Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
87 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
Acne Rosacea
EPID: 1:10, usu adults Lesions: telangectsias, papules, pustules Location: midfacial Path: unknown; (?) type IV hypersensitivity, mite infestation, h. pylori Histo: hyperkeratosis, lymphohistiocytic infiltrate, granulomatous inflamm, perifollicular abscesses C/S: transient erythema after meals/etoh, development of pap/pusutles, sebaceous hyperplasia, rhinophyma sx relating to the eyelids/ conjunctiva (conjunctivitis, blepharitis, telangctesias) Course:↑ inc. of eyelid styes, blepharitis, meibomatitis, conjunctivitis, dry eye, almost all are chronic and progressive Variants: Erythematotelangietatic; Ocular; Papulopustular; phymatous |
|
|
|
Acne Vulgaris
EPID: adolescence, M:F= 2:1 adulthood M:F= 1:2 Lesions: comedo (black/whitehead), pustules, papules Location: face, back, chest, upper arms Path: ↑ sebum production, comedogenesis, inflammation, p.acnes proliferation Course: most abate after several years, 1:3 females and 1:6 males manifest into adulthood Variants: Acne conglobata- cystic, common in XXY; fulminans- rare, systemic immunopathologic rxn; neonatal- d/t dominant circulating androgens |
|
|
|
Actinic Keratosis
EPID: 1:300, usu whites w/ hx of light skin and sun exposure Lesions: Flat erythematous keratotic lesion, <1 cm, may be verroucous Location: face, neck, sun-exposed areas Path: Neoplastic transformation of epidermal keratinocytes into carcinoma in situ (localized to epidermis) Histo: features similar to SSC: atypical, pleomorphic keratinocytes, mitosis, parakeratosis, acanthosis Course: increased incidence of squamous cell carcinoma Risk Factors: chronic UV exposure, fair skin, immunosuppression |
|
|
|
Histological slide of Actinic Keratosis
|
|
|
|
Allergic contact dermatitis
EPID: 1:80 Lesions: Inflammation of skin manifested by varying degrees of erythema, edema, vesiculation Path: Type IV delayed type hypersensitivity rxn, allergens include: poison ivy, nickel, latex, formaldehyde, cosmetics, etc C/S: intense pruritis, erythematous papules that often vesiculate Course: persistent and relapsing until allergen identified Risk Factors: chronic dermatitis which gives access to Langerhans cells Variants: Rhus- d/t urushiol; non-allergic- not immune mediated, d/t direct toxic effect on the skin |
|
|
|
Atopic Dermatitis
EPID: 1:8 children Lesions: ill-defined dry, erythematous areas with scaling and vesiculation common. puritic, linear excoriation d/t scratching Dennie Morgan folds- lines and folds due to edema below the eye Location: Infancy- skin creases, most likely antecubital and popliteal fossae, cheeks, forehead, scalp, anterior surfaces of lower legs. Childhood/ Adults- neck, periorbital areas, buttocks, thighs, hands and eyelids (adults only) Path: (?) d/t disordered rxn of T helper lymphocytes (↑ cytokines) or defect in barrier function of epidermis Histo: epidermal spongiosus, acanthosis, and hyperkeratosis, dermal inflammation & ↑ eosinophils, ↑ IgE Risk Factors: positive fam Hx for bronchial asthma, allergic rhinitis, atopic dermatitis, primary immunodeficiency Variants: Chronic Eczema- exhibits lichenification; Ocular Eczema- eyelids; Hand Eczema- adults only; Kaposi varicelliform eruption- 2o inf. by HSV |
|
|
|
Basal Cell Carcinoma
EPID: 1:300, usu white male adults, MC malignancy in humans Lesions: Erythematous plaques or nodules that commonly grow slowly but finally ulcerates, may be plaque like, morphea like, and/or manifest telangiectatic blood vessels Location: face & neck (85%), other sun-exposed areas Path: arises from pluripotent cells within the basal layer of epidermal or hair follicular structures. Neoplastic proliferation with SHH pathway implicated as the primary molecular defect Course: slow growing, metastasis is rare |
|
|
|
Histological slide of basal cell carcinoma
|
|
|
|
Blue Nevus
EPID: 1:250, M:F= 1:2 any age, but MC during adolescence or YA Lesions: usu single, subcutaneous nodule with blue-gray or gray-black color, usu <10 mm in diameter Location: head, neck, trunk, UE, rarely in mucosa Path: unknown, may be more of a hamartoma than a true clonal proliferation of melanocytes Histo: deep dermis, neoplastic proliferation of melanocytes a/w thickened collagen bundles, scattered macrophages, mitoses absent, absence of junctional involvement Course: persistent, malignant transformation does not occur Variants: Cellular blue Nevus, Atypical Blue nevus; Familial Multiple Blue Nevi Syndrome (all very rare) |
|
|
|
Bullous Pemphigoid
EPID: 1:200,000 usu older adults/elderly Lesions: fluid-filled bullae >1cm, usu puritic Location: flexor surfaces of extremities, groin, axillae Path: Chronic autoimmune, subepidermal, blistering skin disease. IgG autoantibodies directed against basement membrane components and BP Ag 180/230 are deposited in the lamina densa leading to complement activation. Inflammatory cells release proteases which degrade hemidesmosomal components and lead to loss of lamina densa and dermal-epidermal separation Histo: BPAg 1 and 2 by Western Blot/ELISA Course: ↑ incidence of sepsis and bacterial cellulitis chronic if untreated, treated with anti-inflammatory drugs Variants: Drug-Related BP- d/t Lasix, NSAIDS, etc; Localized Pemphigoid of Brunsting-Perry- restricted to scalp and face; Mucous Membrane Pemphigoid; Herpes Gestationis- 2nd/3rd trimester |
|
|
|
Dermatitis Herpetiformis
EPID: 1:3000-1:10,000 usu adults, MC in northern European whites Lesions: groups of vesicles on an erythematous base Location: extensor surfaces, symmetric Path: Cutaneous manifestation of Celiac Disease. Anti gluten IgA against epidermal transglutaminase 3 leads to complement fixation and neutrophil chemotaxis resulting in vesicle formation Histo: granular IgA at the epidermal-dermal junction, epidermal edema, neutrophils and neutrophil fragments in dermal papillae C/S: chronic dz w/ symmetric itching eruptions of vesicles and papules that occur in groups Course: ↑ inc of autoimmune dz, improves with tx and reduction of Celiac Disease |
|
|
|
Dermatofibroma
