types of dermatitis), but it does not present with the smooth, intact epidermal surface that characterizes hives (urticaria). • The epidermal inflammation seen in acute contact dermatitis results in rough, reddened patches but without the thickening and discrete demarcation of psoriasis. • The acute lesions of contact dermatitis are characterized by weeping lesions with numerous tiny vesicles on an erythematous base that is pruritic or has a burning or stinging sensation. The surrounding area in severe cases is also erythematous, with edema and increased heat in the area, making it difficult to rule out secondary bacterial infection in some cases. Lesions in nonallergic and delayed-type hypersensitivity contact dermatitis present in similar fashion, but the typical distribution and the lack of an atopic history are the most helpful factors in the diagnosis. • A clothing- or detergent-related cause should be suspected if the lesions are generalized and primarily affect the borders of the axillae, waist, and upper thighs. • Reactions to toxic plants (e.g., Rhus or Toxicodendronspecies) follow a history of exposure. The characteristic rash is vesicular and linear (or asymmetrical) and is frequently found on the hands and ankles. Rhus dermatitis lesions are sometimes found on the facial area if the patient has inadvertently scratched the face with contaminated fingers. • Lesions in an area where jewelry has been worn recently (e.g., neck, wrist, earlobes) may indicate a hypersensitivity to nickel. Usually, the area of skin that has been the most heavily contaminated will break out first, followed by areas of lesser exposure. • The location of the rash gives the clinician the best clues to the possible etiological agent. For example, a patient with a rash on the scalp and the back of the neck might report a history of the use of a new shampoo, a new hair dye, or other scalp or hair treatments. Diagnostic Reasoning Diagnostic Tests Diagnosis of contact dermatitis is based on the history of exposure to an irritant or allergen and the subsequent appearance of a rash on the exposed skin, either immediately or later on (delayed hypersensitivity). • If scabies is suspected, skin scrapings can be examined under a microscope to rule out that condition. • If tinea (corporis, cruris, pedis, manuum) infection is suspected, skin scrapings should be treated with potassium hydroxide (KOH) and gently heated. A microscopic exam for tinea infection should search for hyphae and spores. • If bacterial infection (impetigo) is suspected, cultures should be taken from the moist areas of the rash or from the discharge. Viral cultures can be done to rule out suspected viral etiology (herpes simplex, herpes zoster). Contact Dermatitis Stages Acute • Erythema and edema • Clear, fluid-filled vesicles or bullae • Exudate, clear fluid • Distinct margins Subacute • Lessening edema • Formation of papules • Less distinct margins Chronic • Minimal edema • Scaling skin • Lichenification • Minimal erythema Diagnostics • Laboratory tests that are done by specialists (allergist) include the scratch and intradermal tests. • Scratch (skin-prick) tests should not be done during an acute episode of contact dermatitis because of an increased rate of false-positive reactions. • The patch test performed by a dermatologist is useful to identify specific irritants in patients with histories that are suggestive of acute contact dermatitis. Allergens that are commonly responsible for such reactions are fixed in dehydrated gel layers and taped against the skin of the patient's back for 48 hours and then removed. A final reading done at 72 to 96 hours after initial application will usually reveal any evidence of contact dermatitis. • • In some patients, a CBC with differential will show eosinophilia, but this blood test is neither sensitive nor necessary for the diagnosis. • Skin biopsy is rarely necessary for diagnosis, particularly in the setting of a convincing contact exposure history. Differential Diagnosis The differential diagnosis of contact dermatitis is similar to that for atopic dermatitis and includes both common and rare disorders. Common disorders that have a similar presentation to contact dermatitis include: seborrheic dermatitis, impetigo, and herpes zoster. • Seborrheic dermatitis rashes, although erythematous, have a greasy and scaly appearance and appear only in certain areas of the body such as the hairline, the ears, the scalp, and the face. • Impetigo, which is caused by gram-positive Staphylococcusor Streptococcus bacteria, is more common in children. A honey-colored crust is seen on top of the erythematous lesions; impetigo also does not have a linear appearance like contact dermatitis. • Herpes zoster is more common in older patients, and the lesions appear as multiple small vesicles on an erythematous base. Although herpes zoster has a linear distribution, it is more likely to occur on the trunk area (contact dermatitis occurs more often on the hands or face) and will follow the path of a dermatome. Management The clinical