00 Dermatology Chp 10. Usmle Step 2 Step Up

Front 1

History and Physical (H/P) = erythema, swollen and painful skin, myalgias, chills; warmth in involved area, fever, lymphadenopathy; skin findings may be near wound (see Color Figure 10-1)

Back 1

Cellulitis
Acute skin infection most frequently caused by Staphylococcus aureus or group A streptococci; methicillin-resistant S. aureus (MRSA) has increasingly evolved as a cause of cellulitis that is difficult to treat because of antibiotic resistance
Risk factors = intravenous drug use, diabetes mellitus (DM), immunocompromise, penetration of skin (e.g., surgery, trauma), previous cellulitis, venous or lymphatic dysfunction
Complications = necrotizing fasciitis; 20–50% recurrence rate

Hint 1

Labs = increased white blood count (WBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP)
Treatment = oral cephalosporins or penicillinase-resistant β-lactams for 10 to 14 days; intravenous (IV) antibiotics for severe cases or bacteremia; linezolid or IV vancomycin used for MRSA or cases not responding to initial antibiotic therapy; diabetics should receive broad coverage antibiotics because of the increased risk for multiorganism infections

Front 2

H/P = erythematous, fluctuant, and localized swelling in skin; tender on palpation; pain frequently relieved by rupture of abscess

Back 2

Skin abscess
Subcutaneous collection of pus most commonly caused by staphylococcal bacteria
Can occur as collection of multiple infected hair follicles (i.e., carbuncle)
Hidradenitis suppurativa
Chronic follicular occlusion and apocrine gland inflammation resulting in recurrent abscesses in the axilla, groin, and perineum
Chronic infection leads to scarring
May require both antibiotics and surgical excision for treatment
Complications = large, eroding facial abscess can cause cavernous sinus thrombosis
Anaerobic bacteria are more commonly a cause of abscesses in the lower back and perineal regions than in other parts of the body.

Hint 2

Labs = culture of abscess contents can determine pathogen, but carries a high rate of false–positive findings if not performed under sterile conditions
Treatment = incision and drainage with healing by secondary intention; antibiotics (cephalosporins initially, then pathogen-specific)

Front 3

H/P = erythematous, warm, and swollen skin; Loss of sensatioN in involved tissue, fever, crepitus in infected skin, purple discoloration, bullae over infected region

Back 3

Necrotizing fasciitis
Quickly spreading group A streptococcus or multipathogen infection of fascial planes leading to extensive soft tissue destruction and systemic infection
Complications = sepsis, gangrene, high mortality (30% patients)

Hint 3

Labs = increased WBC, ESR, and CRP; operative culture useful for determining pathogen
Radiology = x-ray or computed tomography (CT) may detect subcutaneous collections of air
Treatment = prompt surgical débridement, incision and drainage, IV antibiotics

Front 4

H/P = prior skin infection or penetrating wound, severe pain in skin; fever, hypotension, skin crepitus, Rotten-smellinG skin

Back 4

Gangrene
Tissue necrosis because of poor vascular supply or severe infection (occasionally, Clostridium sp.); described as wet or dry, depending on appearance
Dry gangrene, gradual necrosis of skin from vascular insufficiency, features hard and dry skin. Wet gangrene, necrosis caused by acute vascular obstruction or infection, features blistering and swelling of the involved area.

Hint 4

Labs = culture may be useful when caused by infection; ankle-brachial indices should demonstrate asymmetry between limbs
Radiology = subcutaneous air seen on x-ray or CT for wet gangrene; angiography or magnetic resonance angiography (MRA) demonstrates vascular insufficiency
Treatment = incision and drainage, débridement, antibiotics; amputation frequently required

Front 5

H/P = facial pruritus; yellow crusted lesions around mucocutaneous surfaces; erythematous vesicles (blisters) seen in staphylococcal infection; erythematous pustules on face and extremities with streptococcal infections

Back 5

Impetigo
Contagious skin infection most commonly found in children; caused by S. aureus or group A streptococci