EPID: very common, M:F 1:4 Lesions: usu solitary, <1cm, firm, circumscribed, w/ + dimple sign (lateral compression results in surface dimpling d/t tethering) Location: MC lower legs, upper arms and shoulders Path: unk, clonal proliferation of fibroblasts and collagen may be mixed with proliferating histiocytes and produce foamy cytoplasm Histo: epidermal acanthosis, unencapsulated proliferation of spindle cells a/w collagen deposition in the mid-dermis. Most have a grenz (uninvolved) zone of normal dermis overlying the tumor C/S: mildly painful/pruritic, minority have + hx of trauma Course: chronic and persistent, minority recur after surgical excision Variants: Multiple Eruptive Dermatofibromas- 3 or more; Giant Dermatofibromas (rare); Metastasizing; Atypical Fibroxanthoma |
|
|
|
Discoid lupus Erythematous
EPID: 1:5,000 M:F 1:3, more common in blacks Lesions: erythematous papule or plaque with scaling, followed by alterations in skin color with dermal scarring and alopecia Location: sun-exposed areas, scalp Path: Photodamage created a heat shock protein within keratinocytes that acts as an Ag target for T cell mediated epidermal cytotoxicity Histo: Ig and/or complement at the dermal-epidermal jxn in 90% Labs: ↑ ESR, mild leukopenia, ↓ serum complement, minority manifest + ANA, RF, anti-smith Abs, anti dsDNA Abs C/S: systemic symptoms (arthralgias, maculoerethymatous rash) uncommon Course: lesions resolve over weeks with scarring and alopecia Variants: Lupus Panniculitis- deep subdermal inflamm w/ nodules |
|
|
|
Epidermoid Cyst
EPID: very common, M:F 2:1, more common in young adults/ adults Lesions: round, circumscribed, rubbery, subcutaneous nodule that this freely moveable, usu < 2cm, painless, may have a surface opening and fistulous tract Location: MC= face(1), scalp (2), trunk, neck, extremities Path: several routes: benign neoplastic proliferation of the follicular infundibulum, traumatic injury Histo: cystic structure lined w/ stratifies squamous epithelium w/ a granular layer and concentric layers of keratin, “cheesy” w/ odor Course: ↑ incidence of bacterial cellulitis, basal and squamous cell carcinomas Risk Factors: chronic sun exp, gardner’s syn, basal cell nevus syn, cutaneous HPV inf Variants: Milia- tiny discrete white papules; dermoid cyst- developmental cyst, wall contains ectoderm and mesoderm; Multiple epidermoid cysts of the skin |
|
|
|
Erythema Multiforme Minor
EPID: 1:1,000, M:F= 2:1, usu older children, teens, adults Lesions: erythematous, expanding macules or papules that evolve into “target lesions” w/ red borders and central petechiae/ purpura Location: usu symmetric, onset on extremities, expand inward, no more than 1 mucosal surface involved Path: unk, probably hypersensitivity d/t medication, autoimmune, malignancy, or infection (HSV, Mycoplasma, adenovirus) Histo: lymphocytic infiltrate at dermal-epidermal jxn and around dermal vessels, a/w keratinocyte necrosis and bullae C/S: usu spring or fall, malaise, fever, diarrhea Course: almost all undergo spontaneous resolution in few weeks Variants: Erythema Multiforme Major- 1:400,000, 2 or more mucosal surfaces involved, increased incidence of sepsis and 12% mortality rate; Steven-Johnson Syndrome- usu medication related |
|
|
|
Erythema Nodosum
|
EPID: 1:5000, M:F 1:4, more in young adults
Lesions: Erythematous nodules several inches in diameter Location: extensor surfaces of lower legs Path: unk, probably hypersensitivity d/t infection (MC=strep), systemic inflammatory dz, or medication use Histo: septal panniculitis with infiltration by neutrophils, replaced by lymphocytes and multinucleated giant cells. Meischer granulomas in the subcutis is diagnostic C/S: Lymphadenopathy common, arthralgias may be associated with effusions or arthritis Course: Almost all cases resolve spontaneously, Small minority can become chronic Variants: Villanova disease- very rare, usu older adults |
|
|
Senile (cherry) Hemangioma
|
EPID: usu older adults and elderly, us whites
Lesions: well demarcated violaceous or red dome shaped papules, commonly begins small and grows but not >1 cm Location: trunk, upper extremities Path: neoplastic proliferation of dilated small blood vessels Course: increase in # w/ age, remains benign, predisposition to hemorrhage Risk Factors: cyclosporine Rx |
|
|
Impetigo
EPID: young children Lesions: erythematous macules which develop vesicles that rupture to form honey colored crust Location: Bullous- usu on trunk; non-bullous- face or extremities Path: Non-bullous- S. aureus or S. pyogenes entry into an area of skin disruption. Bullous- almost always s. aureus which produces an exotoxin that causes the layers of the epidermis to separate bulla C/S: contact with carriers or infected ind, autoinoculation from area carrying Staph or Strep (nose). Course: Majority resolve spontaneously, Small minority involve deeper layers of skin. If S. pyogenes is pathogen, post-streptococcal glomerulonephritis may occur. Variants: Impetigo of Bockhart- superficial infection of the hair follicles caused by s. aureus |
|
|
|
Keratoacanthoma
EPID: 1: 1000, usu males, whites, adults Lesions: skin colored or reddish papule that rapidly progresses to dome-shaped nodule. May have central crater-ulceration with a keratin plug that projects like a horn. Usu 1-2 cm and solitary Location: face, neck, sun-exposed areas Path: probably arises from cells in the pilosebaceous unit but resembles squamous epithelial cells Course: rapid growth over weeks, most undergo spontaneous resolution, minority evolve into SCC |
|
|
|
Lichen Planus
EPID: 1:100, M:F= 1:2, any age but mc adults, older adults Lesions: 6 P’s pruritic, polygonal, planar, purple papules/plaques Location: flexural surfaces, mucous membranes, genitalia Path: unk, probably T cell dysfunction resulting in an autoimmune attack on the epidermis Histo: globular deposits of IgM and complement, “band” infiltrate of T cell lymphocytes and histiocytes C/S: epidermis manifests hyperkeratosis, acanthosis, colloid bodies Course: almost all undergo spontaneous resolution, commonly w/ atrophy and scarring. ↑ risk of 2o bact. Inf and sepsis Risk Factors: + fam hx, HCV, IBD, Cirrhosis, Hep B immunization, alopecia areata, vitiligo, myasthenia gravis, medication, autoimmune disorder Variants: Oral; Genital; Lichen Planopapilaris- scalp; hypertrophicus- verrucous; actinicus- sun exposed areas; vesiculobullous- blisters superimposed on the plaques; Annularis- form rings; Lichenoid Keratosis- solitary lesion |
