Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Feb 9th board review- Derm.doc.doc


Published on

Published in: Health & Medicine
  • Be the first to comment

  • Be the first to like this

Feb 9th board review- Derm.doc.doc

  1. 1. Feb 9th board review- Derm Question 241 C:herpes simplex virus infection Grouped vesicles (Item C241A) on an erythematous base, as described for the infant in the vignette, suggests neonatal herpes simplex virus (HSV) infection. Lesions may erupt anywhere, but vesicles on the scalp or buttocks are particularly common. Monitoring electrodes may produce sufficient skin trauma to expedite invasion by HSV and induce skin lesions. Vesicles may be present at birth, but onset after delivery is more likely. Up to 30% of infants who have neonatal HSV do not exhibit skin lesions. Mucous membrane involvement is common. HSV in newborns may present as: 1) disseminated disease involving multiple organs; 2) localized central nervous system disease; or 3) disease localized to the skin, eyes, and mouth. In the absence of skin lesions, it is difficult to diagnose neonatal HSV infection. In neonates, HSV infection should be considered in the differential diagnosis of fever, irritability, and abnormal cerebrospinal fluid findings. Neonatal HSV infections are very serious and associated with high mortality and morbidity rates. Initial symptoms of HSV infection may present between birth and 1 month of age. Bullous impetigo (Item C241B) is a common skin manifestation of Staphylococcus aureus infection. As the name suggests, lesions are bullae (or crusted round erosions if the bullae rupture), not vesicles. Gram stain of the contents of a bulla reveals clusters of gram-positive cocci,and a bacterial culture can confirm the presence of Staphylococcus aureus. Congenital varicella is rare, but may mimic HSV infection in the newborn. Affected infants exhibit vesicles in association with abnormalities involving the eye, central nervous system, gastrointestinal system, or limbs. A linear arrangement of vesicles that have minimal erythema at the base is characteristic of incontinentia pigmenti (Item C241C). Rapid development of the "warty" hyperkeratotic stage distinguishes incontinentia pigmenti from HSV infection. Hemorrhagic bullae appear at sites of even minimal skin trauma in newborns who have recessive dystrophic epidermolysis bullosa (RDEB). Removal of the blister roof leaves a raw, bleeding base that heals with scar formation. Early loss of finger nails as a result of blistering and scarring is characteristic of RDEB. Question 33 A: Eosinophils Erythema toxicum neonatorum presents as blotchy, 2- to 3-cm erythematous macules (Item C33A), each of which has a single 1- to 4-mm central papule, vesicle, or pustule. Lesions are not present at birth but appear in the first 24 to 48 hours thereafter. The condition occurs in about 50% of healthy term infants; preterm infants are affected less often. Individual lesions resolve in 4 to 5 days, with new lesions appearing for up to 10 days. A Wright-stained preparation of the pustule contents reveals numerous eosinophils (Item C33B). If obtained, a complete blood count may demonstrate eosinophilia. The condition is benign and self-limited, and no treatment is necessary. A number of neonatal skin conditions are characterized by vesicles and pustules. They may be distinguished from erythema toxicum clinically and by microscopic examination of lesional contents. The pustules caused by staphylococcal folliculitis (Item C33C) contain gram-positive cocci, the vesicles of herpes simplex virus infection (Item C33D) contain multinucleated giant cells (Item C33E), the pustules of transient neonatal pustular melanosis (Item C33F) contain polymorphonuclear leukocytes, and the pustules of congenital candidiasis (Item C33G) contain pseudohyphae and budding yeast (Item C33H).