Hint 5

Treatment = wash all affected areas; erythromycin, cephalosporins, or topical antibiotics; unaffected family members should not share towels or clothing to prevent spread until cure achieved

Front 6

H/P =
Most frequently occurs in adolescents
Erythematous pustules predominantly on face, neck, chest, and back
Cystic lesions can form in severe cases

Back 6

Acne vulgaris
Inflammation of hair follicles and sebaceous glands associated with Propionibacterium acnes, adolescence, androgens, and obstruction of pores by exfoliated skin or personal care products
Complications = cystic acne can result in permanent scarring; oral vitamin A analogues can cause birth defects or hepatotoxicity
Acne usually decreases in severity as adolescence ends. Corticosteroid use and androgen production disorders are common causes of outbreaks in adulthood.

Hint 6

Treatment =
Topical retinoids decrease sebaceous gland activity and are the recommended first-line treatment
Antibiotics (oral or topical) may inhibit bacterial growth (second-line therapy)
Benzoyl peroxide helps prevent follicular obstruction by decreasing oiliness of skin (second-line therapy)
Oral contraceptives may be useful in women with excess androgen production
Oral isotretinoin given for severe cases, but requires close monitoring of liver enzymes (hepatotoxicity risk) and mandatory pharmacologic contraception (high teratogenic risks)
Women should have at least two negative urine pregnancy tests before an oral isotretinoin is prescribed.
Soaps and astringents have little effect on the condition

Front 7

H/P = small painful vesicles around mouth (HSV-1) or genitals (HSV-2) lasting several days (see Color Figure 10-3); primary infection usually presents with more severe symptoms and a flu-like illness; disease affecting eyes causes impaired vision; disease affecting esophagus causes odynophagia and dysphagia

Back 7

Herpes simplex virus (HSV)
Recurrent viral infection of mucocutaneous surfaces caused by HSV-1 or -2
HSV transmitted through contact with oral or genital fluids
HSV-1 causes primarily oral disease; HSV-2 causes primarily genital disease
After primary infection, viral genetic material remains in sensory ganglia; stress will cause reactivation of disease in distribution of involved nerves
Complications =
Contagious whenever vesicles present
Transmission from infected mother to newborn can cause disseminated disease with severe neurologic involvement
Rarely, mother-to-newborn transmission can occur in absence of visible vesicles

Hint 7

Labs = Tzanck smear of lesions shows multinucleated giant cells; viral culture confirms diagnosis
Treatment = incurable, so treatment should be directed at minimizing symptoms and exacerbations; acyclovir, famciclovir, or valacyclovir shortens duration of recurrences and may decrease number of recurrences in patients with frequent eruptions

Front 8

H/P=Small, red macules that evolve into papules and then vesicles that eventually become crusted

Back 8

Varicella
Infection by varicella-zoster virus (i.e., herpes zoster) that can present as primary disease (i.e., chickenpox) or recurrent disease (i.e., shingles)
Immunocompromised patients are at an increased risk for developing encephalopathy or retinitis as complications from varicella infection.

Hint 8

Check varicella immunity status (received vaccine or had chickenpox as child) in all pregnant women; varicella immune globulin should be given to all nonimmune pregnant women who contract the disease.

Front 9

H/P=Small, red macules that evolve into papules and then vesicles that eventually become crusted
Wide distribution
More common in children
Timing=Symptoms 2+ wk after infection occurs; symptoms of headache, malaise, myalgias, and fever precede development of lesions by <3 days
Lesions may develop up to 1 wk and resolve a few days after appearing; infective until lesions crust over

Back 9

Chickenpox (Primary)
Complications=More severe course in older and pregnant patients (increased risk of varicella pneumonia); can have severe consequences if passed from infected mother to unborn fetus

Hint 9

Treatment=Antipruritics aid symptoms; acyclovir used in severe cases or in immunocompromised patients; vaccination has reduced disease incidence significantly

