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39 Cards in this Set
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Case history:
A 47-year old man presented with a one day history of an extremely pruritic vesiculobullous (i.e., blistering) eruption on his hand On the day before the onset of the eruption, he had been clearing shrubs and brush in his backyard Gross features: Allergic Contact Dermatitis |
Acute/subacute form: diffuse erythema, edema, oozing and crusting of skin with formation of vesicles and bullae
Linear lesions may be noted Covered, unexposed sites may be spared Chronic form: scaling, thickened skin (not shown) |
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Histologic features: Allergic Contact Dermatitis
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Acute/Subacute: Spongiosis, intraepidermal vesicles
Chronic: hyperkeratosis, acanthosis (not shown) All stages show a perivascular mononuclear (lymphocytic and histiocytic) inflammatory infiltrate in the upper dermis |
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Allergic Contact Dermatitis: Mech
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Allergic contact dermatitis is a type IV delayed hypersensitivity reaction to haptens
Contact with haptens in a previously non-sensitized individual may not cause a rash, but can lead to the development of immunologic sensitivity over a 10-14 day period Subsequent contact with haptens by the same individual will produce an accelerated reaction within 1 to 2 days Intensity of reaction is variable: depends on: -the concentration of haptens -the body site (thick epidermis is more resistant) -individual sensitivity The eczematous, papulovesicular eruption clears in about 3 weeks |
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Allergic Contact Dermatitis: Offending plant
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Allergic contact dermatitides to the following offending plants are quite common in the U.S. and are clinically the same:
Toxicodendron radicans (poison ivy) T. diversiloba T. quercifolium (poison oak) T. vernix (poison sumac) |
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Toxicodendron dermatitis
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The oleoresin (urushiol) of the Toxicodendron plant sap contains pentadecylcatechols which are the sensitizers
Toxicodendron dermatitis can be acquired from oleoresin-contaminated clothing, animals and tools The fluid of vesicles and bullae in Toxicodendron dermatitis is not antigenic |
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Case history:
A 50-year-old male with a long history of smoking complained of painful lesions in his mouth and weight loss Recently, he noticed the appearance of a number of painful skin lesions PE revealed erythematous and crusted patches with areas of erosion randomly distributed Pemphigus Vulgaris: clinical features |
Clinical features:
PV usually starts as oral lesions which makes it difficult to eat (odynophagia). May lead to noticeable weight loss Oral lesions are followed by generalized bullae 6-12 months later. |
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Gross features: Pemphigus vulgaris
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Lesions commonly involve the oral mucosa, scalp, face, chest, axillae, groin and umbilicus
Large areas of painful erosions are seen in full blown disease Skin lesions consist of a combination of vesicles and bullae that rupture easily |
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Histological features: Pemphigus vulgaris
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Intraepidermal bullae which split the epidermis above the basal cell layer (suprabasal) contain rounded up (acantholytic) keratinocytes
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Histological features: Pemphigus vulgaris-- immunoflorescent
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Direct immuno-fluorescence: IgG and C3 are deposited in the intercellular substance of the epidermis, which looks like a net.
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What Is the Etiology of Pemphigus Vulgaris?
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Autoimmune disease causing loss of normal cell-to-cell adhesion (acantholysis)
Circulating IgG autoantibodies directed against a 130 Kd cell adhesion molecule in the epidermis (desmoglein 3) |
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What Are the Constitutional Symptoms of Pemphigus Vulgaris?
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Weakness, malaise and weight loss
Painful oral lesions make it difficult to swallow resulting in difficulty eating |
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What Is Nikolsky’s Sign?
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Nikolsky's sign involve the superficial layers of skin slipping free from the lower layers with slight pressure.
Pos. Nikolsky's sign is present in scalded skin syndrome (staph infection), toxic epidermal necrolysis, and pemphigus vulgaris. Pressure in the vicinity of the bullous lesion displaces the epidermis leading to skin erosion |
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What is the natural history of this disease
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Without immunosuppressive treatment the disease progresses to death, secondary to debilitation and sepsis
With current medications the side effects of therapy, rather than the skin disease, are the usual cause of death |
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Case history:
A 20-year-old female presented to her family physician with a sudden onset of pruritic lesions on her upper extremities that were present for 3 days Erythema Multiforme: Clinical features |
Inflammatory disease predominantly affecting adults
Oral lesions may occur simultaneously with skin lesions and consist of painful erosions Skin lesions may be asymptomatic or may burn or itch Fever and weakness may be present Skin lesions are usually distributed over the extensor aspects of the extremities Mild and severe forms of the disease exist |
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Gross features:
Erythema multiforme |
Typical lesion: an erythematous papule with a central vesicle that gives the lesion its characteristic target appearance
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Gross features:
Erythema multiforme |
Mucous membrane involvement
Lesions with several different concentric zones of color change may be seen and are bilateral and symmetrical Prominent bullae after sulfonamide ingestion |
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Histologic features
Erythema multiforme |
A perivascular mononuclear infiltrate is present
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What Is the Etiology of EM?
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In some cases, the cause is unknown
EM minor form: commonly observed after recurrent Herpes simplex EM severe form: associated with Mycoplasma pneumoniae infection and a number of drugs |
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What Drugs Is EM Associated With?
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Sulfonamides
Phenytoin Barbiturates Penicillin Allopurinol Nonsteroidal anti-inflammatory agents |
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What Is the Natural Course of EM?
