jdlevenson's version from 2015-06-19 21:02


Question Answer
REtinoids have what affect on acneInhibits follicular epidermal keratinization, loosing keratin plugs of comedones and facilitating their expulsion. And reduces size of sebaceous galnds and inhibits sebum production.
Isotretinoin for severe acne refractory to topical therapies; toxicityHypertriglyceridemia and teratogenicity
Terbinafine mechanismInhibits synthesis of fungal membrane ergosterol by suppressing enzyme SQUALENE EPOXIDASE. Used in treatment of tinea corporis, and other dermatophytes.
PABA esters absorb what kind of lightOnly UVB. UVB radiation is the major cause of UV radiation burns (sunburn), skin damage, photo-aging and photo carcinogenesis by producing reactive oxygen species that damage skin components and cellular DNA. Zinc oxide containing sunscreens have additional UVA wavelength protection.
Atopic eczematous dermatitis histologyIntraepidermal vesicles, superficial epidermal hyperkeratosis producing scales, epidermal hyperplasia/ acanthosis, and or chronic inflammatory infiltrate within the dermis
Dermatitis cured by corticosteroids; however, consequences (histologically)Decreased production of ECM collagen and glycosaminoglycans -> atrophy of dermis with loss of dermal collagen, drying, cracking and or tightening of skin. Sometimes even telangiectasisas, eccymoses, atrophic striae. Sometimes also atrophy of subcutaneous tissues such as adipocytes.
Flexor erythema, papules, vesiscles...Eczema. Extendor – psoriasis.
Eczema, pruritis, erythematous weeping/crusted papules and plaques (that may evolve into thickened scaly plaques) in response to certain environmental antigens or foods** and is a/wAllergic rhinitis and asthma. Eczema thought to be from impairment of skin’s barrier function leading to immunologic exposure to environmental allergens and microbial antigens .
Lichenification in neck, wrists, antecubital fossae...Eczema in older children.
Eczema dx cannot be made withoutINTENSE PRURITUS.
Allergic triadAtopic dermatitis/ eczema; allergic rhinitis and asthma. Usually accompanied by high serum levels of IgE, peripheral eosinophilia, and high levels of cAMP PDE in leukocytes.
Dermatitis 5 typesAllergic contact dermatitis, atopic dermatitis, drug-related eczematous dermatitis, photo-eczematous dermatitis and primary irritant dermatitis
Primary histologic finding in patients with eczematous dermatitisSpongiosis**
Vitiligo basic defPartial or complete loss of epidermal melanocytes and thus complete absence of melanin pigment. 2nd or 3rd decade of life usually but varies. Faces, extremities, axillae, umbilicus, groin, genitalia, hard bony surfaces... Flat macules or patches of absent pigment.
Vitiligo often seen in patients who2nd or 3rd decade and who have variety of other autoimmune disorders – DM1, pernicious anemia, Addison disease, autoimmune hepatitis...
AlbinismMelanocytes that do not produce melanin because of absent or defective tyrosinase.
Café au lait spotsIncreased melanosome aggregates within melanocyte cytoplasm.
Café au lait spots seen inMcCune-Albright syndrome (mutation affecting G-protein signaling; unilateral café au lait spots, polyostotic fibrous dysplasia, precocious puberty, multiple endocrine abnormalities; lethal if happens early but survivable in patients with mosaicism); NF1.
Lentigo vs Nevus vs FreckelsLentigo – hyperplasia of melanocytes which is linear in spread; Nevus – nests of multi-layered melanocytes; Freckels/ ephelis – normal number of melanocytes but increased amount of melanin
Lentigo presentationSun-exposed skin of middle aged or elderly person
Eccymosis vs PurpuraBoth extravasated RBC into skin or subcutaneous tissue that do not blanch since not within the vasculature; petechiae - <5 mm (asymptomatic, not palpable, areas of increased venous pressure); purpursa – 5 mm - <1cm; ecchymosis >1 cm. Eccymoses/ bruises arise from trauma or incomplete hemostasis and also may arise without history of noticeable trauma.
Telangiectasias, blanch or not? Permanent or not?Permanent and YES blanching dilatations of superficial capillaries and venules. Usually in skin or mucous membranes.
Nikolsky skin (new bullae from with gentle traction) positive inPVulgaris (AB against desmosomes, namely desmogleins 3 and 1). Also have Asboe-Hansen sign which is bullae spreading laterally with pressure.
Autoantibodies against desmosomes?Pemphigus vulgaris.
