UWorld Flashcards
Tinea Versicolor (Pityriasis versicolor)
Pathogenesis - Malassezia Globosa skin flora growth in exposure to hot and humid weather
Clinical
1) Hypopigmented, hyperpigmented, or mildly red (salmon color) lesions (face in kids, trunk and upper extremities in adolescents and adults)
2) Plus or minus fine scale
3) Plus or minus pruritus
Dx - KOH prep shows hyphae and yeast cells in a spaghetti and meatballs pattern
Tx - Topical ketoconazole, terbinafine, or selenium sulfide (can take months to resolve)
Patients often consult doctor when hypopigmented areas never seem to tan
Pityriasis Rosea
Appear as oval, fawn-colored plaques that measure up to 2cm in diameter and occur in a “Christmas Tree” pattern. The initial lesion is called the “herald patch” and is followed by a generalized eruption in 1-2w
First symptom is pink or brown scaly plaque with central clearing and a collarette of scale (herald patch) on the trunk, neck or extremities. Followed by development of maculopapular christmas tree pattern along skin tension lines
Tinea corporis
Body ringworm. Ring-shaped lesions with advancing scaly border and central clearing or as scaly patches over the trunk
Any species of dermatophyte can cause it but Trichiphyton Rubrum is most common. Most prominent symptom is itching.
Dx confirmed by microscopic exam with KOH. Should show hyphae.
Topical tx with 2% antifungal lotions and creams (Terbinafine) or systemic treatment with griseofulvin (for extensive disease) offers good relief
Patients with extensive disease should be investigated for underlying disorders that cause immunosuppression (DM, HIV, etc)
Seborrheic dermatitis
Acute or chronic papulosquamous dermatitis characterized by dry scales and underlying erythema. Scalp, central face, presternal, interscapular area, umbilicus and body folds are most common. Pigmentation changes are NOT seen.
Common inflammatory disease that affects the scalp (dandruff), face (eyebrows, nasolabial folds, and external ear canal/posterior ear), chest, and intertriginous areas
Most common in first year of life and again at age 30-60.
Associated with CNS disorders (esp Parkinson) and HIV
Dx is clinical - itchy, red plaques with fine loose yellow and greasy looking scales. Primarily affects areas with alot of sebaceous glands although sebum remains normal
Malassezia may be involved
Topical antifungals (ketoconazole, selenium sulfide) are effective
Vitiligo
Total depigmentation especially around mouth or fingertips .
Specific form of leukoderma which usually peaks in people aged 20-30. Depigmentation has predilection for acral areas and around body orifices. Appears as pale whitish macules with hyperpigmented borders
Autoimmune destruction of melanocytes. Slowly progressive disease. Few experience spontaneous remission.
Inherited absence of melanocytes is Piebaldism. Usually noticed at birth and is confined to head and trunk
SJS and TEN
Nomenclature
1) Less than 10% of BSA is SJS
2) 10-30 is SJS/TEN
3) More than 30 is TEN
Clinical
1) 4-28d after exposure to trigger (2 days after repeat exposure)
2) Acute influenza like prodrome (fever, tachy, hypotension, altered consciousness, sezures and coma)
3) Rapid-onset erythematous macules, vesicles, bullae
4) Necrosis and sloughing of epidermis
5) Mucosal involvement
Common triggers
1) Allopurinol
2) Antibiotics (sulfonamides esp like Bactrim)
3) Anticonvulsants (carbamazepine, lamotrigine, phenytoin)
4) NSAIDs (piroxicam)
5) Sulfasalazine
6) Mycoplasma pneumoniae
7) Vaccination
8) Graft vs Host Disease
It is an inflammatory reaction to drugs or certain infections.
Tx - aggressive fluid support often needed due to poor oral intake and profound cutaneous fluid loss. Secondary infections common so antiseptic precautions are needed. Supportive care with wound care just like burns
Erythema multiforme
Self-limited illness characterized by acute erythematous rash and usually occurs after herpes simplex infection**
EM may cause mucosal lesions similar to 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
Bx shows perivascular lymphocytic infiltrate and epidermal necrosis
Impetigo
Staph or strep skin infection characterized by red macules and papular lesions with honey-colored crusts. Most common in kids.
