dermatology study guide Flashcards
scabies differential diagnosis
contact dermatitis, asteatotic dermatitis, insect bites, animal scabies, seborrheic dermatitis, psoriasis
scabies clinical presentation
variable. Itching which is worse at night
Classic burrow present less than 20% of the time: essential lesion is a small, erythematous, nondescript papule, often excoriated and tipped with hemorrhagic crusts. Burrows are often absent or obscured by excoriation or secondary infection. Miniature wheals, vesicles, pustules, and rarely bullae may also be present.
scabies risk factors
transmitted person to person by direct contact, in young adults, mode of transmission is often sexual contact. Transmission through clothes uncommon, more likely with higher parasite burdens as seen in crusted (Norwegian) scabies. Animals can get scabies but those mites are different and rarely reproduce on human skin. cross infection is unlikely unless the animal is untreated
Scabies diagnostics
” scabies prep” : a drop of mineral oil is placed on a burrow, and the lesion is scraped with a no.15 blade. the sample is viewed under a microscope and examined for mites, eggs or feces. There are usually only a few scabies mites on a infected patient, the majority found on hands and wrists
Scabies TX
topical application of 5% permethrin cream is tx of choice. Cream should be applied from the neck down, giving attention to the interdigtial webs, axillae, umbilicus, gluteal cleft, genitals, areas under the nails, and soles of feet.
in older adults, scabies can infest hairline - cream massaged head to toe.
medication left on 8 - 12 hours and then washed off. Repeat tx in 1 week.
Lubrication and topical corticosteroids are sued to treat any resulting inflammation and pruritus. Antibiotics should be given for infections secondary to scratching.
Actinic Keratosis differential diagnosis
actinic keratoses, basal cell carcinoma, squamous cell carcinoma, malignant melanoma, dysplastic nevi
Actinic Keratosis risk factors
advanced age ( older than 50)
median age of 40 yrs for malignant melanoma
exposure to UV light
fair complexion ( blond or red hair, blue, green or gray eyes)
smokers
skin damaged by burns and/or chronic inflammation
hx of blistering sunburns before 18 years of age increases risk
Actinic Keratosis clinical presentation
persistent or recurrent reddened and roughened area that scales or crusts
Actinic Keratosis diagnostics
biopsy suspicious lesions
shave or punch biopsy
Actinic Keratosis treatment
Liquid nitrogen by a freeze - thaw technique to obtain a 1 to 3 mm rim of freeze, which allows appropriately slow thawing during 20 to 40 sec.
Seborrheic dermatitis differential diagnosis
Psoriasis(main condition in the differential diagnosis of seborrheic dermatiti), atopic dermatitis, rosacea, tinea versicolor, pityriasis rosea, tinea corporis, secondary syphilis, systemic lupus erythematosus (SLE), and pemphigus foliaceous
Seborrheic dermatitis risk factors
possible familial trend, possible link between infantile and adult forms, high association with HIV- infected individuals
Seborrheic dermatitis clinical presentation
Seborrheic dermatitis is a chronic, relapsing, and usually mild form of dermatitis that occurs in infants and in adults. oily, flaky skin on erythemic base around ears, nose, eyebrows and eyelids. red cracking skin in body folds - distribution area in adults: scalp, eyebrows, paranasal area, nasolabial fold, chin, behind ears, chest and groin
Seborrheic dermatitis diagnostics
no diagnostic test, may consider possible skin biopsy to rule out other conditions if suspicious
Seborrheic dermatitis tx
shampoo is the foundation of tx: baby shampoo or medicated shampoo such as salicylic acid shampoo, coal tar, ketoconazole 2%. If shampoo alone fails, topical steroid lotion in combo with shampoo for 2 -3 weeks of tx. For face/groin: low potency agents such as hydrocortisone 1% cream
Impetigo differential diagnosis
contact dermatitis, tinea infection, eczema, varicella, bullous insect bites, mycobaterial fungal infections,
Impetigo risk factors
can develop if bacteria get into healthy skin or into minor cuts, scrapes, or any other small openings (such as those caused by bug bites). The infection usually occurs in warm, humid conditions and is easily spread among people in close contact
The best way to keep from spreading or catching impetigo is to wash your hands often with soap and water. When washing is not possible, use alcohol-based hand rubs. It’s also a good idea to clean the surfaces in your home with a household cleaner.
Impetigo clinical presentation
Non-bullous impetigo is the most common form of impetigo. Lesions begin as papules that progress to vesicles surrounded by erythema. Subsequently they become pustules that enlarge and rapidly break down to form thick, adherent crusts with a characteristic golden appearance; this evolution usually occurs over about one week. Lesions usually involve the face and extremities. Multiple lesions may develop but tend to remain well localized. Regional lymphadenitis may occur, although systemic symptoms are usually absent.
