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Flashcards in Dermatology Deck (134)
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Tinea versicolor

Caused by Malasseziafurfur
- Well-demarcated hypo/hyperpigmented patches on skin

Treat: topical antifungals


Tinea corporis/captis/pedis

T. rubrum, T. Metagrophytes, M. Canis, T. tonsurans
- Annular lesions with peripheral scale

Diagnosis: KOH stain

Treatment: topical antifungals

Mimicker: seborrheic dermatitis
- More common in adults than tinea
- Pityrosporum ovale
- Greasy scale over erythematous plaques (sebaceous areas)
- More common in patients with neurologic disease
- Treatment: topical antifungals


Majocchi's granuloma

Dermatophyte invades and ruptures hair follicle

Mimicker: nummular dermatitis
- Commonly found on extremities
- round, erythematous plaques with scale
- Spongiotic dermatitis
- Treat with topical steroids


Deep fungal infections

Subcutaneous mycoses: chromoblastomycosis
- Caused by Fonasacea pedrosoi

- Verrucous plaques, nodules
- Diagnosis: sclerotic bodies on H&E

Treatment: oral antifungals


Atypical mycobacteria

M. fortuitum, M. chelonei, M. Abscessus
- Infections linked to surgical procedures and nail salon baths

Treatment: debridement, combination antibiotics


Norwegian (crusted) scabies

Immune-compromised, debilitated patients
HUGE mite load
- Hyperkeratotic lesions

BOTH topical or oral therapy needed


Skin conditions involving subcorneal split

1. Impetigo: staph, s. pyogenes
2. Bullous impetigo: staph exfoliative toxin
3. Staph "scalded skin" syndrome: no bacteria in skin samples

1. Pemphigus foliceous: auto-antibodies to desmoglein 1 (cell adhesion complex)
2. Toxic epidermal necrolysis: necrosis of epidermis (deeper splitting)



Epstein Barr virus
Can cause morbiliform eruption
7-10 days after amoxicillin/ampicillin treatment


Epidemiology of basal cell carcinoma

Most common malignant neoplasm in humans
Most common form of skin cancer, and now most common form of cancer in United States
Rarely metastasizes, but can be locally destructive
Associated with long term chronic UV exposure
75% of non-melanoma skin cancers
99% in Caucasians
Majority in patients 40 years and older but not uncommon in 20-40 year olds
85% on head, neck, and trunk


Etiology of Basal cell carcinoma

Pigmentary phenotype-Fitzpatrick I-II
Ultraviolet light exposure- intense episodic
Radiation exposure
Pre-existing skin lesions
- nevus sebaceous
Genetic Syndromes
- Basal cell nevus syndrome
- Xeroderma pigmentosa


Clinical features of basal cell carcinoma

- Smooth translucent, pearly papule, overlying telangiectasia +/- ulceration, pigmentation

- More plaque like with less defined borders

- Erythematous or atrophic macule with raised peripheral borders

- Scar like plaque with ill defined borders


Basal cell nevus syndrome

Range of clinical findings include:
- Numerous BCCs (photodistribution),
- palmar pitting,
- hypertelorism,
- ondontogenic cysts,
- bifid ribs,
- brachymetacarpalism,
- calcification of falx cerebri,
- partial agenesis of corpus callosum,
- ovarian fibromas,
- medulloblastoma

- Transmission sporadic or autosomal dominant
- Chromosomal defect 9q p22


Treatment of basal cell carcinoma

1. Conventional (3-4mm margins)- vertical sections
2. Mohs micrographic surgery- sectioned vertically and horizontally:

Destruction- ED&C, Cryotherapy

- Topical imiquimod (Aldara™)

- elderly, poor operative candidates, or palliation


Indications for Mohs micrographic surgery (MMS)

- Recurrent BCC
- Ill defined borders
- Cosmetically important area/Tissue sparing
- Size > 2.0cm
- Increased risk of recurrence: Location on nose, ears; infiltrating or micronodular histology

- Excision of tumor as complete block
- Horizontal embedding technique
- Peripheral and deep margins embedded on same horizontal plane
- 100% margin evaluation
- Intraoperative histologic evaluation and mapping of residual tumor
- Additional tissue layers taken selectively until negative margins
- Allows for immediate reconstruction


Squamous cell carcinoma: epidemiology

- 20% of non melanoma skin cancers
- Uncommon but not rare in non Caucasians
- Male:Female ratio= 3:1
- Increased incidence with increasing age >40
- Occurs on areas of chronic sun exposure: Head, neck, dorsal hands


Squamous cell carcinoma: etiology

Pigmentary phenotype- Fitzpatrick I, II
Ultraviolet Radiation- chronic
recreational, therapeutic, PUVA
Chemical carcinogens
Chronic ulceration or scar (Marjolins ulcer)
Immunosuppression (transplant- heart 65x increased risk)
Genodermatoses (XP, EDV)


Actinic keratoses

AK is precursor to SCC
- Clinically erythematous scaling macule or papule on sun damaged skin
- Can regress, remain stable, or progress to SCC

Malignant conversion rate ~ 1/200 or 1/1000 per year
- 10% risk of SCC in 10 years with 10 AKs

Treatment : liquid nitrogen, topical 5FU, imiquimod (Aldara™)


SCC- clinical features

SCC in situ (Bowen’s)
- erythematous scaling macule

SCC- invasive
- Erythematous nodule or eroded plaque

SCC/KA type (keratoacanthoma)
- Rapidly growing nodule with central keratin plug

Verrucous carcinoma

Erythoplasia of Queyrat-
- moist red plaque on genitalia


SCC- indications for MMS

High risk for recurrence, metastasis

Perineural involvement (must check patient for palsies, pain, etc)
- spreads along cleavage plane between nerve and sheath (seen in 2-14% of all SCC, 1% of BCC)

