USMLE Dermatology II

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  1. Rosacea
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  2. Erythematotelangiectatic rosacea
    • which typically occurs in fair-skinned individuals age more than 30.
    • 1.Etiology is unknown but may be due to a chronic inflammatory reaction to cutaneous microorganisms, ultraviolet light damage, or vasomotor dysfunction.
    • 2. Symptoms: facial erythema in the nose and medial cheeks (including the nasolabial folds), facial flushing, telangiectasias, roughness or scaling, and burning discomfort.
    • 3. Symptoms are typically precipitated by hot drinks, alcohol, heat, emotion, and other causes of rapid body temperature changes.
    • 4. The episodes are usually intermittent but can progressively lead to permanently flushed skin.
  3. Papulopustular Rosacea
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  4. scabies
    • due to infestation by the Sarcoptes scabiei mite, which burrows into the skin and spreads through direct person-to-person contact.
    • Scabies usually presents with an intensely pruritic rash (often worse at night) in the flexor surfaces of the wrist, lateral surfaces of the fingers, and the finger webs.
    • The rash is due to a delayed type IV hypersensitivity reaction to the mite (feces and eggs included).
    • Scabies can involve other parts of the body (eg, elbows, axillary folds, nipples and areola in women, scrotum and penis in men).
    • However, it is rarely seen on the back and head (except in children).
    • Examination usually shows small, crusted, red papules scattered around the region (sometimes with linear burrows). Patients can also develop small vesicles, pustules, wheals, and extensive excoriations that can obscure the classic burrows in the skin.
    • Scabies often mimics other conditions (eg, eczema, tinea, seborrheic dermatitis).
    • Diagnosis is confirmed by skin scrapings from lesions revealing mites, ova, and feces under light microscopy.
    • Topical permethrin 5% cream (applied from the neck down and left overnight) or oral ivermectin are preferred for treating adults.
    • Antihistamines or low-potency topical steroids can be added to treat the dermatitis.
    • Bedding and clothing should be cleaned or placed in a plastic bag for at least 3 days as the mite can only live away from human skin for 2-3 days.
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  5. Secondary syphilis
    • can present with systemic findings (eg, fever, malaise, weight loss), lymphadenopathy, multiorgan involvement (eg, uveitis), and a rash.
    • The rash is classically diffuse and symmetrical with a macular or papular appearance and involves the extremities, palms, soles, and trunk.

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  6. Seborrheic dermatitis (SD)
    • SD is a common inflammatory disease that affects the scalp (dandruff), face (eyebrows, nasolabial folds, and external ear canal/posterior ear), chest, and intertriginous areas.
    • SD occurs in all ages but peaks in infancy and adulthood and is most common in the first year of life and again at age 30-60.
    • In infants, these areas include the scalp ("cradle cap") eyelids, nasolabial folds, postauricular area, and umbilicus.
    • It is also associated with central nervous system disorders (especially Parkinson disease) and HIV.
    • The diagnosis of SD is clinical, with typical findings characterized by pruritic, erythematous plaques with fine, loose, yellow and greasy-looking scales.
    • SD primarily affects areas with numerous sebaceous glands, although sebum production in affected patients is typically normal.
    • Malassezia species may play a role in the pathogenesis of SD, and topical antifungal agents (eg, ketoconazole, selenium sulfide) are effective in treating this condition.
    • Treatment:
    • • First-line: Emollients, nonmedicated shampoos
    • • Second-line: Topical antifungals or low-potency glucocorticoids
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  7. Seborrheic keratosis (SK [plural, keratoses])
    • is a common epidermal tumor seen in middle-aged or elderly individuals.
    • SKs may be found almost anywhere on the body except the palms and soles.
    • They can vary in appearance from nearly flat macules to raised, wart-like lesions, and can be pink/white, brown, or black. They have a velvety or greasy surface and well-demarcated border and are often described as having a "stuck-on" appearance.
    • SKs are usually asymptomatic but occasionally can be pruritic or tender.
    • They are benign lesions, although sudden onset of multiple SKs may indicate an occult internal malignancy (Leser-Trelat sign).