|
|
|
Malignant Melanoma
EPID: 1:4200 annual incidence, 1:75 lifetime risk, mc in males Lesions: signs of malignant change include: variability in coloration, ↑ in size, irregular/asymmetric borders, itching, erosion, presence of satellite lesions (ABCDE rule) Location: white females- extremities; white males- trunk, head, neck; blacks-hands, feet, nail bed Genetics: familial melanoma gene: 9p21 encodes p16& p14ARF proteins which function to suppress cellular growth. Path: Neoplastic cells originate from melanocytes (usu in normal skin as opposed to from nevi) Histo: Clark’s classification I-V determined by anatomic level of invasion C/S: most grow radially for a # of years followed by an invasive vertical growth with a high probability of metastisis (common sites: liver/lungs) Course: ↑ incidence of membranous glomerulonephritis, risk of metastasis depends on depth of local invasion. Clark level II curable Risk Factors: + fam hx, multiple atypical or congenital nevi, fair skin, chronic immunosupression |
|
|
|
Melanocytic Nevus
EPID: virtually everyone, onset in childhood with more in adulthood Lesions: usu pigmented papules, variable. Junctional- at dermal-epidermal jxn; Intradermal- only in dermis; compound- present in dermis &dermal jxn Location: common in trunk, upper legs, possible anywhere Path: benign proliferation of melanocytes, forming “nests” within the skin, may develop terminal hairs Histo: nevus cells have ovoid nuclei, little cytoplasm, and form nests/syncitia Course: majority remain stable, minority regress, small minority become malignant melanomas Variants: Congenital melanocytic nevi- 1:100 births, present at birth, usu < 1 in; eruptive melanocytic nevi- appear in response to injury; neurocutaneous melanosis- multiple congenital nevi on dorsal surfaces of head, neck, and axilla, mental retardation and seizures |
|
|
|
Molluscum contagiosum
EPID: 1:100, in HIV population 1:5 ROI: Contact with people/fomites infected with MC virus, a ds DNA virus in the Poxviridae family Lesions: multiple, pearly, flesh-colored surface vesicles, commonly manifest umbilication Location: face, trunk, extremities, genital (most common in adults) Path: viral infection of squamous epithelial cells leading to squamous cell proliferation Histo: infected squamous cells exhibit large, eosinophilic viral inclusions Course: progressive spread d/t autoinoculation, majority regress over several months (except in HIV- generally do not regress) recurrences possible |
|
|
|
Pemphigous Vulgaris
EPID: 1:85,000, ↑in Ashkenazi jews & Mediterranean pop, usu older adults Lesions: non-pruritic, flaccid bullae, + nikolsksy’s and abdoe-hansen signs Location: generalized, w/ majority having Oropharyngeal involvement Path: bound and circulating complement-fixing IgG Ab directed against cell surface Ags of keratinocytes which bind to desmosomes causing loss of cell-cell adhesion and subsequent intradermal blister formation Histo: toombstoning of basal layer, + serum antidesmoglein 1 and 3 by ELISA Course: highly variable, ↑ incidence of bacterial cellulitis and sepsis, heals w/o scarring Risk Factors: + fam hx, presence of autoimmune dz Variants: Paraneoplastic Pemphigus- develops in pts with malignancies; Benign familial Pemphigus- AD disorder in the gene for Ca- pump protein ATP2C1, autoantibodies NOT present; Pemphigus Foliaceous- chronic form of PV, no mucous membrane involvement, lesions are “leaf-like”; Drug-induced PV- a/w medication use |
|
|
|
Psoriasis
EPID: 1:75, commonly bimodal incidence (young and older adults) Lesions: pruritic, erythematous plaques with a dry, silvery scale, + Auspitz sign, + koebnerization Location: MC bilateral extensor surfaces of the extremities, scalp, skin folds Path: theories: immune dysregulation in CD4+ T cells resulting in their activation and proliferation, cytokines induce an accelerated cell cycle of keratinocytes resulting in overproduction, hyperadhesiveness of epidermal cells Histo: hyperkeratosis, parekeratosis, acanthosis w/ papillomatosis, mononuclear inflammatory cells around dilated capillaries in the papillary dermis, polymorphonuclear leukocytes (munro microabcesses) in stratum corneum C/S: nail changes common, such as thickening, pitting, onichyolysis Course: chronic and persistent, ↑ incidence of depression, malignant lymphoma, BCC, minority develop inflammatory polyarthropathy Risk Factors: + fam hx, medication use (esp beta blockers, lithium, antimalarials, NSAIAs), HIV |
|
|
|
Scabies
EPID: very common, all ages, epidemics in areas with close and prolonged personal contact ROI: direct contact with mite-infested (S.scabiei) fomites or people Lesions: pruritic (esp at night) linear erythematous lesions (burrows) often a/w inflammatory papules Location: wrists, sides of fingers& feet, antecubital & popliteal fossae, intergluteal& inguinal folds, abdomen, penis, vulva Path: type IV hypersensitivity rxn, to the parasitic infestation in skin Histo: scrapings reveal eggs, mites, or fecal matter C/S: onset weeks after infestation, Course: usu self-limited to weeks or months in immunocompetent, although pruritis may last weeks/months after resolution, ↑ incidence of pyoderma Variants: Nodular scabies- erythematous nodules; crusted scabies- dense infestation w/ markedly thickened skin; infantile acropustulosis- young children, vesicopustular eruption over palms and soles |
|
|
|
Seborrheic Dermatitis
EPID: 1:25, mc in post-pubescent adolescents and young adults Lesions: waxy or greasy scaling over erythematous skin Path: unknown, presence of malassezia sp fungi a likely contributing condition, t cell depression commonly present, activation of alternative complement pathway Histo: non-specific, parakeratosis, epidermal colloid bodies, plasma cell predominant chronic inflammation in superficial dermis Course: chronic, waxes and wanes, ↑ incidence of blepharitis, 2o bacterial infection Risk Factors: + fam hx, excessively oily skin/scalp, HIV, primary immune deficiency Variants: Cradle Cap- SD of newborn scalp; Erythroderma desquamativum- in newborn, SD with exfoliative appearance, a/w lymphadenopathy & diarrhea |