  2. 2. Question 49 D polymorphonuclear leukocytes Transient neonatal pustular melanosis (TNPM) is a disorder of unknown cause that begins in utero. At birth, affected infants may exhibit pustules or small hyperpigmented macules (Item C49A) surrounded by a rim of scale, the remnant of the pustule roof. Pustules resolve within several days, but the hyperpigmented macules may persist for 1 to 3 months, as described for the infant in the vignette. TNPM is more common among African-American infants and may be observed on any skin surface, including the palms and soles. A Wright-stained preparation of the pustular contents reveals a predominance of neutrophils. No treatment is necessary for this self-limited condition. A number of neonatal skin conditions are characterized by pustules or vesicles. They may be distinguished from transient neonatal pustular melanosis clinically and by microscopic examination of lesional contents. The vesicles of erythema toxicum (Item C49B) contain eosinophils (Item C49C), the pustules caused by staphylococcal folliculitis (Item C49D) contain gram-positive cocci, the vesicles of herpes simplex virus infection (Item C49E) contain multinucleated giant cells (Item C49F), and the pustules of congenital candidiasis (Item C49G) contain pseudohyphae and budding yeast (Item C49H). Question 65 E- topical application of selenium sulfide Tinea versicolor typically manifests as multiple round or oval macules with superficial scale arrayed in a yoke distribution that includes the neck, chest, upper back, and shoulders, as described for the boy in the vignette. Commonly, individual macules coalesce to form patches. Lesions may be hypo- (Item C65A) or hyperpigmented (Item C65B), hence, the name versicolor. The infection occurs primarily in adolescents and young adults, perhaps because the organism responsible, Malassezia furfur (Pityrosporum ovale) uses sebum as a nutrient. The infection is most prevalent in hot, humid climates. A potassium hydroxide preparation performed on scale obtained from the lesions reveals the classic "spaghetti and meatballs" appearance (ie, short hyphae and spores) (Item C65C). Initial therapy of tinea versicolor consists of topical application of selenium sulfide 1% (present in some antiseborrheic shampoos) or 2.5% (available by prescription). Although many treatment regimens exist, a commonly employed one advises the application of selenium sulfide to all affected areas for 10 minutes, after which it is rinsed off. An alternative is topical ketoconazole, although this drug typically is more expensive. For patients who have resistant infection or who cannot use topical therapy, treatment with oral fluconazole or ketoconazole may be beneficial. Regardless of the initial treatment employed, infection often returns. For this reason, following initial treatment, topical selenium sulfide often is used prophylactically (ie, as a single 8- to 12-hour application monthly for 3 to 4 months). Patients should be counseled that return of normal skin pigmentation often requires several months. Topical administration of psoralen compounds followed by gradually increasing exposure to ultraviolet radiation may be indicated in the management of vitiligo (characterized by depigmented [not hypopigmented] macules and patches), but it does not have a role in the treatment of tinea versicolor. Postinflammatory hypopigmentation may follow episodes of atopic or contact dermatitis. However, the physical findings exhibited by the adolescent described in the vignette are not consistent with these diagnoses and, therefore, treatment with a topical corticosteroid and epicutaneous patch testing,
  3. 3. respectively, are not warranted. Griseofulvin is used to treat certain dermatophyte infections, particularly tinea capitis, but it is not effective in tinea versicolor. Question 17 C may survive for 36 hours without a blood meal Pediculosis, the infestation of humans by lice, has been documented for millennia. Three species of lice infest humans: Pediculus humanus humanus, the body louse; Pediculus humanus capitis, the head louse; and Pthirus pubis, the crab louse. The hallmark of louse infestation is pruritus at the site of bites. Lice are more active at night, frequently disrupting sleep of the host, which is the derivation of the term "feeling lousy." Adult crab lice can survive without a blood meal for 36 hours. Unlike head lice, which may travel up to 23 cm/min, pubic lice are sluggish, traveling a maximum of 10 cm/d. Viable eggs on pubic hairs may hatch up to 10 days later. Crab louse infestation is localized most frequently to the pubic and perianal regions but may spread to the mustache, beard, axillae, eyelashes, or scalp hair. Infestation usually is acquired through sexual contact, and the finding of pubic lice in children (often limited to the eyelashes) should raise concern for possible sexual abuse. Maculae caeruleae (Item C17A), blue-gray macules observed on the abdomen and thighs at sites where lice have