    • Diagnosis of SK is based on the characteristic presentation.
    • Biopsy is not usually necessary but will show small cells resembling basal cells, with variable pigmentation, hyperkeratosis, and keratin-containing cysts.
    • Simple observation is the preferred management, but bothersome lesions may be treated with excision, cryosurgery, or electrodessication.

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  8. Senile purpura (solar or actinic purpura)
    • is a noninflammatory disorder that is most common in the elderly but can also be seen in middle-aged patients with extensive sunlight exposure.
    • It is caused by loss of elastic fibers in perivascular connective tissue.
    • Minor abrasions that would merely stretch the skin in younger patients can rupture superficial blood vessels in the elderly.
    • The subsequent extravasation of blood leads to ecchymosis over vulnerable areas, such as the dorsum of the hands and forearms.
    • Patients can have residual brownish discoloration from hemosiderin deposition.
    • The incidence and severity are also increased in patients taking anticoagulants, corticosteroids, or nonsteroidal anti-inflammatory drugs.
    • Senile purpura is usually not a dangerous condition and requires no further investigation.
    • However, many older patients with severe skin fragility may require careful wound care measures following even minor lacerations.
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  9. Drug Induced Acne
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  10. Difference between Acne Vulgaris and drug Induced Acne
    • In contrast to acne vulgaris (which displays lesions in various stages of development and typically occurs on the face in adolescents), drug-induced acne can be seen in any age group, is characterized by monomorphic papules without associated comedones, and commonly involves the upper back, shoulders, and upper arms.
    • Some patients may have small pustules, but scarring cystic and nodular lesions are not seen.
    • Drug-induced acne does not respond to typical acne treatment but improves rapidly on discontinuation of the offending agent
  11. Chloracne
    • is a severe skin disorder caused by exposure to halogenated hydrocarbons (eg, occupational exposure to the pollutant dioxin).
    • It is characterized by inflammatory nodules and large comedones affecting the head, neck, and axillae.
  12. SJS Vs TEN
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  13. Stevens-Johnson syndrome (SJS)
    • is a serious inflammatory reaction to drugs or certain infections (eg, Mycoplasma pneumoniae).
    • Clinical features include coalescing erythematous macules, bullae, desquamation, and mucositis.
    • Systemic signs are common and may include fever, tachycardia, hypotension, altered level of consciousness, seizures, and coma.
    • By convention, SJS denotes <10% of body surface area involvement, >30% is designated as toxic epidermal necrolysis (TEN), and 10%-30% is SJS/TEN overlap.
    • The diagnosis of SJS is based on the typical mucocutaneous lesions, systemic signs, and exposure to a likely causative medication.
    • Treatment is supportive, with aggressive fluid support and wound care similar to that for burns. Secondary infections are common, and fatalities may occur despite treatment.
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  14. Erythema multiforme (EM)
    • is a self-limited illness characterized by an acute erythematous rash and usually occurs after herpes simplex infection.
    • EM may cause mucosal lesions similar to those of SJS, but the predominant skin lesions are typically targetoid plaques favoring the distal extremities rather than desquamating bullae; systemic symptoms are not as prominent as in SJS.
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  15. TEN
    • TEN is an inflammatory hypersensitivity reaction to drugs (especially sulfonamides, nonsteroidal antiinflammatory drugs, anticonvulsants and allopurinol) or certain infections (usually Mycoplasma pneumoniae).
    • Clinical features of TEN are variable, but typically include coalescing erythematous macules, bullae, desquamation, and mucositis. Patches of skin slide off with light pressure (positive Nikolsky's sign).
    • Systemic signs are common and may include fever, tachycardia, hypotension, altered level of consciousness, conjunctivitis, seizures, and coma. The exact pathogenesis is unknown.
    • By convention, SJS denotes involvement of <10% of body surface area, >30% is designated TEN, and 10-30% is referred to as a SJS/TEN overlap syndrome.
    • The treatment of TEN and SJS is primarily supportive, with wound care similar to that for burns (and often provided in a designated burn unit).
