niyezuva's version from 2017-10-13 18:25


Question Answer
Stratum corneum roleprotect from water loss, irritants.
Stratum granulosum roleimmune surveillance, make cornified layer
Stratum spinosum roleprotect from friction, trauma
Stratum basale rolegenerates other layers, produces pigment
Basal layer1 cell layer thick. Keratinocytes and melanocytes
Hemidesmosomesadhere BM + keratinocytes
Desmosomeskeratinocytes adhere with each other
Melanocytesmake melanin in melanosomes – transfer to keratinocytes
Spinous layerseveral layers thick. Keratinocytes making keratin. Resists friction. Langerhans cells present for immune surveillance.
Granular layermultiple layers thick. Entirely keratinocytes. 2 types of vesicles: keratinohyaline (aggregation and crosslinking) and lamellar (lipids)
Cornified layerdead keratinocytes and lipids
Basement membranetype IV collagen.
Dermistype 1 collagen. Strength and resistance to tearing. Elastic fibers, capillaries, nerves, lymphatics.
Anagenactively growing hair. Avg 1000 days
Catagenphase of transition. About 10 days
Telogenresting phase. Preparing to restart anagen. At the end, hair falls out.
Nail matrixrapidly proliferating cell that produce nail plate. At base of nail, includes lunula
Nail platehard plate of specialized keratin, no living cells.
Nail bedskin immediately under nail plate. Very vascular.
Eccrine glands 2 kinds of controlthermoregulatory (everywhere but palms), emotional (palms, axillae, forehead)
Aprocrine glandsin axillae, breasts, genital areas. Sweat increases with stress and anxiety. Depends on androgens.
Sebaceous glandsholocrine secretion – cells rupture and extrude contents into duct. Most active on face and scalp. Related to androgenic stimulation.
Tinea capitis epi, dxcommon, esp in African Americans. Dx with KOH, fungal culture.
Tinea capitis clinicallypatchy alopecia with erythema and scaling. Small black dots (hair broken off), diffuse dandruff. Kerion (indurated tender) forms due to severe inflammation. Glows under black light.
Tinea capitis etiologic agentTricophyton – human reservoir, Microsporum canis – dog reservoir
Tinea capitis treatmentoral griseofulvin. Or terbinafine, fluconazole, itracontazole. Antifungal shampoos decrease transmission.
Tinea crurischronic brown/red patches in groin folds. Trichophyton rubrum/mentagrophytes, Epidermophyton. Rare before puberty. Spares scrotum, penile shaft, glans penis. Treat with topical antifungals.
Tinea pedissame critters as tinea cruris. Moccasin distribution. Macerated fissures between toes. Small bullous blisters on sole. Topical antifungal.
Onychomycosisoften associated with tinea pedis. Systemic terbinafine.
Greenish nailgram neg or Pseudomonas. Treat with white vinegar
Tinea versicolorovergrowth of yeast (Pityrosporum ovale). Tx with antifungal shampoos. Hypopigmentation b/c yeast forms dicarboxylic acid inhibiting melanin formation
ImpetigoS. aureus. Honey colored crust. Exfoliative toxin cleaves desmoglein I.
Staph scalded skinDesmoglein I cleavage. Fever, malaise, sloughing bullae
Hot tub folliculitisPseudomonas. Red papules itchy/burn. Tx with antipseudomonals. Improves spontaneously if immunocompetent.
Abscess/Furunclecommonly MRSA. Localized pus collection in red painful nodule. 
Actinic Keratosisthick crusty lesion of skin. precursor for cutaneous squamous cell cancer. UV LOF mutation of p53. Treat with cryosurgery, curettage/dessication, topical 5-FU, declofenac, imiquimod, photodynamic therapy.
Basal cell carcinomarelated to sun exposure. Dysfunction of PTCH gene and p53 mutation. Rarely met. Tx: excise, Mohs, topical imiquimod. Rarely freeze.