Front 10

H/P=Small, red macules that evolve into papules and then vesicles that eventually become crusted
Limited to single or few distinct dermatomes; involvement of multiple dermatomes indicates disseminated disease
Timing=Myalgias, fever, malaise preceding lesions by approximately 3 days. Lesions exist for a week and may be painful; infective until lesions crust over

Back 10

Shingles (Recurrent)
Patient with prior history of varicella-zoster infection
Complications=Postinfectious neuralgia (long-lasting pain at site of eruption), trigeminal neuropathy

Hint 10

Treatment=Analgesics, possible corticosteroids; acyclovir used in immunocompromised patients and trigeminal nerve distribution

Front 11

H/P = well-defined lesions of thickened epithelium, may appear flat (plantar warts) or raised; occasional tenderness to palpation

Back 11

Warts
Benign epithelial tumors caused by local infection by one of many types of human papillomavirus (HPV)
Complications = some forms of HPV that cause genital warts are associated with cervical cancer

Hint 11

Treatment = occasionally self-limited; chemical, laser, or cryotherapy may be required for removal

Front 12

H/P=Small scaly macules most frequently on chest and back

Back 12

Tinea versicolor
Malassezia furfur

Hint 12

Lab=KOH preparation shows short hyphae, Wood's lamp examination shows extent of disease
Treatment=Topical antifungal agent for several weeks or oral ketoconazole for 1–5 days

Front 13

H/P=Pruritic, erythematous, scaly plaques with central clearing

Back 13

Tinea not caused by M. furfur. Described by location: corporis (body), cruris (groin), pedis (feet), unguium (nail beds), capitis (scalp)
Microsporum
Trichophyton
Epidermophyton

Hint 13

Lab=KOH preparation shows hyphae
Treatment=Topical antifungal agent for multiple weeks
Oral antifungal agent for resistant cases

Front 14

H/P=Pruritic, painful, erythematous plaques with pustules most commonly in skin creases

Back 14

Intertrigo
Candida albicans

Hint 14

Lab=KOH preparation shows pseudohyphae
Treatment=Topical antifungal agent, Topical corticosteroid

Front 15

H/P =
Painless, shiny papules with central umbilication (<5 mm diameter)
In children, found on face, back, chest, and extremities; in adults, found in perineal region

Back 15

Molluscum contagiosum
Viral skin infection most frequently seen in children and in patients positive for human immunodeficiency virus (HIV)

Hint 15

Labs = Giemsa and Wright's stains on histology show large inclusion bodies
Treatment = frequently self-limited; chemical, laser, or cryotherapy for removal

Front 16

H/P = severe pruritus at site of involvement (most commonly extremities) that worsens after a hot bath; mite burrows with nearby papules may be seen on close examination of skin
Labs = mites and eggs may be seen in skin scrapings under microscope

Back 16

Scabies
Cutaneous infestation by Sarcoptes scabiei mite
Risk factors = crowded living conditions, poor hygiene
Complications = infection of close contacts common

Hint 16

Treatment =
Permethrin cream or oral ivermectin; diphenhydramine to relieve pruritus
All clothing, towels, and linens must be washed in hot water

Front 17

H/P =
Pruritus, erythematous rash in distinct patterns (lines, shapes) in contact dermatitis
Ingestion of an allergen (e.g., food, drug reaction) can cause rash in a characteristic location or in a poorly defined area
History of drug ingestion, contact with allergen, or previous reaction is helpful for diagnosis

Back 17

Hypersensitivity reactions in skin
Allergic reaction seen in skin because of cutaneous contact or ingestion of a given allergen (e.g., drugs)
Mechanism of reaction
Type I: caused by mast cell degranulation; light, diffuse rash (i.e., urticaria) appears soon after exposure and lasts only several hours
Type IV: caused by lymphocyte activity; measles-like (i.e., morbilliform) rash appears several days after second exposure to allergen (mechanism for most allergic contact dermatitis)

Hint 17

Treatment =
Stop offending agent or remove contact with allergen
Mild cases can be treated with topical corticosteroids and antihistamines
Oral corticosteroids may be required in worse cases