|
|
|
Seborrheic Keratosis
EPID: almost all older adults have 1 or more Lesions: plaque lesions that appear “stuck on” the surface of the skin, commonly manifests an irregular surface, but may be flat, may/may not be pigmented Location: usu on sun-exposed skin Path: benign epidermal neoplastic proliferation that begins as a macule and thickens to a verrucous plaque Course: remain stable after appearance for many years, rarely give rise to SCC/BCC Variants: Dermatosis Papulosa Nigra- common in blacks, multiple brown papular lesions on face and trunk, histologically identical to SK Lesser-Trelat- multiple eruptive SKs a/w internal malignancy (usu GI adenocarcinoma) |
|
|
|
Shingles
EPID: 1:280inUS; incidence >in elderly; chickenpox vaccine incidence in adults Lesions: dermatomal, unilateral vesicle grps Location: propensity for face &trunk but can occur anywhere Path: alpha grp of Herpes family; enveloped dsDNA; humans only reservoir; infection is cytolytic (skin cells & T-cell lymph); latent systemic infection w/i neurons of DRG gets reactivated d/t waning of cell mediated immunity w/ age C/S:; onset of dysesthesia (sim.to anesthesia) several days prior to rash; vesicles rupture and crust that resolve in 2-3wks Course: infectious until all vesicles evolve into crusted plaques; 55% adults dev. Postherpetic Neuralgia; 1:20pt w/Shingles dev 2nd episode |
|
|
|
EPID: range from1:2400 to1:10000; inc in area w/ high sun exposure; usu older&elder; usu men; usu whites
Lesions: erytematous plaque usu evolves into nodule; manifest as scaling keratotic plaque; usu < 1.5cm; ulceration common Location: face; neck; hands; sun-exposed areas Path: arise from epidermal cells (keratinocytes); maj from precancerous lesions (actinic keratosis); maj mainifest p53 mut; min manifest K-ras mut; cytogenetic abnormalities Course: sm min of cutaneous SCC are metastatic @ diagnosis; SCC on lips & ears have highest prob of metastasis (usu to regional lymph & lungs); 5YS 75% Risk Factors:Hx of skin cancer; fair skin; live near equator; chronic immunosuppressive Rx |
|
|
|
Squamous cell Varient
Marjolin Ulcer Arises in an area of chronic cutaneous inflammation such as fistula due to underlying Chronic Osteomyelitis HPV-related SCC Usu located on penis, labia or peri-anal region; very aggressive w/ maj of pt manifesting metastatsis @ time of clinical presentation Primary Cutaneous SCC, Spindle variant More aggressive than Primary Cutaneous SCC; composed of atypical spindle cells that invade dermis Primary SCC of the lip Very aggressive; 1:5 manifest lymph node metastasis @ time of presentation |
|
|
|
another squamous cell variant
|
|
|
Superficial Fungal infection (basic info)
|
Mycology: species pathogenic in humans: trichophyton, microsporum, epidermophyton;
ROF: direct contact from humans or animals Path: remain confined to keratinous zone of skin C/S: vary w/ site & pathogen; Id rxn may occur; non-specific hypersensitivity rxn that occurs in 1:20 cases of superficial dermatophyte infection char. by pruritic erythematous & vesicular lesions in symmetrical distribution@location distant from fungal inf Diagnosis: skin scrapings or nail/hair w/KOH to look 4 fungal elements; skin scrapings to calcofluor white staining; (+) dermatophyte culture |
|
|
|
Tinea Capitis
Tinea Capitis “ringworm of the scalp” EPID: MC pathogen is T. tonsurans (doesn’t fluorescence with Wood Light) C/S: localized area of dry scaling scalp w/o erythema; non-inflammatory alopecia; a/w inflammation (eg. lesion of scalp w/ inflammation & usu secondarily invaded by bacteria); hair shows fungal growth w/ magnification Variants: Favus “crusted ringworm”; rare in US; common in Mediterranea, Asia, N.Africa; severe, chronic ringworm of scalp & nails w/ scarring & formation of crusts called scutula |
|
|
|
Tinea Barbae
Tinea Barbae: fungal inf. of hair follicles |
|
|
|
Tinea Coporis “ringworm”: only involves glabrous skin; usu annular lesion w/ vesicopustular border & central area mild erythema
Variant:Tinea Corporis Gladiatorum EPID: uncommon but occurs in epidemics among teams ROI: direct skin-to-skin; formites (athletic equip) Lesion:annular w/ vesicopustular border; manifest in multiples Location: arms; upper trunk; head & neck Path: skin abrasions & macerated skin from sweating facilitates fungal infection Diagnosis: (+)KOH prep of skin scrapings; (+) dermatophyte cult. |
|
|
|
Tinea Unguium
Tinea Unguium “Onychomycosis” EPID: 1:5 of adult & elder; M:F=2:1 Path: cause is dermatophytes (esp Trichophyton) C/S: nails thickened, distorted, discolored, separate from nail plate distally & a/w subungual hyperkeratosis Course: chronic & persistent w/o Rx; inc of Tinea Pedis, Paronychia, & Bacterial Cellulitis Risk Factors: DM; fam Hx of nail fungus; Psoriasis; chronic immunosuppressive Rx; PVD Tinea Cruris “jock itch”: located in groin; freq a/w Tinea Pedis Tinea Pedis “athlete’s foot”: inflammatory (vesicles & pustules) or non-inflammatory (dry & hyperkeratotic); fissures; 2o bact.inf. common Tinea Manus: inf. of hand w/ symptoms sim. to Tinea Pedis |
|
|
superficial fungal infection (supplemental topic)
|
Tinea Imbricata “oriental ringworm”:
EPID: tropical climates Path: caused by Trichophyton concentricum C/S: erythematous papulosquamous patch consisting of multiple concentric rings of overlapping scales scattered over the body Superficial Fungal Infection (SFI) & Wood Light (WL) -not all sp of fungus cause SFI exhibit UV fluorescence with WL & colors vary -Microsporum cansapple green/yellow green -Trichophyton Schoenleinipale green -Microsporum audouiniyellow green |
|
|
|
Urticaria
EPID: 1:8 in US; causes incl. meds, allergens, inf, idiopathic, change in temp, H2O, sun Lesions: blanching, raised, palpable wheals; may be linear, annular, or arcuate Location: anywhere; migratory Path: occurs following release of serotonin, His, bradykinin, kallikrein, or AchINTRADERMAL edema from capillary & venous vasodilation; MC mech for release of vasodilators is IgEHis release from mast cells C/S: freq w/ itching Course:usu transient & resolves w/o sequelae; may/may not recur |