    • Aggressive fluid support is often needed due to poor oral intake and profound cutaneous fluid loss.
    • Secondary infections are common, and antiseptic precautions are needed.
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  16. Tinea corporis (ringworm)
    • Risk factors:
    • • Athletes who have skin-to-skin contact (eg, wrestling, gymnastics)
    • • Humid environment and warm moist area (eg, shower surfaces, pools, gym mats, seats);
    • • Contact with infected animals (eg, rodents)
    • Etiology:
    • Any species of dermatophyte may cause this condition, but Trichophyton rubrum is the most frequent culprit.
    • Tinea corporis is often more extensive in patients with immunocompromising conditions (eg, HIV, diabetes mellitus)
    • Presentation:
    • • Scaly, erythematous, pruritic patch with centrifugal spread
    • • Subsequent central clearing with raised annular border
    • Patches of tinea corporis are typically round or ovoid but may become confluent to form a "flower petal" shape.
    • Diagnosis:
    • is confirmed using potassium hydroxide (KOH) preparation of skin scrapings, which can show the characteristic segmented hyphae and arthrospores
    • Treatment:
    • • First-line/localized: Topical antifungals (eg, clotrimazole, terbinafine)
    • • Second-line/extensive: Oral antifungals (eg, terbinafine, flucanozole, iatroconazole preferred over griseofulvin)
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  17. Tinea versicolor (pityriasis versicolor)
    • is a superficial fungal skin infection caused by Malassezia species (nondermatophytic, lipid dependent yeasts; eg, M globosa, M furfur)
    • Pathogenesis
    • Malassezia globosa skin flora grows in exposure to hot and humid weather
    • Clinical features
    • •Salmon Colored, Hypopigmented, hyperpigmented, or mildly erythematous lesions (face in children, trunk and upper extremities in adolescents and adults)
    • • +/- Fine scale
    • • +/- Pruritus
    • Hypopigmented areas are frequently noticed following sun exposure due to tanning of the surrounding skin
    • Diagnosis:
    • KOH preparation shows hyphae and yeast cells in a "spaghetti and meatballs" pattern
    • Treatment:
    • Topical ketoconazole, terbinafine, or selenium sulfide
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  18. Clinical features of acute urticaria
    • Clinical
    • presentation
    • • Well-circumscribed, raised erythematous plaques
    • • Lesions can be oval, round, or serpiginous up to
    • several centimeters in diameter
    • • Intense pruritus
    • • Lesions can worsen over minutes to hours, then resolve within 24 hours
    • Etiologies
    • • Infections (viral, bacterial, parasitic)
    • • lgE mediated (antibiotics, insect bites, latex, food, blood products)
    • • Direct mast cell activation (narcotics, muscle relaxers, radiocontrast medium)
    • • NSAIDs
    • • Idiopathic (up to 50% of patients)
  19. Acute urticaria (welts or wheals).
    • Acute urticaria lasts for less than 6 weeks while chronic urticaria lasts for more than 6 weeks.
    • Urticaria is due to mast cell activation in the superficial dermis, which increases release of multiple mediators (eg, histamine) that cause pruritus and localized swelling in the upper layers of the skin.
    • Urticaria can be accompanied by angioedema, which is due to mast cell activation in the deeper dermal and subcutaneous tissues (eg, face, hands, and buttocks).
    • Etiologies of acute urticaria include infections (viral, bacterial, and parasitic), nonsteroidal antiinflammatory drugs, and lgE-mediated (eg, antibiotics, insect bites, latex, food) or direct (eg, narcotics, radiocontrast medium, muscle relaxers) mast cell activation.
    • However, nearly 50% of patients have no known cause (idiopathic urticaria).
    • Chronic urticaria can be due to physical stimuli (eg, cold temperature, skin pressure), serum sickness, or systemic disorders (eg, a.utoimmune disease, vasculitis, malignancy).
    • Patients with acute urticaria usually develop well circumscribed and raised erythematous plaques with central pallor. The lesions can be oval, round, or serpiginous, and up to several centimeters in diameter.
    • Patients usually have intense pruritus that can persist at night.