Front 18

H/P = malaise, myalgias, pruritus; macules (i.e., small, nonpalpable lesions); plaques (i.e., large nonpalpable lesions) or vesicles on extremities (especially palms, soles); target lesions (i.e., erythematous center surrounded by pale inner ring and erythematous outer ring) may be evident

Back 18

Erythema multiforme
More serious cutaneous hypersensitivity reaction caused by drugs, infection, or vaccination
Penicillins, sulfon-amides, nonsteroidal anti-inflammatory drugs (NSAIDs), oral contraceptives, and anticonvulsant medications are agents most frequently associated with erythema multiforme.
HSV and Mycoplasma pneumoniae are common infectious causes of erythema multiforme.

Hint 18

Labs = increased eosinophils; skin biopsy shows increased lymphocytes and necrotic keratinocytes
Treatment = may be self-limited; stop offending agent; corticosteroids, analgesics

Front 19

H/P = similar skin appearance to erythema multiforme, but more severe; more likely to have myalgias, fever, nausea, vomiting, oral pain, and eye pain

Back 19

Stevens-Johnson syndrome
Severe form of erythema multiforme involving mucous membranes, and severe plaque formation
Skin sloughing may be evident; high risk of dehydration

Hint 19

Treatment = stop offending agent; corticosteroids, analgesics, IV fluids; frequently treated in burn unit

Front 20

H/P=significant skin sloughing and full-thickness epidermal necrosis
Labs = - WBC, - Hb&Hct, + ALT & AST

Back 20

Toxic epidermal necrosis (TEN)
Most severe form of hypersensitivity reaction with significant skin sloughing and full-thickness epidermal necrosis

Hint 20

Treatment =
Stop offending agent
Treat patient in burn center, IV hydration, corticosteroids, intravenous immune globulin
Acyclovir may be useful in cases caused by HSV

Front 21

H/P = pruritus; erythematous plaques with Yellow, greasy scaleS
commonly on Scalp or facE

Back 21

Seborrheic dermatitis
Chronic hyperproliferation of epidermis most commonly on scalp or face
Most common in adolescents and infants
Complications = frequent recurrence
“Cradle cap” is seborrheic dermatitis of the scalp in infants.

Hint 21

Treatment = shampoo containing selenium, tar, or ketoconazole when scalp involved; topical corticosteroids and antifungals used for other regions

Front 22

H/P = pruritus; erythematous patches of dry skin with possible vesicles on flexor surfaces, dorsum of hands and feet, chest, back, or face; lesions more commonly on face and scalp in infants

Back 22

Atopic dermatitis (i.e., eczema)
Chronic inflammatory skin rash characterized by dry skin patches with papules
Both infantile (resolves with initial years of life) and adult (recurrent) forms exist
Risk factors = asthma, allergic rhinitis, family history

Hint 22

Treatment = avoidance of precipitating factors, moisturizing creams, topical corticosteroids or tacrolimus; severe cases can be treated with oral corticosteroids and antihistamines

Front 23

H/P = possible pruritus; well-defined red plaques with silvery scales on extensor surfaces (especially knees and elbows) that bleed easily with scale removal (i.e., Auspitz sign), possible small pustules, pitted nails, lifting of nails

Back 23

Psoriasis
Inflammatory skin disorder characterized by epidermal hyperproliferation
Of patients with psoriasis, 20% also have psoriatic arthritis

Hint 23

Labs = negative for rheumatoid factor; skin biopsy shows thickened epidermis, absent granular cell layer, and nucleated cells in stratum corneum; possible increased uric acid, increased ESR
Treatment = topical corticosteroids, tar, retinoids, tacrolimus, or antifungal agents; phototherapy, methotrexate, cyclosporine, or anti-tumor necrosis factor (TNF) drugs can be used in severe disease

Front 24

H/P =
Pruritus; oval erythematous papules covered with white scale located primarily on chest, back, and extremities
Rash begins with appearance of “herald patch” (i.e., single round lesion up to 5 cm in diameter) a few days before generalized eruption

Back 24

Pityriasis rosea
Mild inflammatory skin disorder in children and young adults with possible viral association characterized by papular lesions on the trunk and extremities
Rash distribution in pityriasis rosea occurs in a “Christmas tree” pattern.