|
|
|
Urticaria Pigmentosa
Urticaria Pigmentosa (UP) EPID: very rare; usu children, adolescents & young adults Lesion: flat or slightly elevated; brownish papules which utricate when stroked (Darier Sign) Path: pathogenesis unknown; cutaneous prolif of mast cells d/t excess mast cells in superficial dermis; mast cells may/may not involve other organs C/S: chronic dermatosis composed of lesion Course: chronic w/ minority exhibiting spontaneous resoln |
|
|
|
HPV
EPID: 1:10 in US w/ inc in children (1:5); usu whites Lesions: from contact; well demarcated, rough, hard nodules or plaques w/ irregular surface Location: confined to epithelium-hands,fingers, palms, soles of ft; no systemic dissemination Path: epitheliotropic virus that infects squamous epithelial cells of glabrous (non-hairy) skin & mucous membranescell prolif & hyperkeratotic papule; MC type 2(mc), 1, 4, 7, 27, 57 Histo: dsDNA, lack envelope, replication occurs in differentiated epithelial cells of upper epidermis, viral particles found in basal layer C/S: immunocompetent pts have spontaneous resoln after mths-yrs due to cell-mediated immunity |
|
|
|
HPV (more info)
course risk factors type 2 |
Course:cetain types cause cutaneous & genital warts while others are a/w malignancy
Risk Factors: (+) fam Hx; social contact; raw meat handling; immunodeficiency Type 2: infect keratinized& non-keratinized epidermal surfaces that autoinoculate to genitals, other HPV types don’t infect mucosal surf of genitals; resistance is cell-mediated; cutaneous warts irregular w/ filiform surface; acanthosis; compact orthokeratosis; hypergranulosis; dilated tortuous capillaries w/i dermal papillae; vertical tiers of parakeratotic cells; elongated rete ridges; granular layer of cells manifest keratohyaline granules & koilocytosis |
|
|
HPV Varients
|
Verruca Plana: sm flat warts in immunodef pt
Bowen Disease: SCC in situ on head & neck , sm amt pt manifest HPV type 16 neoplastic epithelia cells Bowendoid Papulosis: uncommon; flat, wart-like growth on genitals; may/may not be a/w oncogenic HPV; little propensity to invade Epidermodysplasia Verruciforms: very rare; most autosomal recessive; genetic cell-mediated immunodef w/ numerous Verruca Plana most on hands & ft but can go anywhere; onset during childhood; sm warts coalesce; inc of SCC of skin Heck Disease (focal epithelial hyperplasia): MC in Native Americans & Inuit; due to papovaviruses; mult soft nodular verruciod lesion of lips, buccal mucosa, tongue & oral sites in children & adolescents: spontaneous regression |
|
|
|
More HPV variants
|
|
|
|
HPV Variant
Heck Disease (focal epithelial hyperplasia): MC in Native Americans & Inuit; due to papovaviruses; mult soft nodular verruciod lesion of lips, buccal mucosa, tongue & oral sites in children & adolescents: spontaneous regression |
|
|
|
Dysplastic (atypical) Nevus
EPID: usu whites; extremely rare in dark skinned pop Lesions: pigmented macule w/ irregular borders, pigmentation, & surface; any size but majority are >5mm dia Location: M: MC back then chest; F: lower legs; uncommon for MorF butt, breast, scalp Path: neoplastic prolif of melanocytes forming “nests” w/i skin; nevus cells present @ dermo-epidermal junct or both this & upper dermis; melanocytes exhibit cytologic atypia w/ enlarged, hyperchromatic nuclei Histo: lamellar & concentric dermal fibroplasias; lymphocytic infiltrate superficial dermis C/S: onset usu in childhood/adolescence Course: pt w/ numerous Dysplastic Nevi @ higher risk for melanoma Risk Factors:fam Hx of malignant melanoma |
|
|
|
Epidermolysis Bullosa
EPID: 1:45000 live births; the more severe type the rarer Path: inherited defect in keratin proteins loss of normal desmosome strength & cell-cell adhesion; blister formation w/i epidermis C/S: (+) Nikolsky sign Course: inc of dehydration a/w electrolyte loss & protein loss through the skin, dermal scarring, scarring alopecia, milia, bacterial cellulitis & sepsis; all types but EB Simplex may manifest in oral mucosa, nasopharyngeal mucosa, cornea, airway lining, genitourinary lining, bowel mucosa Variant:Epidermolysis Acquista EPID: extremely rare; usu in adults Path: IgG target the non-collagenous domain of type VII collagen leading to separation of epidermis from dermis blisters C/S: Koebner phenomenon & healing w/ scars; on elbows, knees, ankles, butt; inc autoimmune disease like SLE &IBD |
|
|
|
Epidermolysis Bullosa Simplex (EBS)
EPID:MC type of EB; MC autosomal dominant; mutation in keratin 5 gene on chrom 12q or keratin 14 gene on 17q Location: MC on hands & feet after traumatic injury Path: Keratinocyte abnormalities such as clumping; blisters form by cytolysis w/i basal or spinous layers of epidermis Course: only on skin; heals w/o scarring Types: Weber-Cockayne—MC EBS; onset of Sx during late childhood; on hands ft w/o scarring; over time skin on hands & ft thickens Koebner—onset of @ birth/infancy; greatest on extremities Dowling-Meara – most severe EBS; onset @ birth; severe blistering in clusters; a/w nail dystrophy; course includes inc failure to thrive, bacterial cellulitis & sepsis |
|
|
|
Dystrophic Epidermolysis Bullosa
EPID: 2nd MC EB; AD or AR; onset @birth or childhood; mutation in gene for type VII collagen on chrom 3p Path: basement membrane remains attached to epidermis & blister cavity forms beneath lamina densa d/t abnormalities in anchoring fibrils; dermal scarring after bullous separation of epidermis from dermis C/S: progressive scarification Course: inc of pseudosyndactyly, progressive dysphagia d/t esophageal stricture; corneal ulceration & perforation; AR type a/w inc of cutaneous SCC Junctional Epidermolysis Bullosa Path: AR; epidermis separates from basal lamina; nonscarring blistering C/S: onset as neonate, persistent & nonhealing perioral & perinasal crusted lesion Course: inc bacterial sepsis, dehydration, failure to thrive |
|
|
|
Ichythiosis Vulgaris