Nodular basal cellpearly appearance with telangiectasias. Head and neck.
Superficial basal cellcommon on trunk. Pink, thin scaly patches or plaques
Morpheaform basal cellfirm, ill-defined plaques.
Squamous cell carcinomamalignant proliferation of keratinocytes. From actinic keratosis or de novo. Presents as keratotic papules, plaques, nodules. Tx: excise, Mohs. Curettage/dessication, radiation.
SCC epimore common in transplants, immunosuppressed
Subtypes of SCCSCC in situ (Bowen’s), invasive, keratoacanthoma, marjolin’s ulcer
Melanomamost common cause of cancer deaths in women 25-30. 1/80 lifetime risk. CDK2NA gene.
Melanoma warning signsAsymmetry, Border irregular, Color variations in red/black/brown/white, Diameter >5 mm
Prognostic factors of melanomaBreslow thickness – from top of granular layer to deepest invasion of dermis. (better than Clark’s in localized melanoma)
If melanoma > 1 mm deep, or with regression/ulceration or papablebiopsy sentinel nodes
Melanoma 10 yr survival<1 mm (90%), 1-2 mm (80%), 2-4 mm (60%), >4 mm (<50%)
Mycosis fungoides (Cutaneous T cell lymphoma)malignant CD4+ T cells. Red brown scaly patches. May evolve into plaques, tumors, erythroderma. Can spread to LN/blood, int. organs
Mycosis fungoides treatmentUVB, PUVA, topical nitrogen mustards, BCNU, IFN, chemo, local radiation
HPV1plantar warts
HPV2peringual warts
HPV3flat warts
HPV 6,11benign genital warts
HPV 16,18,31,33genital warts with malignant potential
Genital wartsmay be contagious after visible resolution
Genital/anal cancer risksuppressed cell-mediated immunity
Molluscum cause/epipox virus. More common in kids with atopic dermatitis/immunocompromised. 
Molluscum appearance/treatment1-3 mm shiny papule with central. May be much larger with HIV. May resolve spontaneously. Treat if symptomatic.
HSVdsDNA virus. Pain, burning, tingling before lesions. Vesicles on erythematous base. Rupture is painful ulcer. Latent in DRG.
HSV1orolabial > genital (80-90% pop with Ab)
HSV2genital > orolabial (20% pop with Ab)
Neonatal herpesexposure from primary HSV infection in mom. 75% with skin lesions. May have severe multisystem fatal infection.
Scabies organism/epiSarcoptes scabies, kids, nursing home residents, hospitalized. 
Scabies symptomsintense nighttime pruritis. 10-20 mites on body – react to mites/feces. Involves finger webs, abdomen, breast, groin, penis. 
Scabies lesions“borrows” – thin white lines. If crusted – 1000’s scabies
Scabies treatmenttopical permethrin. Oral ivermectin. Wash bedclothes, treat contacts.
Pediculosis capitis epipreschool/elementary. Uncommon in African American
Pediculosis capitisintense scalp pruritis, lice saliva/stool irritate
Pediculosis pubisintensive pruritis in genital region. Treat with permethrin cream/oral ivermectin if resistant.
Salmon patchlight pink, probably due to immaturity of blood vessels. Eyelid lesions fade, neck lesions persist. Blanch on pressure.
Sturge-Weber syndromeport wine stain, seizures, mental retardation, glaucoma.  (V1 port wine)
Parkes-Weberport wine stain of extremities, elongated/hypertrophied extremities
Hemangiomas epifemales, preemies, chorionic villus sampling
Superficial hemangiomabright red, sharply demarcated
Deep hemangiomabluish, less defined
Seborrheic keratosisv. common after age 30. Waxy, verrucous, brown/black. 1 mm – 6 cm. Completely benign. “senile wart”
Junctional nevusbtw epidermis and dermis. Flat and brown. 
Compound nevusproliferation between epidermis and dermis and within dermis – raised and brown.