Hint 24

Treatment = self-limited; topical steroids, phototherapy, or erythromycin may decrease duration of exacerbation

Front 25

H/P = malaise, arthralgias; tender erythematous nodules (usually pretibial), fever

Back 25

Erythema nodosum
Inflammation of subcutaneous fat septa resulting in painful erythematous nodules most commonly on anterior tibias, but can also affect trunk and other extremities

Caused by delayed immunologic reaction to infection, collagen-vascular diseases, inflammatory bowel disease, or drugs
SPUD BITS: Streptococcal infection, Pregnancy, Unknown (idiopathic), Drugs, Beçhet's disease, Inflammatory bowel disease, tuberculosis (TB), Sarcoidosis.

Hint 25

Labs = possible positive antistreptolysin O titer (when associated with streptococcal infection), increased ESR; skin biopsy may show fatty inflammation
Treatment = self-limited; NSAIDs, potassium iodide, corticosteroids

Front 26

H/P = Painful, fragile blisters in oropharynx and on chest, face, and perineal region; blisters rupture easily and erosions are common
Patients usually middle-aged or elderly

Back 26

Pemphigus vulgaris
Autoimmune disorder characterized by autoantibodies to adhesion molecules in epidermis
Complications = sepsis, high mortality without treatment, osteoporosis (chronic corticosteroid use)

Hint 26

Labs = skin biopsy shows separating of epidermal cells (i.e., acantholysis) with intact basement membrane; immunofluorescence demonstrates antiepidermal antibodies
Treatment = corticosteroids, azathioprine, or cyclophosphamide

Front 27

H/P = widespread blistering (especially on flexor surfaces and perineal region), pruritus; erosions can form with blister rupture
Most patients >60 yr of age

Back 27

Bullous pemphigoid
Autoimmune disorder characterized by autoantibodies to epidermal basement membrane

Hint 27

Labs = immunofluorescence shows antibasement membrane antibodies
Treatment = oral or topical corticosteroids or azathioprine

Front 28

H/P = chronic blistering on sun-exposed skin, ruptured blisters heal poorly and result in erosions and hyperpigmented skin

Back 28

Porphyria cutanea tarda
Disease resulting from deficiency of hepatic uroporphyrinogen decarboxylase, an enzyme involved in heme metabolism
Risk factors = alcoholism, hepatitis C, iron overload, estrogen use, smoking

Hint 28

Labs = decreased uroporphyrinogen decarboxylase, increased porphyrins in serum, urine, and feces
Treatment = periodic phlebotomy, chloroquine

Front 29

H/P = erythematous papule with rough, yellow-brown scales <5 mm in diameter; lesions found in sun-exposed areas

Back 29

Actinic keratosis
Precancerous skin lesion that can progress to squamous cell cancer
Risk factors = sun exposure
Complications = 0.1%/yr risk of progression to squamous cell carcinoma (60% of squamous cell carcinomas arise from actinic keratosis)

Hint 29

Labs = biopsy (must to r/o squamous cell cancer) shows dysplasia of epithelium (deeper epithelial cells show variations in shape and nuclei with increased staining)
Treatment = topical 5-flurouracil or imiquimod, cryotherapy

Front 30

H/P = painless, erythematous papule with scaling or keratinized growths in sun-exposed area; progressive lesions may bleed, ulcerate, or be painful

Back 30

Squamous cell carcinoma
Skin cancer involving squamous cells of epithelium
Risk factors = sun exposure (particularly UVB radiation), actinic keratosis, arsenic exposure, fair complexion, radiation
Complications = progresses slowly, but can be a large lesion by time of diagnosis if located in poorly visualized region (back, scalp); 5–10% of cases metastasize