fed, is a useful, although less common finding. Crab lice affect all races and ethnic groups. This is in contrast to head lice, which rarely infest African-Americans, perhaps because the oval cross-sectional shape of their scalp hair does not permit lice to grasp the hair effectively. The preferred treatments for pubic lice infestation are permethrin 1% or pyrethrin with piperonyl butoxide. Other options include permethrin 5% or malathion (although the latter agent is expensive, potentially flammable, and may be irritating when applied to the groin). Lindane is effective, but concerns about toxicity if used improperly or ingested inadvertently limit its use. It is considered a second-line therapy, is contraindicated for use in neonates and pregnant women, and should be used with caution in those weighing less than 110 pounds. If the eyelashes are affected, petrolatum may be applied to them three to five times daily for 10 days. Question 177 C: with clinical follow-up only at 4 to 6 weeks Griseofulvin remains the preferred treatment for tinea capitis. The desired dose is 20 mg/kg per day for at least 6 weeks. Although many rare severe adverse effects, including agranulocytosis and aplastic anemia, have been reported, griseofulvin remains a safe drug for use in children, and laboratory monitoring at baseline or during therapy is not required in an otherwise healthy child. Clinical follow-up at 4 to 6 weeks is adequate surveillance for the adverse reactions. Newer antifungal agents have been introduced, but none have the longstanding safety profile of griseofulvin. Question 81 C: glaucoma Port-wine stains (PWSs) are permanent capillary vascular malformations that are present from birth, as reported for the infant in the vignette. Unlike hemangiomas, PWSs do not proliferate, but grow proportionally with the child's somatic growth. Although a PWS may occur anywhere on the body, facial lesions should raise concern about possible Sturge- Weber syndrome (SWS).SWS is the association of a facial PWS in the V1 distribution with central nervous system leptomeningeal angiomatosis (that may cause seizures) and/or glaucoma. One study found that only 8% of individuals who have a facial PWS have SWS; all of those affected had a PWS in the distribution of V1 (upper lid) and/or V2 (lower lid). The risk of SWS was increased if the facial PWS was bilateral or if unilateral, involved the distribution of all three branches of the trigeminal nerve.
  4. 4. Congestive heart failure is not associated with SWS; it is an occasional complication in children who have multiple cutaneous hemangiomas and liver involvement or in those who have arteriovenous malformations. Consumptive coagulopathy (along with thrombocytopenia and anemia) is a feature of Kasabach-Merritt syndrome (Item C81A), in which patients have an atypical-appearing hemangioma (actually a hemangioepithelioma or tufted angioma). Ocular axis occlusion that prevents stimulation of the visual cortex is a concern with enlarging hemangiomas located near the eye (Item C81B). A tethered spinal cord results when a thickened, ropelike filum terminale remains firmly attached, reducing cord mobility. Tension on the cord and compromised blood supply produce neurologic findings, such as abnormal gait and secondary enuresis. A midline lumbosacral PWS might herald the existence of this or another occult spinal lesion. Question 97 C: benzoyl peroxide topically and tretinoin topically Acne affects 85% or more of adolescents and is the skin disorder most often treated by physicians. Multiple factors contribute to acne, including bacteria (that induce an inflammatory response, leading to erythematous papules and pustules (Item C97A), androgens (that cause increased sebum production), and abnormal follicular keratinization (that causes blockage within pores, resulting in blackheads and whiteheads (Item C97B). The treatment of acne depends on the types of lesions present (eg, blackheads/whiteheads, inflammatory, or both), the extent of disease (face versus face and trunk), and the severity of disease (more severe disease involves scarring and the presence of numerous and larger inflammatory lesions). The patient described in the vignette has facial acne characterized by a few small inflammatory lesions and numerous obstructive lesions (ie, blackheads and whiteheads) (Item C97C). As a result, he requires treatment with two agents, one to control inflammatory lesions and one to control obstructive lesions. Because the inflammatory component of his acne is mild and limited to the face, it may be treated topically with benzoyl peroxide applied each morning. Alternatives might include a topical combination product (eg, benzoyl peroxide combined with either clindamycin or erythromycin) or possibly a topical antibiotic alone (although bacterial resistance to these agents when they are used without benzoyl peroxide is common). Although benzoyl peroxide may be of some benefit in mild comedonal acne, the numerous lesions