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Two clinical presentations: mild and severe
The mild form (EM minor) is often associated with prior Herpes simplex infection Usually seen on the trunk and extremities, lacks systemic symptoms and may involve oral mucous membranes Acyclovir may prevent further eruptions Eruptions are self-limited and resolve within several weeks |
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What Is the Natural Course of EM? The severe form (EM major or Stevens-Johnson Syndrome)
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The severe form (EM major or Stevens-Johnson Syndrome) is often related to drug ingestion and involves mucous membranes and variable amounts of skin
Multiple target lesions and/or bullae are present Systemic symptoms are seen Erosive mucous membrane involvement leads to cheilitis (inflammation of lips), stomatitis (inflammation of the mucous membrane of the mouth) and genital involvement (vulvitis and balanitis (infl of glans or clitoris) Involvement of the ocular mucosae may lead to a keratitis and corneal ulceration, which may result in blindness A laryngotracheobronchitis may be seen Steroid therapy may be of value if initiated early on Suspect or unnecessary drugs should be stopped and M. pneumoniae infection, if present, should be treated |
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Case history:
The patient is a 22-year-old woman who presented with a six year history of a bilateral symmetric pruritic eruption over her elbows, knees, scalp and sacral area These lesions appear as red papules and plaques covered by white adherent scales Gross features: Psoriasis |
Sharply demarcated erythematous papules and plaques covered by white, silvery scales
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Gross features: Psoriasis, what areas are commonly involved?
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The scalp, sacral region and extensor surfaces of the extremities, umbilicus, penis and nails are commonly involved
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Gross features: Psoriasis
Pustular variant |
Multiple pustules on erythematous plaques
Benign if localized to hands and feet Life-threatening if generalized |
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Histologic features: Psoriasis
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Parakeratosis (keratinized cells with abnormal retention of nuclei)
Acanthosis (thickening of the epidermis) Elongation of the rete ridges Elongation of the papillary dermis Neutrophils and Munro microabscesses in the parakeratotic layer |
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What is Auspitz sign?
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Fine bleeding points that can be produced by peeling off a psoriatic scale
Caused by delicate capillaries in the papillae that almost reach the surface of the epidermis |
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Genetic Basis of Psoriasis
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Higher incidence among the offspring and relatives of patients, high concordance in monozygotic twins and HLA associations (HLA-B13, HLA-B17, particularly HLA-Cw6)
The more severe the disease, the greater the likelihood of familial predisposition A family history of psoriasis is reported by about one-third of affected patients |
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What Is Koebner Phenomenon?
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The Koebner (pronounced “curb-ner”) phenomenon is the induction of a specific type of skin lesion by trauma
The lesion is confined to the site of trauma The trauma can consist of various types of skin injury such as burns, tattoos, excoriations, dermatitis and infection The Koebner phenomenon is characteristic of psoriasis but can also be seen in vitiligo, lichen planus, lichen nitidus, etc |
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Case history:
A 80-year-old male presents with several large, elevated dark brown papules and small plaques on his face Clinical features: Seborrheic Keratosis |
Common benign tumor seen in older individuals usually on the face, trunk or extremities, but can occur anywhere
Lesions increase in number and size with age Lesions are generally asymptomatic but may occasionally itch or become irritated |
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Gross features: Seborrheic keratosis
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Begin as small 1-3 mm papules
Enlarge to 1-3 cm and develop a warty or greasy surface, and have a “stuck on” appearance May resemble a piece of tan or brown chewing gum that has been pressed flat against the skin until it sticks and hardens Lesions are round to oval in shape and can vary in color from flesh-colored to yellow, tan, brown and black May resemble an intradermal nevus |
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Histologic features:
Seborrheic keratosis |
hyperkeratosis
acanthosis papillomatosis melanocytic hyperplasia **>>horn cysts<<** |
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What Is Etiology of SK?
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The pathogenesis is unknown
We can tell patients that it’s caused by wisdom, because young people who have not yet acquired wisdom don’t get seborrheic keratoses |
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What Other Skin Lesions Are in the Differential?
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Early lesions may be confused with:
pigmented actinic keratosis lentigos warts nevi Larger lesions are mistaken for: pigmented BCC melanoma squamous cell carcinoma warts |
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Case history:
A 15-year-old presents with a hyperkeratotic, rough-surfaced, wart-like growth on his ring finger Clinical Features: Verruca Vulgaris? |
The common wart (verruca vulgaris) is due to infection with human papilloma virus, types 1, 2, 4 and 7
Warts can be classified based on clinical presentation, histologic classification or based on the type of HPV virus The typical lesion presents as a solitary, small papule, usually less than 1 cm in diameter with a hyperkeratotic surface - may be multiple Warts are more common in school age children and decrease in incidence after the age of 25 The hands, fingers and knees are common sites of involvement |
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What viruse is repsonsible for Verruca Vulgaris (warts)?
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human papilloma virus, types 1, 2, 4 and 7
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Gross features: Verruca
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Most are small, well circumscribed, skin-colored or pink papules
Reddish-brown to black dots on the surface, due to thrombosed capillaries, are a characteristic feature |
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Histologic features:
Verruca |
Hyperkeratosis, acanthosis, papillomatosis and elongation of the rete ridges which curve inward at the margins of the lesion
Foci of vacuolated cells, clumped keratohyalin granules and vertical tiers of parakeratotic cells |
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What's Verruca's relationship to SCC?
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Can mimic verruca, and warts may resemble squamous cell carcinoma
The age of the patient and the location of the lesion helps to differentiate between these two entities |
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What are some population types affected by Verruca?
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Large or extensive numbers can be seen in immuno-compromised states such as in HIV infection or in organ transplant patients on immunosuppressive drug therapy
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