Pemphigus vulgaris
Caused by autoantibodies to desmosomes. Like SJS, it can cause mucosal lesions and desquamating bullae. However, systemic signs (fever) are less prominent and the course is typically more chronic, with oral lesions appearing weeks to months prior to skin syndromes
1) Autoantibody target - desmosomes (desmogleins 1 and 3)
2) Clinical - Flaccid bullae and ulcers; mucosal erosions; separations of epidermis by light friction (Nikolsky sign)
3) Histo - Intraepidermal cleavage, acantholysis (detached keratinocytes), Tombostone cells along basal layer
4) IF - Netlike intercellular IgG and C3 (chicken wire pattern)
5) Tx - Systemic glucocorticoids, corticosteroid-sparing agents, aggressive wound care
Staph Scalded Skin Syndrome
Usually in kids less than 6. Syndrome of acute exfoliation caused by toxins produced by staph aureus
Toxic Shock Syndrome
Inflammatory response caused by a staph exotoxin and presents with fever, rash, hypotension, constitutional symptoms and multiorgan injury. Rash is characterized by diffuse erythema resembling sunburn, with desquamation involving palms and soles.
Exfoliative dermatitis (erythoderma)
Widespread, scaly eruption of the skin. May be drug-induced, idiopathic, or secondary to underlying derm or systemic disease
Actinic keratosis
Erythematous papules with a central scale due to hyperkeratosis. A sandpaper-like texture on palpation of affected areas is typical for this condition.
lesions are small and flat at first, but may enlarge and become elevated. Usually their size does not exceed 10mm in diamater. Hyperkeratosis in such lesions may become prominent and turn into “cutaneous horns”
They develop in genetically predisposed people 40-60 years old under influence of excessive sun exposure.
Most commonly face, ears, scap and dorsa of arms and hands, but any other sun exposed site (legs, back, upper chest) can be involved.
Microscope:
1) Acanthosis (thickened epidermis)
2) Parakeratosis (retention of nuclei in stratum corneum)
3) Dyskeratosis (Abnormal keratinization)
4) Hyperkeratosis (thickening of stratum corneum)
5) keratinocytes have dif degrees of atypia
6) Mitoses and inflammatory infiltrate present
Actinic keratosis is a premalignant condition or carcinoma-in-situ. Fever than 1% of AKs evolve into frank SCC though
Psoriasis
Well-circumscribed raise papules and plaques covered with thick silvery scale.
Lesions are on scalp, trunk, extensor areas of extremities (elbows and knees)
Seborrheic keratosis
In elderly individuals and presents with stuck on, deeply pigmented or flesh-colored lesions with velvety or greasy surface
Usually appears after age 50 as solitary or multiple well circumscribed hyperpigmented lesions. Can have the stuck on or warty appearance and usually occur on trunk, face, upper extremities
Can be itchy or tender especially in areas that come in contact with jewelry
Waxy. Some are flat and lie just above surface of surrounding normal skin. Scalin on surface may be there. Can be pink/white to pale brown to dark.
naturally slow enlargement with increasing thickness
Dx is visual. Bx rarely needed. No tx needed unless lesions become irritated or the patient desires them removed for cosmetics. Tx options include removal by snip/shave excision, cryosurgery and electrodessication
They are benign, though sudden onset of multiple SKs may indicate occult internal malignancy (Laser-Trelat sign)
cutaneous verrucae
Warts
Most common cutaneous manifestation of HPV
HPV can cause warts in various locations like plantar, palmar, genital areas. Plantar is mostly in young adults and patients with decreased cellular immunity (AIDS, organ transplant)
Virus enters through tiny cuts or skin abrasions after direct contact with HPV infected individual. Patients can develop lesions weeks to months later.
Hyperkeratotic papules on sole of the foot (sometimes with thrombosed capillaries and visible skin lines) that can be painful with walking or standing. Dx is clinical
Calluses
Hyperkeratotic lesions next to bony prominences on feet or sometimes on hands.