described for the patient indicate the need for a topical retinoid (eg, tretinoin or adapalene). Beyond this, many experts believe that topical retinoids are an essential part of any acne treatment program (regardless of lesion type observed) because they normalize the keratinization process and prevent new lesion formation. To avoid skin irritation, the patient is advised to apply the medication sparingly (a pea-sized amount is sufficient to cover the entire face) and use it every second or third night, progressing to nightly application as tolerated. Benzoyl peroxide inactivates tretinoin and, therefore, should not be applied simultaneously (ie, it is applied in the morning and tretinoin at night). Systemic antibiotics such as tetracycline, erythromycin, doxycycline, minocycline, and others are indicated in the management of severe or widespread inflammatory acne or inflammatory disease that does not respond to appropriate topical therapy. Using topical clindamycin alone would not address the obstructive component of the patient’s disease, just as tretinoin used alone may be insufficient to control inflammatory lesions. Question 49 C: observation
  5. 5. Hemangiomas represent benign vascular tumors that are present in 1% of newborns and approximately 10% of 1-year-olds. They may be separated clinically into three types: • Superficial: Bright red plaques or dome-shaped papules or nodules (Item C49A) • Deep: Compressible nodules or tumors that have a bluish hue and often surface telangiectasias (Item C49B) • Mixed: Lesions that have both superficial and deep features (Item C49C) Most hemangiomas follow a benign course and do not threaten vital structures. Typically, they grow rapidly during the first 6 to 9 months after birth, stabilize, and subsequently begin to involute. The clinical hallmark of involution is the appearance of a gray or white discoloration on the lesion's surface (Item C49D). Complete involution is seen in 30% of children by 3 years of age, 50% by 5 years, 70% by 7 years, and 90% by 9 years. The infant described in the vignette has a superficial hemangioma that is exhibiting signs of involution. Therefore, no intervention is necessary, and the family should be counseled about the lesion and its natural history. A variety of treatment options are available for problematic hemangiomas. Intralesional corticosteroids may be used for localized lesions, such as those involving the nasal tip (Item C49E) or ulcerated lesions in the diaper area (Item C49F). Proliferating lesions that threaten a vital structure (eg, the eye (Item C49G) or airway), are large, or are associated with systemic symptoms (eg, thrombocytopenia or disseminated intravascular coagulation as part of Kasabach-Merritt syndrome (Item C49H) typically are treated with oral corticosteroids. Interferon-alfa is an inhibitor of angiogenesis that often is beneficial in the management of hemangiomas that fail to respond to systemic corticosteroid therapy. Hemangiomas that do not involute completely or ulcerated lesions that do not respond to local care may benefit from pulsed dye laser treatment. Question 129 B: erythema multiforme The girl described in the vignette has round erythematous plaques that have a central violaceous discoloration (ie, target lesions) concentrated on acral surfaces and no mucosal involvement. These findings suggest a diagnosis of erythema multiforme (EM), previously called EM minor. EM is a hypersensitivity reaction that usually is precipitated by infection with herpes simplex virus (HSV) type 1. Although a recent history (within the previous 2 weeks) of herpes labialis is reported in 50% of cases, HSV DNA can be recovered from target lesions in 80% of patients. The eruption of EM begins abruptly without prodromal symptoms. Early lesions are round erythematous macules, wheals, or plaques that later develop a central violaceous discoloration, vesicle (Item C129A), or concentric rings. The lesions remain fixed in location until they resolve, typically in 7 days or more. Oral ulcers may be present in up to 50% of patients, but other mucosal sites are spared. EM resolves in 2 to 3 weeks, and treatment is supportive. For children who experience recurrences, given the association with HSV infection, prophylactic acyclovir therapy may be employed. Stevens-Johnson syndrome (SJS) (previously termed EM major) and toxic epidermal necrolysis (TEN) represent hypersensitivity reactions to drugs and, less commonly, infections. They are believed to represent the same disorder, differing only in the extent of epidermal loss: SJS is diagnosed when less than 10% of the epidermis is lost, SJS/TEN overlap when the loss is 10% to 30%, and TEN is diagnosed when the loss is greater than 30%. Unlike in EM, patients who develop SJS or TEN manifest prodromal symptoms such as fever, malaise, cough, sore throat, or headache 1 to 14 days before the eruption appears. Target lesions are uncommon or absent; rather, individuals develop erythematous or violaceous macules or patches (Item C129B) that may develop blisters (Item C129C) that rupture, leaving denuded areas. Multiple mucosal sites are involved,