challenge in the treatment of contact dermatitis is to provide symptomatic relief to the patient while attempting to identify the underlying allergic precipitant. • Identifying the antigen or irritant in contact dermatitis is critical, both to eliminate or minimize the current contact and to avoid future exposure. • The responsible irritant should be identified and eliminated to prevent the cycle of itching, scratching, and skin disruption, which can lead to chronic changes in the skin. • A careful history of exposures is key in addition to a thorough skin examination. • The effects of Rhusdermatitis (from poison ivy, poison oak, or poison sumac) may be lessened if the exposed skin is thoroughly rinsed in soap and water or with isopropyl alcohol, as soon as possible after exposure. Exposed clothing should be discarded. For localized contact dermatitis with weeping lesions, treatment with moist compresses and simple drying agents or antipruritic lotions (e.g., Burow's aluminum acetate solution, Calamine lotion) applied several times a day is usually effective. • For more extensive and severe cases, potent topical steroids in cream form (avoid the use of ointments on wet lesions because they can cause skin maceration) can be applied twice daily for the first few days to help decrease pruritus and inflammation. • If treatment is necessary beyond 2 weeks, a less potent (mild or moderate) topical steroid may be used twice daily until the rash resolves. • High-potency steroids should not be used on the face or in bodily folds (intertriginous areas) because of their ability to thin the skin and cause hypopigmentation. Oral systemic steroids may be indicated in acute and particularly severe cases of contact dermatitis offering relief within 12 to 24 hours. • Relatively high doses of oral prednisone can be given for 10 to 14 days (or up to 21 days in the most severe cases). • Abrupt cessation of high-dose systemic corticosteroids that are given for more than 5 days’ duration should be avoided. Potential adverse effects of oral prednisone therapy are more likely with long-term use and may include any of the following: suppression of the hypothalamic-pituitary-adrenal axis, hypokalemia, hypocalcemia, masking or worsening of infection, increased likelihood of secondary infection, carbohydrate intolerance and worsening of • diabetes, glaucoma, cataracts, osteoporosis, dermal atrophy, skin hypopigmentation, and psychiatric disorders including depression, euphoria, or even acute psychosis. • It should also be noted that even systemic steroids will likely prove ineffective if exposure to the offending allergen or irritant is not limited. Follow-up and Referral Follow-up and referral are determined by the patient's condition and response to therapy. Severe cases should be referred to a dermatologist or an allergist. Patient Education The provider should teach the patient and family about the disease and the appropriate use of medications, as well as adverse effects or exacerbations that should prompt the patient to contact the health-care provider. The mainstay of prevention is helping patients identify the agents causing the dermatitis and teaching them to avoid exposure or to use protective clothing and gloves. SEBORRHEIC DERMATITIS Seborrheic dermatitis is one of the most common skin conditions seen in primary care among adults and the elderly. • It is a chronic condition that is marked by remissions and exacerbations. • Seborrheic dermatitis commonly manifests in patients with HIV infection. A severe or resistant case on a patient should prompt investigation for risk factors of HIV infection. • The rashes of seborrheic dermatitis are seen on skin that is rich in sebaceous glands. (It is associated with an increased production of sebum.) • The affected skin is pink, edematous, and covered with yellow to brown scales and crusts. • These rashes are most easily seen on the scalp, the forehead, the eyebrows, and the area surrounding the nose and the ears. Epidemiology and Causes • Seborrheic dermatitis affects approximately 2% to 5% of the adult population. • It runs in families and has a known genetic component. • It may be an inflammatory reaction to Malassezia furfur yeasts. • The occurrence of seborrheic dermatitis is most common during early infancy on the scalp (“cradle cap”), after the second decade of life, and in the elderly or immunocompromised patients. • A strong association with HIV infection and AIDS is well established. Pathophysiology • This type of dermatitis was originally defined by excess oil secretion from the sebaceous glands and is thus found on areas of the body where such glands are most concentrated, that is, in decreasing order, the scalp, face, chest, upper back, pubic area, and axillae. • Interestingly, however, overproduction of sebum is not seen in all cases of seborrheic dermatitis, nor is the composition of the sebum the main factor in this condition. • Skin biopsies typically reveal parakeratotic scale heaped around hair follicles and an inflammatory lymphocytic infiltrate. Thus, mild