EPID: 1:280; MC type of ichthyosis; AD Lesions: noninflammatory dryness & scaling of skin a/w abnormalities of cutaneous lipid metabolism Location: scaling on extremities & trunk sparing flexor areas, palms &soles have hyperkeratosis Path: formation of defective keratin; a defect in filaggrin protein results in dysfunction of keratocytes leading to inability to normally desquamate Histo: hyperkeratosis, follicular plugging, thinning or absence of granular layer; absent keratohyalin granules in granular layer C/S: onset @ infancy/early childhood; pruritis Course: improvement in adulthood; normal life span Variants: acquired ichthyosis vulgaris (rare; onset as adult; dermis manifests granulomas; majority a/w medication or systemic disease) |
|
|
|
Kaposi Sarcoma
EPID: 1:6 in AIDS pt, HIV related occur @ any age Lesions: brown, red to bluish macule that get lg & coalesce into nodules & dome-shaped tumors, ulceration may occur Location: MC head/neck and lower extremities, can be on mucosal tissue Path: arise from endothelial cells; cytokines work w/ HIV tat gene to induce neoplastic proliferation of endothelial cells; HHV-8 present in many cases carrying an oncogene that aids in neoplastic transformation w/i endothelial cells; neoplastic angiogenesis lacking basement membrane leak C/S: lymphedema; requires a skin biopsy for diagnosis Classic Kaposi Sarcoma: very rare, M:F = 6:1, usu adults, usu Mediterranean or eastern Europe, not related to HIV, usu on lower legs/ft, slow growing and indolent, inc a/w Hematopoietic malignancy Iatrogenic type – related to chronic immune suppression Endemic & Epidemic Types--related to HIV/AIDS; aggressive |
|
|
|
Mucocutaneous Candidiasis
Histo: lesion has neutrophils mixed w/ budding yeasts & hyphae; scales Path: most d/t C. albicans; virulence factors are surface molecules, secretion of acid prodeases, and ability to convert hyphal forms Course: if immune competent or Rx – resolves on own or discontinued Rx Note: cultures are only informative in relation to blood because Dandida is normal flora Oral candidiasis EPID: MC type; rare in immunocompetent no taking antibiotics;1:60 if taking antibiotics; almost all pt w/ AIDS get Candidal sp infection Lesions: erythematous plaques w/ adherent white material Location: tongue & mucosa of mouth Path: is a superficial mucocutaneous fungal infection; Course: immunocompromised inc Esophageal Candidiasis & Disseminated infection |
|
|
|
Cutaneous Candidiasis
Lesions: scattered erythematous lesions a/w “cottage cheese” exudates, scaling erythroderma that manifest satellite lesions, folliculitis Location: intertrigionous areas, perineum in children from diaper Path: caused by immune defect or disruption in normal bacterial flora C/S: heat, moisture & chronic skin irritation promote fungal growth Course: immunodeficient neonates lack resoln extension of infection Risk Factors: antibiotic Rx, primary or secondary immunodeficiency Candidal Balanitis -- C/S: erythematous macules manifest vesicle or shallow erosion, usu on glans penis but can involve shaft |
|
|
|
Candidial Onychomycosis
EPID: 1:5 adult; M:F=2:1; Path: MC dermatophytes (Trichophyton) although can be from C.albicans C/S: thick, discolored nails Course: chronic w/o Rx, inc of Paronychial & bacterial cellulitis; Risk Factors: DM, fam Hx, Psoriasis, PVD Candidial Vulvovaginitis Path: change in flora caused by Rx distruption, pregnancy, oral contraceptive use, DM, hypothyroidism, iron deficiency anemia, HIV C/S: vaginal epithelium manifest erythema & white curd-like discharge; burning sensation; vulvar pruritis |
|
|
|
Mucocutaneous Herpes Simplex: Neonatal Herpes Infection
Virology:dsDNA; pathogenic only to humans EPID: 1:4000 live births Path: after contact, HSV replicates in epidermal & mucosal epithelial cells; cytolytic to cells and persistent infection in lymphocytes & macrophagesvesicles; most d/t HSV2; can create a latent infection in peripheral neurons C/S: onset from days to wks after birth Risk Factors: maternal herpes infection Hx; prolonged rupture of membranes; vaginal delivery Neonatal herpes keratoconjunctivitis: onset after 2 wks, majority have skin or mucous membrane lesions; erythema of palpebral & bular conjunctivae a/w lid & peri-orbital soft tissue swelling and discharge |
|
|
|
Neonatal Mucocutaneous Herpes: any skin by contact; grps of 1-2 mm vesicles on erythematous base that progresses to ulcer forms a honey-colored crust; heals w/I 3 wks; develop disseminated infection if anti-viral Rx is not given
Neonatal herpes encephalitis: both HSV1&2 cause; MC HSV2; infect inferior frontal and medial temporal lobes; majority manifest localized disease prior to encephalitis; majority manifest post-infection morbidity Neonatal disseminated herpes: MC type; multi-organ infection; Majority manifest localized disease prior to onset of dissemination; onset @10-30days old; hypo/hyperthermia, poor feeding, tachypnea, seizures; inc of DIC & multi organ failure, morbidities same as encephalitis |
|
|
|
Herpes Gingostomatitis: caused by HSV1; lip, mouth, tongue lesions; grp of vesicles on erythematous base rupture forming crusting lesion or aphthous-like ulcer; possible fever cervical lymphadenopathy; often drool
Cutaneous Herpes: either HSV1 or 2; variants:Eczema Herpeticum, Herpetic Whitlow (healthcare workers like dentist get), Herpes Gladiatorum (wrestlers get), Herpes Rugbeiorum (rugby) Herpes Genitalis: 1:450; commonly caused by HSV2 but oral sex has # infection by HSV1; same lesions but on genitals; a/w inguinal lymphadenopathy |
|
|
|
Other Mucocutaneous Herpes Simplex examples
|
|
|
|
Other Mucocutaneous Herpes Simplex examples
|
|
|
|
Pityriasis Rosacea
EPID: 1:2500 in us: M:F=1:2; usu children/young adult Lesions: majority have intial lesion is single, lg salmon-colored scaling plaque “herald patch” (prior to onset, herald patch is commonly misdiagnosed as Tinea Corporis; oval papulosquamous Location: commonly on trunk, proximal extremities Path: unknown; probably HHV7; seasonal variation, generalized rash following primary patch, limited course, rarity of second attack, familial clustering; PR-like eruption reported in Rx use Histo: acanthosis, focal parakeratosis in mounds, epidermal spongiosis w/ exocytosis of lymphocytes, C/S: onset usu spring or fall; mild pruritis common; Course: depending on intensity of inflammation, some lesions manifest post-inflammatory pigmentations change; spontaneous resoln over 8-10wks Variant: inverse pityriasis rosea-distribution confined to distal extremities |