  6. 6. including the conjunctivae (Item C129D), mouth (Item C129E), genitalia, urethra, and rectum. During the early disseminated phase of Lyme disease, multiple erythema migrans lesions occasionally may be observed (Item C129F). Unlike the lesions of EM, however, those of erythema migrans generally lack the typical targetlike appearance. The appearance of the wheals of urticaria may mimic those of EM. However, individual lesions in urticaria disappear within 24 hours (usually within 2 to 3 hours), vary in size, often have unusual shapes (incomplete circles, large plaques with serpiginous borders), and lack the central epidermal change (eg, vesicle or crust) characteristic of the target lesions of EM (Item C129G). Question 236 E: washing the skin immediately after contact with poison ivy may lessen the severity of the eruption A rash caused by poison ivy, oak, or sumac (Rhus dermatitis) is one of the most common forms of allergic contact dermatitis. Damaging any part of the plant (Item C236A) liberates sap that contains urushiol, a potent antigen that penetrates the epidermis and sensitizes T lymphocytes. Re-exposure to the antigen results in a rash within 12 to 24 hours. If a person is aware that he or she has contacted poison ivy, oak, or sumac, washing the skin promptly (ideally within 10 to 15 minutes) may prevent or attenuate the rash. Several myths surround the acquisition and spread of Rhus dermatitis. Although it often is stated that poison ivy may be handled safely during winter months, the sap retains its activity and can induce a rash. Many believe that fluid from vesicles and bullae can spread the rash. This may be based on the observation of new lesions continuing to appear for several days following a single exposure. However, this phenomenon occurs because areas that received the greatest concentration of resin erupt first, while those that have a lesser exposure develop the rash later. Thus, the eruption only occurs at sites that have come into contact with plant sap; once it has been removed by bathing and clothing has been changed, the rash cannot be spread. When poison ivy dermatitis is extensive or severe or affects critical areas, treatment with an oral corticosteroid for 14 to 21 days is indicated. Discontinuing therapy earlier may result in a flare of symptoms. Although Rhus dermatitis can be prevented by avoiding offending plants or by the use of barrier preparations, desensitization is not recommended due to lack of efficacy, need for prolonged treatment, and potential adverse reactions. Question 65 C: psoriasis The boy described in the vignette has findings typical of psoriasis: well-defined, round or oval plaques that have a thick, white, or silver scale. The scale is adherent, and when removed, pinpoint areas of hemorrhage may be observed (Auspitz sign) (Item C65A). Psoriasis is an inherited disorder that begins before age 16 in 25% to 45% of individuals. The disease has a predilection for the eyebrows, ears, extensor surfaces of the elbows and knees (Item C65B), umbilicus (Item C65C), and gluteal cleft. Most children exhibit scalp involvement with thick adherent scale (Item C65D). Pitting, yellowing, or thickening of the nails occurs in some patients (Item C65E). Lesions may appear in areas of trauma, such as scratches or abrasions (the Koebner phenomenon) (Item C65F). A variant, called guttate (droplike) psoriasis, begins on the trunk as multiple erythematous macules that may mimic a viral exanthem. With time, the lesions become elevated and develop scale (Item C65G). Guttate psoriasis often is preceded by
  7. 7. pharyngeal or perianal infection with group A beta-hemolytic Streptococcus, and patients who have the disorder should be evaluated for this possibility. The morphology and distribution of psoriatic lesions generally permit their differentiation from lesions associated with other disorders. In particular, a psoriatic lesion typically has a thick, adherent scale that covers its entire surface. A unique form of eczema, termed nummular eczema (from the Latin word nummulus, meaning small coin), produces round, oozing, crusted erosions (Item C65H) or dry macules that have fine scale. The generalized eruption of pityriasis rosea may mimic guttate psoriasis. However, the lesions are small, oval, thin plaques that have fine scale located centrally, and they are oriented with their long axes parallel to lines of skin stress (Item C65I). Seborrheic dermatitis is characterized by erythematous macules or patches that have a greasy scale (Item C65J); the eyebrows, alar folds, or posterior auricular or presternal regions typically are involved, and there may be scaling of the scalp. Finally, tinea corporis causes one or several scaling annular lesions. Unlike the lesions of psoriasis, those of tinea corporis exhibit central clearing and peripheral scale (Item C65K).