Hint 30

Labs = biopsy shows anaplastic epidermal cells extending to dermis
Treatment = surgical excision; Mohs' excision (i.e., serial shallow excisions with histologic analysis to minimize cosmetic damage) may be performed for lesions on face; radiation may be helpful in large lesions

Front 31

H/P = pearly papule with fine vascular markings (i.e., telangiectasias)

Back 31

Basal cell carcinoma
Skin cancer arising in basal epidermal cells
Risk factors = sun exposure
Complications = lesions metastasize in <0.1% of cases
Basal cell carcinoma is the most common type of skin cancer.

Hint 31

Labs = biopsy shows basophilic-staining basal epidermal cells arranged in palisades
Treatment = surgical excision, Mohs' excision, radiation, or cryotherapy
Shave biopsy should never be used to study a suspicious lesion because it does not provide sufficient tissue for clear diagnosis and cannot be used to measure lesion depth.

Front 32

/P =
Painless, pigmented lesion with recent changes in appearance
Lesions have irregular borders, multiple colors, and can be large or rapidly growing (see Color Figure 10-16)
In contrast, melanocytic nevi are more symmetric, have more regular borders, are homogenously colored, and remain relatively the same size over time (see Color Figure 10-17)

Back 32

Melanoma
Malignant melanocyte tumor that spreads rapidly
Risk factors = sun exposure, fair complexion, family history, numerous nevi
Superficial spreading: most common type; grows laterally before invasive growth occurs
Nodular: grows only vertically and becomes invasive rapidly; difficult to detect
Acral lentiginous: involves palms, soles, and nail beds
Lentigo maligna: long-lasting in situ stage before vertical growth
Complications = aggressive cancer; lesions can have metastasized by time of discovery (most commonly, lung, brain, and gastrointestinal tract)
The most important prognostic factor for melanoma is thickness of lesion (>0.76 mm associated with increased risk of metastasis).
Periodic skin checks should be performed in anyone with a history of significant sun exposure and a positive family history for melanoma

Hint 32

Nevi should be followed to look for the ABCDEs of melanoma: Asymmetry, Border (irregular), Color (variable), Diameter (>6 mm), and Enlargement.
Labs = excisional biopsy shows atypical melanocytes and possible invasion into dermis
Treatment = surgical excision (0.5 cm margin if in situ, 1 cm margin if <2 mm thick, 2 cm margin if >2 mm thick) with possible lymph node dissection; chemotherapy and radiation therapy if metastatic

Front 33

Skin Graft Indicated & Donor Site
Skin replacement in wounds; useful to cover extensive surface area (contracts over time)

Back 33

Split-thickness graft
Skin graft composed of epidermis and part of dermis

Hint 33

Common Donor Site= Abdomen, thighs, buttocks

Front 34

Skin Graft Indicated & Donor Site
Defects on face, hands

Back 34

Full-thickness graft
Skin graft composed of epidermis and full dermis

Hint 34

Common Donor Site=Above ears (for face), forearm, groin

Front 35

Skin Graft Indicated & Donor Site
Site-specific anatomic reconstruction

Back 35

Composite graft
Skin grafts that also contain other tissues (cartilage, nail bed, fat)

Hint 35

Common Donor Site= Fingertip, ear, etc.

Front 36

Skin Graft Indicated & Donor Site
Large defects with good vascular supply requiring padding

Back 36

Fasciocutaneous flap
Skin and subcutaneous tissue with attached vascular supply

Hint 36

Common Donor Site= Forehead, groin, deltopectoral region, thighs

Front 37

Skin Graft Indicated & Donor Site
Areas requiring increased vascularized tissue, exposed deep tissues, severe radiation injury

Back 37

Muscle flap
Transferred muscle that either includes skin (myocutaneous flap) or requires additional skin graft

Hint 37

Common Donor Site=Tensor fascia lata, gluteal muscles, sartorius, rectus abdominus, latissimus dorsi