Antibodies against hemidesmosomesBullous pemphigoid. Bullae remain intact and mucosal involvement is uncommon. Itchy. Elderly. Fluid filled, tense, usually 2 cm in diameter. Most common in inner thighs, flexor forearms, axillae, groin...AB result in complement fixation and recruit neutrophils and eosinophils that can cause tissue injury.
Lichen Planus 5 p’sPolygonal, planar, pruritic, purplish plaques on wrist hands trunk legs with finely reticulated scale – wickham’s striae
Epidermolysis bullosa acquisita and cicatricial pemphigoid have autoantibodies againstBM of skin.
Pemphigus vulgaris most common in what locationOral mucosa.
Hyperparakeratosis, acanthosis, elongation of rete ridges, mitotic activity above epidermal basal cell layer ,reduced or absent stratum granulosumPsoriasis
Sharply demarcated salmon-colored round plaques covered with loosely adherent silvery scalePsoriasis
Psoriasis most commonly atElbows, knees, gluteal cleft, lumbrosacral area, glands penis, scalp.
Psoriasis is also frequently associated with (non skin complication)Psoriatic arthritis.
Urticaria/ hives (IgE or not Ige but def mast cell degranulation) is characterized bySuperficial dermal edema and lymphatic channel dilation with excess transudae; not epidermal changes
Spongiosis isIntercellular epidermal edema
Acantholyiss ( loss of cohesion between keratinocytes) a/wSpongiotic dermatitis.
DyskeratosisAbnormal premature keratinization of individual keratinocyts; a/w SCC
Psoriasis pathogenesisCD4+ T cells -> CD8+ after interacting with APC of skin -> production of cytokines, GFs, keratinocytes proliferation, inflammation and angiogenesis.
Erythema nodosum – painful reddish nodules on shins in response toOCPs, strep pharyngitis, IBD, sarcoidosis.
Erythema multiformeAcute onset of spectrum of lesions that are on libms and extremities and especially palms. HSV is most common cause. May be recurrent and are common in children and young adults. Also a/w mycoplasma, sulfa trugs, b-lactams, phenytoin, cancers, autoimmune diseases.
Molluscum contagiosum, white umbillicated papules on penis, vulva or groin caused byPoxvirusf
VelvetyAcanthosis nigrans; hyperkeratotic, hyperpigmented plaques with or without skin tags (pedunculated outgrowths). Most often axillae, posterior neck, groin but also soles, oral mucosa, etc.
AcanthosisIncrease in thickness of stratum spinosum/ prickle cell layer (between granular and basal layer)
Benign Acanthosis nigransInsulin resistance. Insulin aind insulin like growth factors stimulate epidermal and dermal proliferation.
Malignant Acanthosis nigransUnderlying neoplasms – GI and GU especially gastric adenocarcinoma.
Small scaly erythematous lesions with a sandpaper texture on sun-exposed areas; ‘erythematous plaques with overlying whitish scale’Actinic keratosis (AK)
Lesions that are ‘felt more than seen’ with sandpaper-like textureAK.
Hyperkeratosis (HP of corneum), parakeratosis, atypical keratinocytes** with pleiomorphic nuclei and multiple mitosesActinic keratoses; may also be pigment irregularities, dilated blood vessels too and may enlarge and become elevated and form cutaneous horns that are real gross.
AKs in what age group40-60 under influence of excessive sun exposure
AKs do or do not invade dermisDo NOT invade dermis. Premalignant lesions. Recall, seborrheic keratosis is benign, not premalignant. AKs can transform into invasive squamous cell carcinoma, a change reflected by increase in lesion size and thickness, dermal invasion and metastatic potential. Rarely to BSS.
Stuck on papules in elderly individualsSeborrheic Keratoses. Deeply pigmented or flesh colored lesions. Granular or velvety quality.
Most common skin cancerBasal cell carcinoma. Sun exposed areas and low tendency to metastasize unlike melanoma. So usually head nd neck.
Melanoma, key risk factorUV radiation. Solar and tanning bed UV sources.
Melanoma pathogenesisSunlight + hereditary factors + history of pre-existent dysplastic nevus in same location; light skinned > dark skinned
Melanoma, what key geneBRAF; activating mutation; BRAF -> MEK -> ERK -> Cyclin D1 -> growth and survival.
What drugs can treat melanoma BRAF pathwaysTYR K inhibitors such as imatinib, nilotinib, and dasatinib. Also Vemurafenib too which is a potent inhibitor of mutated BRAF.