|
|
|
Porphyria Cutanea Tarda
EPID: MC type in US; majority acquired rather than inherited Path: deficiency in uroporphyrinogen decarboxylase; marked elevation of circulating porphyrin intermediates elevated skin levels of intermediates & sun exposurephotoactivation of metabolites & toxic skin injury Histo: subepidermal separation a/w festooning of dermal papillae C/S: minor trauma causes blistering; healing show hypo/hyperpigmentation; dermal scarification & scleroderma-like plaques; hypertrichosis over malar areas Diagnosis: dark red urine; elevated8-&7-carboxyl porphyrin, fewer 6-, 5-, 4-carboxyl porphyrins; does NOT manifest elevated porphobilinogen Course:elevated porphyrin intermediates cause liver injuryinc of hepatic cirrhosis, hepatic adenocarcinoma, and more so in pt w/ predisposition or Ethanol use |
|
|
|
secondary syphilis
Path: manifest following asymptomatic period, involves dissemination of bacteria; most contagious phase of syphilis due to # of organisms in body Histo: mononuclesar infiltration into upper dermis; vasculitis w/ endothelial swelling & proliferation, lymphocyte & plasma cell infiltration into the vessel wall; use Treponemal stains; motile spirochetes C/S: follows healing of genital ulcer after 2-8 wks (some don’t manifest for mnths), fever, sore throat, headache, malaise, myalgias, arthralgias Course: rash lasts wks & disappears as pt enters latent phase; inc Uveitis, hepatitis, optic neuritis, membranous glomerulonephritis; if untreated 30% will progress to tertiary syphilis |
|
|
|
Spitz Nevi
Neoplastic lesion w/ atypical melanocytes highly suggestive of malignant melanoma but lacks invasive behavior EPID: 1:60,000 in US (malignant melanoma is 10xMC than Spitz); MC in children/young adults Lesions: single, dome-shaped papule-nodule; color varies (nude-red) Location: face, legs Path: arise de novo on normal skin or pre-existing melanocytic nevus; majority manifest compound nevus appearance Histo: epithelioid & spindle-shaped melanocytes growing in nests & arranged in vertical pattern, multinucleated melanocytes present; acanthosis & hyperkeratosis C/S: lesion manifests a growth phase of several months & then goes static Course:benign |
|
|
|
Tinea Versicolor
Caused by a fungus that lack ability to synthesize medium-chain & long-chain fatty acids & requires an exogenous supply of lipids for growth EPID: 1:8 in US Lesions: faintly erythematous macules or raised flat papules that have scales; common discoloration Location: chest, upper back, trunk Path: caused by a fungus (Malassezia furfur) normal to skin flora C/S: occur @ any age; MC in adolescents/young adults in US Course: majority multiple recurrences, minority have spontaneous resoln Variants: inverse tinea versicolor-involvement of face & flexural areas |
|
|
|
Varicella (chickenpox)
EPID: 1:25; since vaccine in 1995; MC 4-10 yo; occur in epidemics ROI: aerosol or direct contact Lesions: multiple erythematous papules 2-4 mm udergo vesiculation & shallow ulceration; common for pt to have mixture of lesions @ various stages of development (some papules, vesiculated papules, & crust) Location: begin on face & trunk then spread full body sparing distal extremities; can occur in mouth & conjunctiva & cornea Path: 2-3wk incubation period; virus gains entrance via respiratory epithelium and disseminates to lymph nodes, replicates then goes systemic; becomes latent w/I sensory ganglia & can reactivate => shingles C/S: HHV3, dsDNA; occur anytime during yr but MC in winter/early spring; fever, arthralgias/myalgias; spontaneous resoln 7-10 days Course: contagious until all skin lesions have eschar; inc of bacterial cellulitis, reye syndrome, varicell encephalitis, & systemic vasculitis |
|
|
|
Vasculitis
EPID: 1:50,000 is avg in US; M:F =2:1; MC in older adults/elder; MC adult types giant cell arteritis microscopic polyangitis, Wegener granulomatosis; MC children types Henoch-schonlein purpura, Kawasaki disease Path: disorders classified by caliber of blood vessels involved: C/S: fever; weakness; recurrent headache; cutaneous palpable purpura, usu lower extremities; polyarthralgias; peripheral neuropathy Lab findings:leukocytosis; elevated ESR & CRP; proteinuria; hematuria Diagnosis: difficult because subtlety of presentation; should be on differential diagnosis if either unexplained multiple organ dysfunction or unexplained ischemia w/o atherosclerosis |
|
|
|
Vitiligo
EPID: 1:60; onset @ late childhood/young adult; familial cases occur Lesions: face, neck, scalp Location: sharply defined, nonpigmented white patches, symmetrically distributed, bordered by hyperpigmented areas, depigmented lesions manifest a scalloped border, white hair in depigmented areas Path: epidermal melanocytes are completely lost, melanocyte destruction is autoimmune mediated Course: chronic & progressive & lesions tend to enlarge w/ time; commonly a/w other autoimmune disorders |
|
|
|
Xeroderma Pigmentosum
EPID: 1:650,000 to 1:250,000; higher inc in Japan; most AR Path: rapid ageing of exposed skin d/t inability to repair UV-induced DNA damage; mutation rate inc of neoplastic transformation in skin cells Histo: excessive chromosomal fragility C/S: onset during infancy/early childhood; photosensitivity w/ severe sunburn; develop pigmented spots like freckles & multiple actinic keratoses; corneal opacities blindness; photophobia Course: inc of cutaneous cancers (BCC, SCC, MM) as a young child; MC cause of death is metastatic malignancy |
|
|
|
Drug Eruption (Generalized)
|
EPID: 1:20-1:100, M:F 1:2, more common in adults and elderly
Path: immunologic- majority are type IV hypersensitivity rxns in which the drug (hapten) binds to an endogenous macromolecule which is processed as an Ag inducing T cell mediated resp. non-immunologic- mechanisms include: direct toxic effect, mast cell degranulation, phototoxicity, or idiosyncratic Histo: possible peripheral blood eosinophilia and drug related Abs C/S: + hx of medication use, pruritis common, fever and other systemic sx may be present Course: most undergo resolution w/discontinuation of Rx, minority develop severe cutaneous injury Risk Factors: Polypharmacy, Atopy hx, 1o/2o immune deficiency, + family hx |