    • Individual lesions appear and enlarge over minutes to hours before disappearing within 24 hours.
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  20. Warts (cutaneous verrucae)
    • Most common cutaneous manifestation of human papillomavirus (HPV) infection.
    • HPV can cause warts in various locations including the plantar, palmar, or genital areas.
    • Plantar warts occur most commonly in young adults and patients with decreased cellular immunity (eg, AIDS, organ transplant patients).
    • The virus usually enters through tiny cuts or skin abrasions after direct contact with an HPV-infected individual.
    • Patients can develop lesions weeks to months later; these appear as hyperkeratotic papules on the sole of the foot (sometimes with thrombosed capillaries and visible skin lines) that can be painful with walking or standing.
    • Diagnosis is made clinically based on the appearance and location of the lesions.
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  21. Vitiligo
    • Vitiligo is caused by regional destruction of melanocytes, most likely due to an autoimmune etiology. Genetic and environmental factors may also play a role.
    • Clinical manifestations
    • • Depigmented macules on acral areas & extensor surfaces; face commonly affected
    • • Lesions may be symmetrical, dermatomal, or unilateral
    • Clinical course
    • • Most cases progress gradually
    • • Repigmentation is spontaneous in 10%-20% of cases
    • • Increased incidence of other autoimmune disorders (eg, lupus, Rheumatoid Arthritis, autoimmune thyroid disease, pernicious anemia,Sjogren Syndrome, Alopecia areata, Addison disease)
    • Autoimmune thyroid disease (eg, chronic lymphocytic (Hashimoto) thyroiditis, Graves disease) is especially common, and many experts advise patients with vitiligo be assessed for thyroid function.
    • Diagnosis of vitiligo: is usually made on clinical grounds.
    • Biopsy: can be considered in uncertain cases and will show loss of melanocytes, often with scattered lymphocytes at the lesion border
    • Treatment:
    • • Limited disease: Topical corticosteroids
    • • Extensive/unresponsive disease: Oral corticosteroids, topical calcineurin inhibitors, PUVA
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  22. Pathophysiology of Varicella Zooster
    • After an initial VZV infection (chicken pox), latent infection is established in the sensory dorsal root ganglia. Shingles occurs when there is reactivation of this latent infection.
    • It most commonly occurs in older individuals, immunosuppressed patients or during periods of stress. Pain usually precedes the vesicular eruption by 48 hours or more.
    • The eruption is most commonly unilateral and occurs in a band-like fashion along the affected dermatome.
    • Disseminated disease can occur in severely immunosuppressed patients.
  23. Atopic dermatitis (eczema)
    • It is characterized by pruritus, erythema, and scaly lesions on the skin.
    • Pathogenesis involves epidermal dysfunction due to improper synthesis of stratum corneum components.
    • Allergens can enter the disrupted skin barrier and generate an inflammatory response.
    • Excessive bathing, dry environments, stress, overheating, and irritating detergents can trigger flares.
    • Risk factors
    • • Low humidity
    • • Relatives with eczema, allergies, or asthma
    • Clinical features
    • • Infant: Itchy, red, scaly, crusted lesions on extensor
    • surfaces, trunk, cheeks & scalp
    • • Child/adult: Lichenified plaques in flexural creases
    • Treatment
    • Treatment includes trigger avoidance, frequent application of thick bland emollients, and use of hypoallergenic cleansers for bathing and laundry.
    • Moderate and severe eczema may require topical anti-inflammatory ointments (eg, hydrocortisone).
    • Complications
    • • Eczema herpeticum
    • • Cellulitis/abscess
    • • Discomfort interfering with daily activities & sleep
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  24. Signs of deliberate scald Injury
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  25. Child Abuse
    • Child abuse (neglect, physical abuse, psychological maltreatment, sexual abuse) is a common cause of death in young children.
    • Red flags for child abuse include a caregiver's history of an injury that is inconsistent and does not correlate with physical findings.
    • Splash or drip marks are also characteristics of unintentional injury.
    • In addition, burns that spare flexor surfaces (where the ankles, knees, hips are flexed) should immediately raise suspicion of a deliberate immersion injury.