How many cases of melanoma a/w BRAF40-60%
Melanoma, most important prognostic factorDepth of invasion/ breslow thickness. Prominent cellular atypia is not considered important risk factor; dense lymphocytic infiltrate is actually thought to improve prognosis.
Dermatitis herpetiformis, IgA and IgG against gliadin also againstBM of epidermis. Leads to microbscesses containing fibrin and neutrophils at dermal papillae tips.
Pearly papules with central depression or ulcerationBSS. Nests of basaloid cells and peripheral palisading of nuclei.
DermatofibromasSueprficial benign fibrous histiocyotomas; benign proliferation of fibroblasts; lower extremities as solitary nodules.
GlomangiomaRed bluish very tender and small neoplasm frequently under nail bed
Glomus body functionThermoregulation – shunt blood away in cold and vice versa, heat to skin surface in hot temperatures to facilitate dissipation of heat. Found in nail bed, pads of fingers and toes and ears. Composed of afferent arteriole connected to richly innervated muscular arteriovenous anastomaosis and then efferent vein. Modified smooth muscle** cells.
Solitary pink or brown scaly plaque with central clearing on trunk, neck or extremities (herald patch) followed by ovoid maculopapular rash with lesions oriented in an oblique pattern along skin tension linesPityriasis rosea
Christmas tree patternPityriasis rosea
Multiple firm violaceous nodules on arm post radical mastectomy with chronic lymphedema (12 years)Stewart-Treves syndrome, refers to chronic lymphedema being risk factor for development of cutaneous angiosarcoma; cutaneous angiosarcoma**/ lymphangiosarcoma. Poor prognosis. Histology -> infiltration of dermis with slit-like abnormal vascular spaces.
Soft rubbery asympatomic cutaneous nodules in 2nd or 3rd decade of lifeNeurofibromas.
Why are burn victims at riskLoss of barrier function of skin; post-burn immune dysfunction; lack of blood flow to necrotic areas
Burn patients, after pseudomonas, thinkStaph aureus and enterococcus
Hemangiomas/ Cavernous hemangiomas
Question Answer
Strawberry vs Cherry hemangiomas, which one in elderlyCherry. Dilated capillaries and post-capillary venules in papillary dermis and do not regress spontaneously.
Strawberry hemangiomas is also known asSuperficial hemangioma; bright red if near surface and more purple if deeper
Spider angiomas common inPregnancy, liver disease and OCP/ estrogen supplements. Dilated cutaneous arterioles that present as central papule with radiating blanching capillaries.
Cavernous hemangiomas vs strawberryCavernous – soft blue compressible masses vs Strawberry – more superficial
Cystic hygromaLymphatic cysts lined by thin epithelium; present at birth and most commonly located on posterior neck and lateral chest wall; Turner and Downs syndrome. CAN BE REALLY BIG.
Cherry Hemangiomas what age3rd and 4th decade of life; most common benign vascular tumors in adults
Yellowish eyelid papule or plaque containing lipid laden macrophagesThink xanthelasma, a form of xanthoma which are from primary or secondary hyperlipidemia (secondary could be in case of obstructive biliary lesions and PBC)
How are xanthelasmas correctedCorrection of underlying lipid defects can lead to slow resolution of these lesions
Thinning hair, pretibial myxedema, alopecia areataHypothyroidism
Keloids present asSoft or firm nodules that grow beyond borders of wounds with claw like extensions into normal tissue. Large disorganized collagen bundles and excess cellular connective tissue.
Keloids form in which kind of woundsAll wounds. Sometimes in absence of wounding!
Wound healing – inflammatory (first 24 hrs neutrophils, 2-3 days macrophages to damaged area and phagocytosis); proliferative (3-5 days later; fibroblasts and endothelial vasc cells proliferate/ neovascularization; granulation tissue that looks pink friable edematous); maturation (fibrosis, 2nd week after injury; active fibroblasts synth collagen, elastin.....6-8 weeks – initial scar formation is complete; 30-40% of tensile strength)
Question Answer
Keloids vs hypertrophic scarsHypertrophic scars – limited to area of the wound and may regress spontaneously; parallel arrangement of CT of fibroblasts, myofibroblasts and collagen vs Keloids - Excess collagen formation; beyond borders of original wound; do not regress; recur after resection; disorganized arrangement of CT of fibroblasts etc.
Tender erythematous brown or purple papule, nodule or plaque after suture placementGranuloma