epidermal hyperproliferation has been cited as a contributing factor. However, it is not known whether this occurs in response to infection by saprophytic skin fungi or vice versa. • Malassezia furfur commonly colonizes affected individuals. Recurrence of symptoms has been linked to an increase in the number of M furfur organisms found on the skin surface. Fungalspecific stains of affected skin reveal large numbers of M furfur spores within the stratum corneum, the uppermost skin layer. Clinical Presentation Subjective • The typical patient is an adult male who complains of a pink, scaling rash located on the face and scalp. • Seborrheic dermatitis can also be an incidental finding; some patients, especially elderly patients, are not bothered by the cosmetic effect of the rashes. • The lesions are usually asymptomatic in most patients, but pruritus may be present (and is aggravated by perspiration), especially in scalp lesions. Objective Seborrheic dermatitis presents as scaly patches that may be slightly papular; each patch is surrounded by erythema. • The lesion borders are poorly defined, and the scales may be greasy and appear yellow. • The most frequently involved area is the scalp, and the condition is differentiated from common dandruff (pityriasis sicca) by the appearance of erythema, which may be minimal or moderate. • The affected areas may include the forehead at the hairline, eyebrows, nasal folds, and the retroauricular and presternal areas. • In more severe cases, intertriginous areas, as well as the external ear canal and umbilicus, are involved. • The rashes may be more difficult to recognize in fastidious patients because daily bathing removes some of the scale. Diagnostic Reasoning Diagnostic Tests Diagnosis of seborrheic dermatitis is based on clinical findings and the history. Dermatologists and allergists can test for Malassezia furfur using antigen-specific skin-prick or serum RAST testing. Fifteen percent to 65% of patients with seborrheic dermatitis have positive responses to skin-prick tests with Malassezia extracts. Malassezia antibodies have also been found in young adults with head and neck dermatitis. Fungal-specific periodic acid Schiff and Gamori Methenamine Silver stains identify hyphae and spores in skin scraping or biopsy samples; however, these specialized stains typically require specialist referral and are not commonly used in the primary-care setting. Rather, the diagnosis of seborrheic dermatitis is most commonly based on the characteristic appearance and distribution of the rash, as well as its response to empiric therapy. Differential Diagnosis Skin conditions that mimic seborrheic dermatitis include impetigo, atopic dermatitis, psoriasis, scabies, tinea capitis, and Langerhans cell histiocytosis. • A history of the same rash recurring at characteristic locations on the body (e.g., the scalp and hairline, sides of the nose and upper lip, eyebrows and eyelashes, cheeks, or ears) will give the clinician the best clues to identify seborrheic dermatitis correctly. • Impetigo, a bacterial infection of the skin caused by Staphylococcus or Streptococcus bacteria, has an acute onset and tends to occur on the extremities (a location not seen in seborrheic dermatitis) or on the face. • The most useful distinguishing feature between atopic dermatitis and seborrheic dermatitis is the increased number of lesions on the forearms in the former, compared with the increased number of lesions in the axillae in the latter. • The erythema of seborrheic dermatitis typically has a pinkish hue, rather than the bright-red appearance of psoriasis. Seborrheic dermatitis is also associated with several chronic conditions, including Parkinson's disease, HIV infection and AIDS, phenylketonuria, cardiac failure, zinc deficiency, and epilepsy. • Other dermatological disorders, such as acne vulgaris, rosacea, and psoriasis, may also be associated with these diseases, however. importantly, florid manifestations of seborrheic dermatitis may be an early cutaneous indicator of HIV infection, and these patients may demonstrate extensive symptoms that are often resistant to therapy. Management • The high incidence and chronic benign nature of seborrheic dermatitis present a therapeutic challenge. Mild to moderate cases do not seem to bother some patients, especially elderly patients who frequently refuse treatment or are noncompliant. • Younger patients who are bothered by the cosmetic effects of the rashes on the face frequently request treatment. The therapeutic approach is aimed at managing symptoms and reducing the yeast count on the skin. • The regular use of an OTC dandruff shampoo is sufficient to control most scalp symptoms. The preparations must remain on the scalp for at least 5 to 7 minutes to be effective. Commonly used ingredients in these products include selenium sulfide, zinc pyrithione, tar, salicylic acid, sulfur, or ketoconazole. Zinc pyrithione and selenium sulfide are classified as keratolytic agents. • They appear to be both fungicidal and cytostatic. The combination of