Invasion into bone



UVR exposure and skin cancer

Skin Cancer (SCC)
- Peak effect at 300nm (UVB) in mice
- Elastosis
- Irregular pigmentation
- Telangiectasia
- Peak effect at 340nm (UVA)

1. DNA Damage
- Pyrimidine dimer formation
- Activation of oncogenes or inactivation of tumor suppression genes
- Damage to two alleles leads to neoplasia
2. Immunologic Suppression
- Decreased immune surveillance by down regulation of Langerhans cells
- Altered cytokine production


Basal cell nevus syndrome and hedgehog pathway:

Candidate gene for BCNS localized to chromosome 9q22.3
- PTC - putative tumor suppressor gene
- Two hit hypothesis:
1. BCNS associated with inherited mutations in one allele
2. UVR produces additional defective allele leading to neoplasia

The "patched" gene=
- Tumor suppressor gene that encodes a transmembrane protein in ‘Hedgehog’ signaling pathway
- regulates cellular proliferation and organ development during embryogenesis
- Implicated in the development of sporadic BCC and other tumors: lung, prostate, pancreatic, gastric, hepatocellular, neural

1. Cyclopamine (inhibits HH pathway)
- Steroid alkaloid and teratogen
- Foundin Rocky Mtn wildflower= Veratrum californicum
2. Vismodegib: FDA-approved BCC tx


p53 and skin cancer

Tumor suppressor gene on chromosome 17p13.1
- Mutations found in 50% of human cancers including skin cancer

Transcription factor for genes controlling apoptosis
- Loss of suppressor functions can lead to neoplastic proliferation

Mutations in skin cancers are pyrimidine dimers c/w UV induction
- Mutations in 60% of AKs, 90% of SCC, 50% of BCC
- P53 mutations prevent apoptosis of UV damaged cells
- Additional UVB can lead to clonal expansion, carcinogenesis


Xeroderma pigmentosa

Rare AR genodermatoses

Defective DNA endonuclease
- Inability to perform normal DNA excision repair

Clinical features:
- Severe actinic damage, early onset cutaneous neoplasia
- Cataracts, photophobia, keratitis
- May be associated with neurologic impairment (De Sanctis-Cachione syndrome)


Characteristics of UVA/UVB

- Penetrates into epidermis/dermis
- Not filtered by glass
- Leads to dermal collagen damage
- Seen throughout day, all year

- Absorbed in epidermis
- Erythema of sunburn
- Seen in late spring, summer, autumn, midday

- Cause photo aging
- Skin cancer (more UVB)


MED= minimal erythemal dose

Minimal erythemal dose
- Smallest dose of UV radiation that can induce sunburn
- Not necessarily correlated with skin type

Ex: Burn after 1 minute of sun exposure
- SPF 30= 30 minutes to get burned from sun exposure


Pruritic disorders: skin changes

Follicular accentuation
Post-inflammatory pigmentary alteration
Picker's nodules/ Prurigo nodularis


Differential diagnosis of pruritis

Primary: skin diseases:
- Xerosis (dry skin, eczema craquele, senescence)
- Scabies
- Urticaria (comes and goes rapidly)
- Dermatitis herpetiformis
- Urticarial stage of bullous pemphigoid
- Contact dermatitis

- Medication-induced pruritis

Secondary: Systemic disease
- Chronic renal disease
- Liver disease (cholestasis)
- Iron deficiency
- Polycythemia vera
- Thyroid disease
- Parasitic infestation
- Lymphoma
- Diabetes


Treatment of pruritis

No effective specific antipruritic drugs:
- Topical agents (corticosteroid, phenol, menthol, opioid)
- Oral antihistamines
- Systemic corticosteroids
- UVB radiation


Venous insufficiency

Incompetent one-way bicuspid valves in veins of legs prevent backflow--> chronic inflammation, fibrosis, etc.
- With aging, valves compromised (incompetent)--> dilated veins

Seen in 6-7% population > 50 years:
- Superficial veins (most common): saphenous veins, tributaries
- Deep veins: anterior and posterior tibial, peroneal, popliteal, deep femoral, superficial femoral, iliac veins
- Perforating veins

- Congenital, abnormal valves
- Age-related
- Trauma (injury, vein stripping)
- Venous thrombosis

- Throbbing, burning, aching, heaviness, restless legs, leg fatigue

Clinical manifestations:
- Spider veins
- Varicose veins
- Stasis dermatitis (often confused with bilateral cellulitis)
- Acroangiodermatitis of Mali (tumor-like veins)
- Stasis ulcers
- Lipodermatosclerosis (loss of hair, shiny scar-like skin)

- Compression
- Sclerotherapy
- Vein stripping with ligation
- Valvuloplasty


Toxic epidermal necrolysis

TEN= acute widespread blistering eruption caused by drugs

- Antibiotics (bactrum, sulfonamides, ampicillin)
- Anticonvulsants (phenytoin)
- Allopurionol

- Eruption preceded by morbilliform, generalized erythema
- Nikolsky sign (blister expands with physical manipulation)
- Mucositis
- Diff diagnosis: staph scalded skin

- Supportive care (similar to burn pt: fever, hyperthermia, hypotension due to volume losses, tachycardia, pneumonia, sepsis)
- Corticosteroids (only if early)
- High dose IVIG

Mortality= 25-50%