    • Immersion burns typically involve the buttocks, back, and legs if the child is forced into a bathtub with hot water.
    • A stocking or glove burn distribution can be seen if an extremity was forced into hot liquid.
    • Intentional burns are also usually uniform depth, with a sharp line of demarcation between burned and normal skin.
    • If a mandated reporter such as a physician suspects that a child has been abused or neglected, he or she must notify child protective services immediately.
  26. Hypersensitivity Reaction
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  27. Neonatal Rashes
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  28. Erythema toxicum neonatorum (ETN)
    • Asymptomatic blotchy, erythematous papules and pustules support the diagnosis of ETN.
    • "Toxicum" is a misnomer as the rash is benign and evanescent.
    • It is common in full-term neonates.
    • The rash can change appearance and can occur on any part of the body (sparing the palms and soles) in the first 2 weeks of life.
    • The etiology is unknown.
    • Parents should be reassured that treatment is unnecessary as the rash resolves spontaneously without sequelae.
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  29. Superficial infantile hemangioma
    • It is the most common benign vascular tumor in children.
    • Infantile hemangiomas are composed of capillaries separated by connective tissue.
    • Superficial infantile hemangiomas, also known as strawberry hemangiomas, are bright red, sharply demarcated plaques that blanch with pressure.
    • Capillary hemangiomas can also be found in deep tissues and the viscera (eg, liver).
    • Infantile hemangiomas appear during the first days or weeks after birth and grow rapidly during the first 1-2 years of life.
    • The majority of these lesions regress spontaneously during childhood with minimal consequence.
    • A minority of lesions can be disfiguring, ulcerating, disabling (eg, strabismus from eyelid hemangioma), or life-threatening (eg, tracheal lesions).
    • Beta blockers (eg, propranolol) are recommended for patients at risk for complications.
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  30. Henoch-Schonlein purpura
    • It is immune (lgA) mediated, is the most common systemic vasculitis of childhood.
    • Pathogenesis:
    • • lgA-mediated leukocytoclastic vasculitis
    • Clinical manifestations: It typically follows an infection (often minor) and presents with the classic tetrad of palpable purpura on the lower extremities, arthralgias, abdominal pain, and renal disease.
    • • Palpable purpura (typically involves the buttocks, thighs, and legs and is distributed symmetrically).
    • • Arthritis/arthralgia
    • • Abdominal pain, intussusceptions: Abdominal pain is typically colicky and is thought to be secondary to localized vasculitis of the bowel wall
    • • Renal disease similar to lgA nephropathy (Renal manifestations include hematuria, non-nephrotic-range proteinuria, and a mildly elevated serum creatinine)
    • Diagnosis: diagnosis requires the presence of lower extremity purpura or petechiae with at least one of the following: arthritis or arthralgia, renal involvement, abdominal pain, or positive histopathology
    • Laboratory findings:
    • • Normal platelet count & coagulation studies
    • • Normal to Increased creatinine
    • • Hematuria +/- RBC casts +/- proteinuria
    • Renal biopsy: deposition of lgA in the mesangium will be seen
    • Treatment:
    • • Supportive (hydration & NSAIDs) for most patients
    • • Hospitalization & systemic glucocorticoids in patients with severe symptoms
  31. Infectious Complications of Atopic Dermatitis
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  32. Eczema herpeticum
    • It is a complication caused by a superimposed primary herpes simplex virus (HSV) infection (usually type 1 ).
    • An open area that is exposed to HSV type 1 can develop painful vesicles with an erythematous base that evolve to "punched-out" erosions with hemorrhagic crusting.
    • The lesions can be localized or disseminated, and fever, irritability, and lymphadenopathy are typical. The infection may be life-threatening in infants;
    • Treatment: Systemic acyclovir treatment should be initiated as soon as possible.
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  33. Congenital dermal melanocytosis ("Mongolian spot")
    • benign, flat, blue-grey patches that are usually present over the lower back and buttocks but can also be seen in other parts of the body.