Bullous impetigo is a form of impetigo seen primarily in young children in which the vesicles enlarge to form flaccid bullae with clear yellow fluid, which later becomes darker and more turbid; ruptured bullae leave a thin brown crust – in an adult should prompt investigation about HIV
Ecthyma is an ulcerative form of impetigo in which the lesions extend through the epidermis and deep into the dermis. They consist of “punched-out” ulcers covered with yellow crust surrounded by raised violaceous margins
Impetigo diagnostics
The diagnosis of impetigo often can be made on the basis of clinical manifestations. The key clinical findings of non-bullous impetigo, bullous impetigo, and ecthyma include:
●Non-bullous impetigo – Papules, vesicles, and pustules that rapidly break down to form golden adherent crusts; often located on the face or extremities
●Bullous impetigo – Flaccid, fluid-filled bullae that rupture and leave a thin brown crust; often located on the trunk
●Ecthyma – “Punched-out” ulcers with overlying crusts and raised violaceous borders
Impetigo treatment
Bullous and non-bullous impetigo can be treated with either topical or oral therapy. Topical therapy is used for patients with limited skin involvement, whereas oral therapy is recommended for patients with numerous lesions
Mupirocin and retapamulin are probably equally effective topical therapies. Mupirocin is applied three times daily and retapamulin is applied twice daily. The recommended length of treatment is five days
Oral therapy should be administered to patients with numerous impetigo lesions or ecthyma. Dicloxacillin and cephalexin are appropriate treatments because S. aureus isolates from impetigo and ecthyma are usually susceptible to methicillin. A seven day course of antibiotics is recommended.
Stevens - Johnson syndrome
a severe, life -threatening systemic reaction with fever, malaise, cough, sore throat, chest pain, vomiting, diarrhea, myalgia, arthralgia and sever skin manifestations with painful bullous lesions on mucous membrances
Dermatophytoses: tinea capitus; tinea coporis; tinea pedis
dermatophytes are the most common fungi that invade the skin and nails, proliferate within the nonviable keratinized tissues.
capitus: head/scalp
coporis: body
cruris: jock itch
pedis: athletes foot
manus: hand
unguium: nail
Dermatophytoses differential diagnosis
atopic dermatitis; figurate erythemas; granulomatous dermatoses; papulosquamous eruptions; psoriasis; skin cancer; uticaria; alopecia areata; impetigo; pediulosis; erythema multiforme; cutaneous lupus erythematous; secondary syphilis; contact dermatitis; dyshidrosis
Dermatophytoses risk factors
usually acquired through inhalation of endemic fungi in the environment, also transmitted through close contact with infected people or animals. tinea corpis is the second most common infection passed from dogs and cats to humans.
Dermatophytoses clinical presentation
characterized and named by thier location. start out as patchy, scaly areas, erythemtous plaques and papules(ringworm of the body in circular formation), intergitial scaling, maceration and fissuring.
depending on the oranism, the lesions may become inflamed, boggy and pustular
Dermatophytoses diagnostics
KOH microscopy preparation is valuable and cost effective: provides rapid confirmation of many types of fungal infections. An adequate specimen is obtained by scraping the active, leading border of the infection. Under the microscope, look for the diagnostic branching appearance typically seen with these organisms, a positive result.
other lab tests include: skin culture on sabourauds medium
woods lamp examination
skin or nail biopsy
Dermatophytoses TX
Most dermatophyte infections can be managed with topical treatments. For patients with limited tinea pedis, tinea corporis, or tinea cruris,treat with a topical antifungal drug with anti-dermatophyte activity rather than systemic therapy.
Examples of effective topical antifungal agents are azoles, allylamines, ciclopirox, butenafine, and tolnaftate. Oral antifungal therapy is used for extensive infections or infections refractory to topical therapy. eg; griseofulvin for 2 to 4 months
Nystatin is not effective for dermatophyte infections
Tinea versicolor differential diagnosis
pityriasis alba; pityriasis rosea; vitiligo; seborrheic dermatitis; secondary syphilis;
viral exanthem
Tinea versicolor risk factors
high heat and humidity - condition is more prevalent during the summer and in hot, humid regions.
Tinea versicolor is not related to poor hygiene.
hyperhidrosis, and the use of topical skin oils
Tinea versicolor clinical presentation
macules, patches, and thin plaques of tinea versicolor can be hypopigmented, hyperpigmented, or mildly erythematous
A fine scale is often present on affected skin
In adolescents and adults, tinea versicolor is most commonly found on the upper trunk and proximal upper extremities, and less often on the face and intertriginous areas. In contrast, when tinea versicolor occurs in children, it is likely to involve the face
mild pruritis
Tinea versicolor diagnostics
KOH preparation
skin cluture if indicated
Tinea versicolor TX
common antifungal creams such as imidazoles. oral antifungal agents can also be used.