May sometimes cause pain and discomfort and occur in response to repeated shear or frictional forces
Lichen planus
Purple flat-topped papules or plaques that are pruritic, planar, or polygonal
Most commonly occur on flexural surfaces of extremities, trunk, genitalia
Molluscum contagiosum
Common condition caused by a poxvirus
Single or multiple skin-colored papules with central punctum (umbilicus or central pit)
Children are most commonly affected, but teens and adults can get it too. Transmission is skin-skin contact or via contaminated fomites with subsequent autoinoculation to additional sites.
On kids - lesions are on extremities, face, trunk.
Adults - sexual transmission may lead to lesions on lower trunk or anogenital region
Self-limited (resolution within 6-12months), but treatment with curettage, cryo, or topical podophyllotoxin may be considered to prevent further spread, reduce symptoms or improve looks
Patients with impaired cellular immunity*** (HIV) may have prolonged course with widely distributed papules, facial involvement, and lesion counts numbering in the hundreds. HIV testing should be considered for patients with MC esp if they have large (more than 10mm), numerous, or widespread lesions
SCC
Typically presents with erythematous lesions that are scaly, ulcerate, or grow irregularly
Should be suspected in patients with a slow growing and non-resolving lesion in sun-exposed areas
Much less common than BCC and faster growing. Often arises from a precursor lesion like actinic keratosis and typically has overlaying hyperkeratosis
Look out for outdoor occupation (farmer) who has developed a persistent, indurated, ulcerating lower lip lesion (SCC is most common type of cancer of lower lip vermillion - BCC is upper lip usually).
Light exposure, alcohol, tobacco, fair skin, chronic inflammation, scar formation, immunosuppression are all risk factors for SCC
Confirm dx with bx. It will show invasive cords of squamous cells with keratin pearls. Prognosis is usually very good for cutaneous SCC with curative resection seen in over 90%
Most lesions do not metastasize, but untreated SCC can cause extensive local destruction and may eventually spread to LN or distant structures.
Adverse prognostic signs - larger size, deeper, involvement of regional LNs
Risk factors
1) UV, ionizing radiation
2) Immunosuppression
3) Chronic scars/wounds/burn injuries
Clinical features
1) Scaly plaques/nodules
2) Plus or minus hyperkeratosis or ulceration
3) Neuro signs with perineural invasion
Dx - Bx shows dysplastic/anaplastic keratinocytes
Small or low risk lesions - tx is cryo or electrodessication. Lesions that are high risk or in sensitive areas should get Mohs
SCC doesnt usually met, but SCC arising in wound or burn (Marjolin ulcer) has higher risk of mets
Allergic contact dermatitis
Path - type 4 hypersensitivity (cell mediated instead of antibody mediated. Helper T cells. Delayed)
Triggers
1) Poison oak/sumac
2) Rubber/latex
3) Leather dyes
4) Meds
5) Formaldehyde
6) Nickel
7) Skin care products
Appearance
1) Primarily on exposed skin, well demarcated
2) Erythema
3) Papules/vesicles
4) Chronic lichenification
Red rash with vesicles and small bullae at site of exposure.
Poison ivy/oak/sumac
Toxicodendron
Grows as small shrubs or vines and produces urushiol, a highly allergenic resin
Most common in undeveloped, wooded areas but can be seen in urban/suburban neighborhood
Rash can appear days after exposure. Usually limited to exposed skin and frequently forms linear streaks where skin is brushed against plant leaves.
Diffuse or atypical patterns can be seen after exposure to contaminated cloth, pets or smoke from burning plants
Irritant contact dermatitis
Path - physical or chem irritation
Triggers
1) Soaps/detergents
2) Chemicals
3) Acid/alkali
Appearance
1) Commonly on hands
2) Erythema
3) Fissures
Cellulitis
Localized, expanding erythema and swelling. It is rarely bilateral.
Most caused by strep and staph
Coagulase neg staph are common contaminants in skin cultures, but true infection is rare in healthy patients
Hidrandenitis suppurativa
AKA acne inversa
Chronic, relapsing disorder with painful nodules and abscesses in intertriginous areas (axilla). But can occur in any hair-bearing skin.
Due to chronic inflammatory occlusion of folliculopilosebaceous units which prevents keratinocytes from properly shedding from the follicular epithelium.
Risk factors include FHx of it, smoking, obesity, diabetes, mechanical stress on the skin (friction, pressure)
Usually presents as solitary, painful inflamed nodules that can last for several days to months. The nodules may regress or can progress to abscesses that open to the surface with purulent or serosanguinous drainage.