Dermal nevusstrictly in dermis. Skin colored raised lesion.
Atypical nevusirregular borders/shape/colors, larger than typical nevi
Halo nevussurrounded by white rim – immune response to melanocytes. Associated with vitiligo or MELANOMA. Need full body exam
Lentiginesliver spots, larger than freckles. Associated with sun exposure, but do not fade.
Cherry angiomassmall bright red papules. Small proliferation of superficial blood vessels. Hormone responsive sometimes. No treatment required.
Xanthelasmayellow/whitepapules near medial canthus of eye. Lipid deposits in superficial dermis macrophages. Approx 50% will have hyperlipidemia as well. Can be removed for cosmetic reasons.
Keloidexcessive scar formation, common in African Americans. Extends beyond borders of initial wound. Earlobes and central chest. Treat with massage, intralesional steroids, silicone patches, removal.
Acute Cutaneous Lupus Erythematosismalar rash. Develop or have systemic lupus. 
Subacute Cutaneous Lupus Erythematosiswidespread cutaneous lesions – polycyclic and psoriaform. About 50% have systemic symptoms. Associated with SS-A/Ro. Photosensitive. May be triggered by meds.
Chronic Cutaneous Lupus Erythematosischronic, potentially scarring. 5-20% have systemi symptoms. Atrophy, scarring, dilated pores, scaling, hypo/hyperpigmentation. Conchal bowl of ear is frequently involved.
Treatment of cutaneous lupussun protection. Immunsuppresion.
Dermatomyositisassociated with inflammatory myopathy, anti Jo-1 antibody. Approximately 20% of those >40 have underlying MALIGNANCY (ovarian, gastric, lung CA, lymphoma)
Dermatomyositis clinicallyheliotrope eyes (violaceous), Gottron’s papules over knuckles, shawl sign, abnormal cuticles (erythema, dilated capillaries), scalp erythema
Dermatomyositis systemicallyproximal muscle weakness, esophageal involvement, cardiomyopathy, pulmonary fibrosis 
Dermatomyositis treatmentphotoprotection. Rheum/neuro if systemic symptoms.
Recurrent blisters over weeks and monthsprobably autoimmune
Pemphigus vulgarisIgG to desmoglein 3 (oral) and/or desmoglein 1 (cutaneous), intraepidermal blisters that easily rupture. Fatal if not treated w/immunosuppressants
Oral pemphigusdesmoglein 3
Cutaneous pemphigusdesmoglein 1
Bullous pemphigoiddisease of the elderly. IgG to basement membrane hemidesmosomes @ dermal/epidermal junction. SUBepidermal blisters, difficult to rupture. Give topical steroids, systemic if severe
Psoriasis – don’t givesystemic steroids – upon stopping will have relapsing inflammatory response
Plaque psoriasismost common. Elbows, knees, scalp, sacrum. May be itchy. Elbows/knees respond to topical therapy, hands don’t.
Guttate psoriasis2nd most common. More common in kids, related to STREP infections. Trunk most often involved. May resolve spontaneously. Looks like “raindrops”
Pustular psoriasismost acute. Can be life-threatning. Fevers, elevated WBC, hypocalcemia. Can be caused by withdrawal of systemic steroids. Can get high output cardiac failure because skin needs so much blood. 
3 steps of Psoriasis treatment1. Topical therapy. 2. Phototherapy. 3. MTX
Noninflammatory acneopen and closed comedones. Treat with salicylic wash, tretinoin, benzyol peroxide
Inflammatory acnecomedones, red papules, pustules. Inflammatory mediators released by Propionobacterium acne. Doxy or minocycline. Topical tretinoin/benzoyl perox
Nodular acnered tender nodule with deep component. Individual lesion may persist for weeks. Send to dermatologist
Rosaceamild is red cheeks, moderate includes red papules, severe includes pustules. Treat with topical metronidazole, oral doxy.