Psoriasis differential diagnosis
lichen planus; lichen simplex chronicus; flat warts; pityriasis rosea; rheumatoid Arthritis; reactive arthritis; seborrheic dermatitis; atopic dermatitis; ; fungal infections; gout; pseudogout; syphilis; nummular eczema; SCC
Psoriasis risk factors
genetic factors; smoking; obesity; drugs (eg; beta blockers, lithium, etc..); infections; alcohol; vit D defeciency
the peak times for disease onset are ages 30 to 39 and ages 50 to 69 years
The scalp, extensor elbows, knees, and back are common locations for plaque psoriasis.
Psoriasis clinical presentation
thick, red plaques with sharply defined border and adherent silvery scale
Psoriasis occurs in a variety of clinical forms. The major clinical categories include:
●Chronic plaque psoriasis ●Guttate psoriasis ●Pustular psoriasis ●Erythrodermic psoriasis ●Inverse psoriasis ●Nail psoriasis
Psoriasis diagnostics
diagnosis usually based on presentation of silvery scales on red, erythematous plaques
biopsy useful in pustular disease
nail cultures useful to differentiate for fungal dx
Psoriasis TX
not curable
to treat symptoms a combination of therapies centered on topical tx can manage the disease:
moderate to high potency topical glucocorticosteroids applied two or three times per day over 2 to 3 weeks.
UV light
oral medications such as oral retinoids and methotrexate
biologic agents such as TNF antagonists
coal tar preparations
Onychomychosis differential diagnosis
psoriasis; eczema; trauma; lichen planus; onychogryposis; herpetic whilow; subungual malignant melanoma; PVD; pityriasis; medications; trophic changes; black nail paronychia; darier’s disease; endocrine disorders
Onychomychosis risk factors
risk factors include advanced age, swimming, tinea pedis, psoriasis, diabetes, immunodeficiency, genetic predisposition, and living with family members who have onychomycosis
Onychomychosis clinical manifestations
onychomycosis is any infection of the nails caused by a fungus. Tinea unguium is a dermatophyte infection of the nail plate, although the terms are often used interchangeably
Onychomychosis clinical manifestations
onychomycosis is any infection of the nails caused by a fungus. Tinea unguium is a dermatophyte infection of the nail plate, although the terms are often used interchangeably
Onychomycosis is marked by nail thickening, yellowish nail discoloration, onycholysis, and subungual debris. If left untreated, nail infections can lead to total nail dystrophy.
Paronychia (erythema and swelling surrounding the nail plate) may be an associated finding.
Onychomychosis diagnostics
KOH smear and culture
CBC and differential
LFTs
Onychomychosis TX
Treatment of onychomycosis is not mandatory in all patients. We suggest treating onychomycosis in:
●Patients with a history of cellulitis of the lower extremity, especially if repeated, who have ipsilateral toenail onychomycosis
●Patients with diabetes and toenail onychomycosis who have additional risk factors for cellulitis (ie, prior cellulitis, venous insufficiency, edema)
●Patients who are experiencing discomfort or pain associated with infected nails
●Immunosuppressed patients
●Patients who desire treatment for cosmetic reasons
Although 50% of nail dystrophies are due to onychomycosis, a patient should never be treated with systemic antifungal agents without confirmed infection based on direct microscopy, fungal culture, or histopathology. Systemic antifungal agents are costly and can have rare, undesirable side effects and toxicities.
Treatment options for onychomycosis include topical and systemic antifungal drugs, laser treatment, photodynamic therapy (PDT), and surgery. In addition, patients with symptomatic onychomycosis may benefit from measures to reduce discomfort regardless of whether they proceed with curative treatments.
The most effective therapy for onychomycosis is terbinafine 250 mg p.o. daily for a duration of 12 weeks for toenail infections and 6 weeks for fingernail infections. As a less expensive alternative regimen, pulse dosing of terbinafine can be used with only a slight decrease in efficacy (250 mg p.o. for 7 days, for 1 week per month for 3 months).
Topical urea is a keratolytic agent useful for removing hyperkeratotic nail debris in patients who forgo antifungal treatment (symptom relief)
Warts differential diagnosis
seborrheic keratosis; callus; lichen planus; SCC; molloscum contagiosum; amelanotic melanoma; foreign body
Warts risk factors
infection occurs when the virus comes in contact with skin that is broken or has been traumatized. The virus enters the hosts epidermal epithelial cells and uses the hosts resources to replicate. warts can occur singly or in groups and can coalesce to form plaques called mosaic warts. auto inoculation can come from cutaneous trauma, such as from shaving or scratching.
transmission is usually through direct skin contact. Genital infection is usually acquired through sexual contact. individuals with decreased cellular immunity are at risk for more recalcitrant HPV infection.
more common in kids and young adults
more common among certain occupations such as handlers of meat, poultry, and fish
Warts clinical manifestations
benign epidermal neoplasms caused by various forms of HPV virus