sulfur and salicylic acid has keratolytic, antifungal, and antiseptic actions. Coal tar agents must be used with caution in fair-haired persons because they may cause an undesirable change in color. • Resistant seborrheic dermatitis may require a prescription shampoo. A 2.5% selenium sulfide shampoo, a ketoconazole shampoo (Nizoral shampoo), and a detoconazole shampoo are available. Keratolytic or oil-based lotions are recommended to soften heavy crusts. • A topical corticosteroid may be necessary when significant erythema is present. Hydrocortisone cream 0.5% to 1.0% (OTC) for the face or betamethasone valerate 0.1% for the scalp should be applied after cleansing. • Facial application and long-term use of topical corticosteroids should be avoided because of the risk of telangiectasia and dermal atrophy. • These risks are not present with the topical use of ketoconazole. Exudative lesions may require compresses of Burow's solution applied for 30 minutes three times daily. Ketoconazole shampoo every other day is recommended for resistant cases. Ketoconazole 2% cream may be applied to the affected areas twice daily when there is facial or chest involvement. Calcineurin inhibitors that lower the activity of the immune system may be effective for recalcitrant cases although these drugs are not FDA approved for seborrheic dermatitis. • Such agents include tacrolimus (Protopic) and pimecrolimus (Elidel), which are available in topical formulations. As indicated for second-line therapy in atopic dermatitis, the FDA cautions against the chronic, long-term use of these medications in any age group, given concerns over their long-term safety, including rare reports of malignancies. • Once symptoms resolve, maintenance therapy may be required with a once to twice a week application. • The prophylactic use of a ketoconazole shampoo (Nizoral) once a week is safe, easy, and at times very rewarding. For a superinfection of gram-positive skin bacteria, cephalexin 7 to 10 days is required. • Because a strong association with HIV infection and AIDS is well established, treating the underlying HIV infection with effective antiretroviral therapy is often the key to resolution of the patient's skin findings. Follow-up and Referral • Repeated secondary infections or resistance to standard management require a prompt referral to a dermatologist. Patient Education • Patients should be reassured that seborrheic dermatitis is not contagious or progressive. • They must, however, understand the chronic nature of the condition and the need for continued management. The role of emotional stress in acute flare-ups should be explained. If topical steroids are used, the patient needs to be instructed in the proper application and the potential adverse effects. A list of effective OTC preparations should be provided, so each patient can select one that meets his or her personal preferences. Daily shampooing of oily hair is recommended for the first week, decreasing to two or three times a week as maintenance therapy. 3. Common viral exanthems ● Rubeola (measles) pt will appear very sick, high fever, red moucosal membranes , skin appears reddish purple generalized macular and papular rash. Lesions start out on the head then spread down body in 1-2 days, treatment-symptomatic care with pain reliever ● Rubella- skin rash will be rose pink , macules and papules ● Varicella (chicken pox) erythematous papules & macules rash starts on face then spreads to body ● Fifth disease (roseola) caused by human herpes, mild and common in children , skin appears with light pink erythematous macules and papules on the face, neck & extremities, usually resolves 1-3 days ● Pityriasis rosea- more common in spring time, 2-4 plaque or patch or plaque on trunk occurs 2-3 weeks before general rash known as herald patch, rash may be itchy , pink- erythematous, round to oval plaques or papules with possible scaly orders, rash resembles a christmas tree on the trunk ● Hand foot & mouth disease contagious, usually occurs in children, skin has vesicles on hands and feet and mouth sores, pt is contagious ● Molluscum contagiosum - skin presentation is tiny pustules that are 2-5 mm, may be single or multiple lesions that are spread by contact, scratching, autoinoculation or shaving. Most common place in children is are thighs and arms, in adults genital area, the virus can last 8 months or longer, can be treated with OTC Zymaderm 4. Acne Acne is a condition that is manageable but not curable. ● A provider must emphasize this to their patients so there are realistic expectations. ● Acne can occur at any age, and there are different levels of severity. Acne is classified into three categories mild, moderate, and severe. ● Mild is a patient with a few papules and some pustules. Moderate acne patients have papules, pustules, and nodules. Severe acne consists of papules, multiple pustules, and multiple nodules that can be painful. Acne lesions can appear on the face, neck, chest, back, and upper arms. The differential diagnosis should include: rosacea, folliculitis, pe