Rhinophymaenlargement of nose with chronic rosacea. Lumpy. Only in men. Treat with surgery
Seborrheic dermatitisvery common. Dandruff on scalp or other parts of body. More in Caucasians, men > women. Red plaques or patches with yellow-white/greasy scale. Nasolabial folds, eyebrows, scalp chest. Hospitalized patients. Worse with malassezia. Treat with ketoconazole cream or wash face with dandruff shampoo.
Pityriasis roseastarts with “herald patch” and then many smaller patches develop quickly. Itches slightly. Resolves in 6-8 weeks, but may last up to 6 mo. Treat with sunlight and oral antivirals (may be due to HHV 6+7). 
Atopic dermatitis15-20% of toddlers/school aged children. Defect in skin barrier function, relative deficiency in lipid ceramide. Pruritic rash. Treat with aggressive moisturization. 
Atopic dermatitis distribution in kidsInvolves face, extensor surfaces of extremities, popliteal/antecubital fossae, wrists, ankles. 
Atopic dermatitis distribution in adultsFace/hands/flexors. Often severe and widespread.
Atopic triadatopic dermatitis, asthma, allergic rhinitis
Contact dermatitisCD4+ T cells recognize a substance – rash 8-48 hr later. Lasts 7-28 days. Very itchy. Nickel, fragrance, preservatives. Treat: avoid the substance, steroids for flares
Poison ivyblister fluid does not spread response – dose response causes variation in blister formation times. Treat with prednisone x 3wk
Neosporin dermatitisitchy more than painful (differentiates between infx and hypersentivity). Use muciprocin instead
Irritant hand dermatitisHCW repetitive soap and water washing. Dish soap is worse. Apply cream after handwashing
Exanthematous drug rash1-14 days post drug exposure. Itchy, trunk. Caused by NSAIDs, narcotics, beta lactams, sulfas, diuretics, anticonvulsants. Treat with topical steroids and oral antihistamines
Anticonvulsant hypersensitivity syndromeoften favors face 2-8 weeks after drug started (buildup of toxic metabolites). Associated with sore throat, fever, eosinophilia. May be life threatening. Stop the drug! 
Erythema multiformeon mucous membranes, often related to HSV. Treat with steroids, antihistamines
Stevens Johnson rashacute death of epidermis. Pain, multiple mucus membranes involved. Skin sloughing. Stop med and send to burn unit. 
Alopecia areataimmune reaction against melanin in hair bulbs
Telogen effluviumhair falls out 3 mo post stressful event. Made worse by iron deficiency or hypothyroidism
Nephrogenic systemic fibrosisacquired progressive systemic fibrosing disorder. Develops in setting of renal disease. Linked to gadolinium. 
Nephrogenic systemic fibrosis clinicallywoody induration of skin, involves skeletal muscle, myocardium, diaphragm. Joint contractures, burning pain, pruritis, impaired limb function.
Pyoderma gangrenosumulcer with necrotic border. Nonspecific pathology. 50-70% with associated disease: IBD, arthritis, AML, myelofibrosis, monoclonal gammopathy (esp IgA)
Erythema nodosum35-55% idiopathic. Strep is most common infectious cause. Also URTI, mycoplasma, TB, cocci, histo. Sulfa, PCN. Sarcoid. Crohn’s > UC
Yellow nail syndromelymphedema, chronic bronchitis, bronchiectasis, pleural effusions, sinusitis
Distal splinter hemorrhagestrauma, psoriasis, onychomyosis
Mid/proximal splinter hemorrhagesendocarditis, vasculitis, trichinosis, APL Ab syndrome
Beau’s linestransverse depressions of nail plate. Most often traumatic. If multiple digits likely systemic disease, if all at the same level – febrile illness/drug/toxin
Koilonychiathin concave nails. Iron deficiency in adults. May be physiologic in kids.
Progressive systemic sclerosis/sclerodactylyscleroderma – tightening and thickening of skin around fingers with underlying soft tissue atrophy