    • Most infants of African, Asian, Hispanic, and Native American ethnicity have Mongolian spots at birth, and the hyperpigmentation usually fades spontaneously during the first decade of life. It is important for physicians to document the presence of Mongolian spots as these can be mistaken for bruises, which are also flat, nonblanching, and similar in color.
    • Extensive bruising would raise concern for coagulopathy or child abuse.
    • Skeletal survey is mandatory in suspected physical abuse to evaluate for patterns of intentional injury. However, bruises are tender, more varied in color, and fade quickly, making further workup inappropriate for this patient
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  34. Staphylococcal scalded skin syndrome (SSSS)
    • is caused by exfoliative toxin-producing strains of S. aureus.
    • The toxins target desmoglein 1, which is responsible for keratinocyte adhesion in the superficial epidermis. Prodrome of fever, irritability, and skin tenderness. Erythema starts on the face, and generalizes within the ensuing 24-48 hours. Superficial flaccid blisters soon develop, with flexural accentuation and perioral crusting.
    • The Nikolsky sign is positive (gentle lateral pressure on the skin surface adjacent to a blister causes slipping and detachment of a superficial layer of skin).
    • Blisters of SSSS are fragile, and when unroofed reveal a moist erythematous base.
    • Subsequent scaling and desquamation continue for about 5 days, and the entire process usually resolves within 1-2 weeks.
    • Cultures from intact bullae are usually sterile, because this is a toxin-mediated process.
    • Goal of treatment: is to eliminate any inciting focus of infection with appropriate anti-staphylococcal antibiotics, and to provide supportive wound care of all denuded areas.
    • SSSS is primarily a disease of children, but adults with renal disease or immunocompromise may also be affected.
  35. Impetigo
    • is a localized epidermal infection caused by S. aureus or group A beta -hemolytic streptococcus.
    • There are bullous and non-bullous variants.
    • Impetigo is more common in children than adults. Bullous impetigo is usually caused by a strain of exfoliatoxin-producing S. aureus.
    • The blisters are flaccid and rupture easily, leaving a tell-tale honey-colored crust. The Nikolsky sign is negative.
    • The lesions are asymptomatic and affected patients are usually not ill-appearing.
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  36. Erysipelas
    • is a bacterial infection of the dermis that typically manifests as a well-demarcated, red, indurated, warm, tender plaque.
    • In severe cases, there may be overlying vesicles and bullae.
    • There may also be lymphangitic streaking away from the plaque.
    • Constitutional symptoms like fever, chills, and malaise are common.
    • Group A streptococcus is the classic cause of erysipelas, but it may also be caused by other organisms.
    • The face and lower extremities are common sites of involvement.
  37. Sunburn
    • Sunburn is an inflammatory response to excessive exposure of ultraviolet (UV) radiation.
    • Excessive exposure to UV light increases the risk of photoaging and skin cancer.
    • Regardless of skin type, everyone is at risk of the carcinogenic effects of excessive UV exposure and could benefit from education regarding photo protection.
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  38. Prevention and Treatment of Sunburn
    • The best method of photo-protection is sun avoidance, especially during peak hours of UV intensity.
    • Sunscreen should be applied 15-30 minutes before sun exposure to allow the formation of a protective film on the skin and reapplied at least every 2 hours.
    • Because sunscreen is washed off with swimming and sweating, reapplication is needed even for products labeled "water-resistant" or "very water-resistant."
    • In addition, patients should be informed that cloud coverage does not block UV rays and that UV rays can be reflected off water, sand, snow, and concrete. As a result, patients can burn in the shade or while skiing in the winter.
    • Sunscreen is generally avoided in infants age <6 months="" because="" of="" their="" thin="" skin="" and="" high="" surface="" area-to-body="" weight="" ratio="" which="" increases="" exposure="" to="" sunscreen="" chemicals="" br="">However, a small amount of sunscreen can be used if sun exposure is unavoidable and additional protection is necessary.
  39. Lyme Disease
    • Oral doxycycline is first-line treatment for Lyme disease, which can present with erythema migrans, often described as a "bull's-eye" rash.
