Skin Flashcards
Sx of bullous pemphigoid
Blisters of the skin most commonly in extremities (Negative Nikolsky sign); oral mucosa is spared (vs. Pemphigus vulgaris)
Etiology of bacterial skin abscess
Almost always staph
___lesions are characterized by central, ulcerated crater surrounded by telangiectatic (dilated) vessels
Basal cell carcnioima (“pink-pearl-like”)
Superficial skin infection not associated w/ systemic sx
Impetigo
Histology of pemphigus vulgaris
1) Acantholysis of stratum spinosum keratinocytes
2) “Tombstone” appearance- due to basal layer cells that remain attached to BM via hemidesmosomes
Mutation that drives dysplastic nevi/ melanonva
BRAF kinase, which results in loss of CDK inhibitor
Another type of lesion (besides skin) found in pemphigus vulgaris
Oral mucosal bullae (blisters)
Present as pigmented raised lesion w/ central darker shade
Dysplastic nevi
Melasma and risk factors
Hyperpigmentation of cheeks (can be elsewhere); risk factors include pregnancy (“mask of pregnancy”) and OCP use
Presented as pigmented raised lesion w/ central darker shade
Dysplastic nevus
_________: condition characterized by auto IgG antibodys against hemidesmosome components, particularly _________
Bullous pemphigoid; BP180
Histology of psoriasis (3)
1) Acanthosis w/ elongation of rete ridges + dermal papillae
2) Parakeratosis
3) Munro microabscesses
Signs + sx of SJS/TEN
Fever, bullae/ skin necrosis, sloughing of skin, involvement of mucous membrane (lip/ oral mucosa)
__________is the most important prognostic factor in predicting metastasis of melanoma, not the size
Breslow thickness
Two growth phases of melanoma and main difference
1) Radial growth- melanocytes grow horizontally along DE junction; lack metastasizing ability
2) Vertical growth- melanocytes grow vertically into dermis- tumor gains metastatic potential
Premalignant lesoin to squamous cell carcinoma
Actinic keratoses; many lesions show dysplastic changes; risk of SCC proportional to degree of epithelail dysplasia
Condition in which there is IgA deposition at the tips of dermal papillae
Dermatitis herpetiformis
Presentation of actinic keratosis
Small, rough + scaly (“sand-paper like”), red or brownish papules or plaques
Disease associated w/ dermatitis herpetiformis
Celiac
Risk factor of development of basal cell carcinoma
UVB induced damage- sunlight, albinims, xeroderma pigmentosum
Diseases associated w/ positive Nikolsky sign
1) Pemphigus vulgaris
2) Scalded skin syndrome
Infection associated w/ Lichens Planus
Chronic hep C
How is scalded skin syndrome + TEN/SJS distinguished from each other?
Level of skin separation using histology- separation in SJS/TEN occurs between dermal-epidermal junction (Hemidesmosomes), while scalded skin syndrome involves stratum granulosum w/ spinosum
Presentation of melanoma
Mole-like growth w/ ABCDE
Asymmetry, borders irregular, color not uniform, diameter > 6 cm, evolution over time
What embryological tissue derives melanocytes
Neural crest
Bacterial infection that involves epidermis, deeper dermis, subcutaneous fat
Cellulitis
Presentation of intradermal nevi vs. junctional nevi
Intradermal nevi- papules
Junctional nevi- flat macules
Causes of impetigo
S aureus, S pyogenes
Rosacea
Inflammatory skin disorder characterized by eryhtematous papules + pustuels but no comedones; occurs in ages 30-50 (vs. acne vulgaris)
Well-defined, slightly raised eryhthematous, shiny lesion
Erysipelas
Xeroderma pigmentosum
Autosomal recessive defect in enzymes necessary for nucleotide excision repair (sunlight can induce formation of pyrimidine dimers, which are normally excised by DNA repair). Increased risk for all 3 types of skin CA
Location of melanin synthesis and precursor molecule involved
Melanocytes synthesize melanin in melanosomes, using tyrosine (tyrisinase) as precursor molecule.