Most patients have a chronic, relapsing course
Complications include sinus tracts, comedones, and scarring
Severe scarring can lead to dense, rope-like bands in the skin with strictures and lymphedema.
Clinical dx without need for bx or cx
Sporotrichosis
Fungal infection acquired by direct traumatic inoculation of the skin. Ulcerating, pustular nodules at the site of inoculation with associated lymphatic channels
Melanoma
Melanoma occurs as solitary lesion, and can occur anywhere on the skin. The back is most common location in men while legs is most common in women.
Patients often complain of a mole that has changed in size or color (either darkened or lightened) or a mole that has become symptomatic (itchy, painful or bleeding)
ABCDEs help screen and detect early. Asymmetry, Border irregularities, Color variegations, Diameter more than 6mm and Enlargement
Risk factors: Fair skin, history of blistering sunburns, family history, dysplastic nevus syndrome, atypical nevi and greater than 100 typical nevi
Keratocanthoma
Low grade malignancy that pathologically resembles SCC.
Appears as solid, firm, round, skin-colored or reddish plaque that develops into a nodule with a central keratin plug
Rapidly growing, volcano-like nodule with central keratin plug. Although these lesions may regress on their own, many are treated as well-differentiated SCCs
Early tx is indicated if lesion is near an important structure like the eye
Bullous pemphigoid
Autoimmune blistering disease that causes itchy, tense bullae in flexural surfaces, groin and axilla. Mucosal lesions occur in only some. Bx shows subepidermal cleavage with linear IgG deposits at Basement membrane on IF
Usually in patients over 60.
Variable prodrome of eczematous or urticarial lesions and subsequently develop tense bullae and plaques affecting flexural surfaces, groin and axilla
First line tx - high potency topical steroids (clobetasol), which is effective even if severe. Systemic steroids are NOT more effective and have more complications. Can be used if topical isn’t practical
Acrochordon
Skin tag. Usually flesh colored or pedunculated papules in regions of the body subjected to friction such as neck, axilla, and inner thighs
BCC
Most common presentation of BCC is slow-growing papule or nodules with a pearly, rolled border and overlying telangiectasia (dilated blood vessels). Ulceration is commonly seen as is bleeding following minor trauma
Possible features include:
1) Persistent open sore that bleeds, oozes or crusts
2) Reddish patch or irritated area (superficial BCC)
3) Pearly or translucent nodule that is pink, red, or white in color (Nodular BCC)
4) Elevated or rolled border with central ulceration
5) Pale scar-like area with poorly defined borders
BCC only rarely spreads to other parts of the body, but it should be treated (removed) to prevent invasion of nearby tissues/structures like nerves*, bones, and brain
Low risk lesions on trunk or extremities can be easily managed with electrodessication and curettage.
Nodular BCC on the trunk or extremities may be easily managed with standard surgical excision, typically with 3-5mm margins
BUT, for the face and other delicate or cosmetically sensitive areas, Mohs is used more.
Low risk superficial BCC can be treated with topical 5-FU or imiquimod (less effective in nodular)
Hypersensitivity rashes caused by circulating autoantibodies
Can be of either type 2 (antibody-dependent cellular cytotoxicity) or type 3 (immune complex deposition)
Type 2 rashes are more likely to manifest as blisters or bullae (pemphigus vulgaris, bullous pemphigoid) than papules
Type 3 rashes tend to be more erythematous and maculopapular
Rosacea
Chronic inflammatory disorder with flushing, erythema, telangiectasias, papules/pustules, and tissue hyperplasia. Usually in fair skinned people over 30.
Most often involves central face and scalp
1) Erythemato-telangiectatic: Persistent facial redness/flushing, telangiectasias
2) Papulopustular: Papules and pustules on central face
3) Ocular: Conjunctival hyperemia and lid margin telangiectasias
Treatment
1) Avoid triggers (alcohol, spicy foods)
2) Sun protection
3) Gentle cleansers and emolients
4) Topical metronidazole for papulopustular type
5) Laser or topical brimonidine (vasoconstrictive alpha-2 agonist) for erythematotelaniectatic type.