    • Transmission of Lyme disease requires >48 hours of tick attachment, and the rash usually appears > 7 days later.
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  40. Tinea capitis
    • a dermatophyte infection occurring most commonly in children and immunocompromised patients.
    • Most common form: in the United States is black dot TC (BDTC), which is due to Trichophyton tonsurans, but other dermatophytes (eg, Microsporum canis, Microsporum audouinii) can also cause TC.
    • Transmission is usually through human-to-human contact or fomites (eg, shared combs).
    • Clinical features:
    • • Scaly erythematous patch on scalp
    • • Hair loss with residual black dot
    • • Possible lymphadenopathy
    • • Other findings can include inflammation, pruritus, occipital or postauricular lymphadenopathy, and scarring
    • Management:
    • • KOH examination of hair shaft to confirm diagnosis
    • • Treatment: Oral terbinafine, griseofulvin, itraconazole or fluconazole
    • As dermatophyte carriers can be asymptomatic, many experts recommend that household contacts be treated with selenium sulfide or ketoconazole shampoo.

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  41. Wound Infections after Burn
    • Wound infections are common, and patients with large surface area (>20%) burns are at highest risk.
    • The earliest sign is usually a change in appearance (partial-thickness injury turns into a full-thickness injury) of the wound or the loss of a viable skin graft.
    • Burn wound sepsis can develop rapidly and is associated with some or all of the following systemic findings:
    • • Temperature <36.5 c="" 97="" 7="" f="" as="" in="" this="" patient="" or="">39 C (1 02.2 F)
    • • Progressive tachycardia (>90/min)
    • • Progressive tachypnea (>30/min)
    • • Refractory hypotension (systolic blood pressure <90 mm Hg)
  42. Diagnosis and Treatment of Burn Infections
    • Oliguria, unexplained hyperglycemia, thrombocytopenia, and mental status changes are also common.
    • Diagnosis requires quantitative wound culture more than 10^5 bacteria/g of tissue) and biopsy for histopathology (to determine tissue invasion depth).
    • Treatment involves empiric, broad-spectrum intravenous antibiotics (eg, piperacillin/tazobactam, carbapenem) with the addition of potential coverage for methicillin-resistant Staphylococcus aureus (eg, vancomycin) or multidrug-resistant Pseudomonas aeruginosa (eg, an aminoglycoside). Local wound care and debridement are usually necessary.
  43. Kaposi sarcoma
    • is most commonly seen in the setting of coinfection involving HIV and human herpes virus 8.
    • The lesions typically begin as papules and later develop into plaques or nodules.
    • The color can change from light brown to violet, and patients often have multiple lesions.
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  44. Mycosis Fungoidis
    • Mycosis fungoides, a hypopigmented rash that typically appears on the trunk, may be an initial presentation of cutaneous T-celllymphoma. Severe pruritus is common.
    • The presentation is less acute, and lesions relapse and remit over time regardless of season or sun exposure
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  45. Pityriasis rosea
    • Pityriasis rosea classically begins with a single salmon-colored macule (herald patch) followed by the development of multiple lesions on the trunk and extremities, often in a "Christmas-tree" distribution.
    • Lesions are erythematous and eventually desquamate, causing itching. I
    • t does not present as multiple hypopigmented spots.
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  46. Candidiasis
    • Cutaneous candidiasis causes an erythematous, vesiculopapular rash in warm, moist areas (eg, skinfolds).
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  47. SPF Of Sunscreens
    • Sunscreens are rated by the strength of their SPF. The amount of UVB radiation filtered by SPF 15, 30, and 50 sunscreens is 93%, 97%, and 98%, respectively.
    • Sunscreens with SPF more than 50 provide a negligible increase in UV protection (eg, SPF 100 sunscreen filters 99% of UVB rays).
  48. Discoid Rash SLE and Malar Rash Of SLE
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  49. Psoriasis and Guttate Psoriasis
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  50. Tuberous Sclerosis Ash Leaf Spots
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Card Set:
USMLE Dermatology II
2017-09-11 09:34:02

Acne , Rosacea, BCC
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