|
|
|
Drug Eruption (Variants)
|
Papulopustular DE- inflammatory papules/pustules that have a follicular pattern
Acute Generalized Erythematous Pustulosis- scarlatiniform erythema w/ many small, sterile, nonfollicular pustules, generalized and symmetrical involvement w/ sparing of palms and soles, fever and other systemic sx present Drug Rxn w/ Eosinophilia & Systemic Sx-(DRESS syndrome) EPID: 1:15,000-1:8,000 pts taking anti-convulsants Lesions: pruritis, follicular centered erythematous macules progressing to generalized symmetric papulopustular eruption Path: severe, idiosyncratic multisystem adverse drug rxn, 1-8 weeks after med exposure, similar to SIRS, mc caused by antibiotics & anti-convulsants Labs: peripheral blood eosinophilia and atypical lymphocytes, ↑ AST/ALT, BUN & creatinine C/S: clinical triad: fever, skin rash, multi-organ dysfunction Risk Factors: + fam hx |
|
|
|
Drug Eruption (Variants)
|
Drug-related Acral Erythema- erythema a/w tenderness & edema, symmetric involvement of the hands & feet including the palms and soles, commonly a/w chemotherapy
Drug-Related Erythema Nodosum- very rare, path unk, probably a hypersensitivity rxn, systemic sx common, light microscopic findings show a septal panniculitis w/ infiltration by neutrophils early replaced by multinucleated giant cells Lichenoid Drug Rxn- intense pruritis, distribution consistent w/ LP Drug-related Subacute Cutaneous Lupus Erythramatosus- deposition of Ig and or complement at the dermal-epidermal jxn, common causes: thiazide diuretics, Ca-channel blockers, ACE inhibitors, terbifine Morbiliform Drug Reaction- MC type of generalized drug eruption, onset of sx w/in 1-2 weeks of first dose, no fever, pruritis common, erythematous exanthem, generalized and symmetric w/ sparing of palms and soles |
|
|
|
Drug Eruption (Variants)
|
Secondary Porphyria Cutanea Tarda- disruption of the conversion from uroporphryrinogen III to coprophyrinogen III, marked elevation of circulating porphyrin leads to photoactivation and toxic skin injury. MC meds are antibiotics and NSAIAs
Drug-related serum sickness- very rare, caused by immune complex deposition followed by complement activation. MC drugs are antibiotics, sulfa drugs, allopurinol. Lesions and generalized and symmetric but highly variable. Labs: ↓ total complement, hypergammaglobinemia, proteinuria, hematuria Leukocytic Vasculitis Path: very rare, type III hypersensitivity rxn, medication acts as an Ag inducing the production of autoantibodies which bind and activate complement. The circulating Ag-Ab complexes deposit in tissues and blood vessels resulting in inflammation. Common meds are: hydralizine, proainamide C/S: palpable purpura, livedo reticularis, urticaria, systemic sx common Lab: ↑ ESR, CRP, ↓ total complement, presence of immune complexes, + ANA |
|
|
|
Drug Eruption (Variants)
|
Drug-related urticaria- urticaria occurs following the release of serotonin, histamine, bradykinin, kallikrein, or Ach, resulting in intradermal edema and blanching, raided, palpable wheals
Drug-related Photodermatosis- accounts for 4-10% of adverse drug reactions, ranges from mild erythematous sunburn like rash to broad areas of erythema w/ vesiculation and bullae. Only on sun-exposed areas. prerequisite: exogenous compound in the skin that can be photochemically changed. MC drugs: Sulfa (1), tetracycline (2), thiazide diuretics, NSAIA, retinoid acid, sulfonylureas, benzodiazepines Drug-induced Bullous disease – severe drug eruptions a/w the highest mortality, greatest incidence w/ semisynthetic penicillins, drug acts as a hapten and binds to an endogenous protein (carrier). The hapten-carrier complex is antigenic resulting in activation of CD8 T cells which invade the skin and form bullae, oropharyngeal involvement is common. |
|
|
|
Fixed Drug Eruption
|
EPID: 1:75 treatment courses, 20% of all cutaneous drug eruptions
Lesions: sharply demarcated, erythematous macules that may or may not manifest vesiculation Location: more common on lips, hands, feet, hip, genitals, reoccurs in same site Path: Drug binds to skin protein resulting in antigen complex which activates CD8 T cells, which manifest in localized area Histo: peripheral blood eosinophilia possible C/S: pruritis is common. Course: Commonly has post-inflammatory hyperpigmentation, Almost all resolve spontaneously with elimination of drug, Recurrences with repeat exposure Risk Factors: polypharmacy, primary immunodeficiency, HIV. Common causes: antibiotics, phenytoin, NSAIA, phenothiazines |
|
|
|
Cutaneous Hemangioma (infantile)
|
EPID: 1:9 live births, increases with prematurity, M:F= 1:3, usu white
Lesions: well-demarcated, soft red areas, may be flat or raised Location: head/neck (mc), trunk, extremities, if midline, ↑ a/w underlying hemorrhage Path: benign neoplasm of proliferating epithelial cells which form vascular channels. Lots of mast cells in associated stroma. May be capillary or cavernous (deeper dermis and large dilated vessels) Course: significant growth in 1st year followed by slow involution, ↑ incidence of ulceration. a/w CNS hemangiomas, Dandy-Walker syndrome, and R-sided coarctation of the aorta Variants: salmon patch- 1:2 live births, may be d/t persistent fetal vessels or be a neoplastic proliferation of vessels |
|
|
|
Malignant Melanoma (variants)
|
Superficial Spreading melanoma- majority of cases of malignant melanoma, epithelium manifests atypical Pagetoid cells scattered through the epidermis. Macular lesion with asymmetric borders, may have a pink halo.
Primary Nodular Melanoma- 2nd mc type of melanoma, arises de novo with rapid vertical growth w/o the initial radial growth. Highly aggressive, high potential for metastisis. Lentigo Melanoma- melanotic freckle, usu females, usu older adults/elderly. Atypical contracted melanocytes in the lower epidermis a/w solar damage in the dermis & atrophy of the epidermis. Tan-brown macule w/ differing shades throughout, common in sun-exposed areas |
|
|
|
Malignant Melanoma (variants)
|
Acral lentiginous melanoma- very uncommon, usu in older adults/ elderly, mc type of malignant melanoma in blacks and Hispanics
Mucosal lentiginous melanoma- 1:100 cases of malignant melanoma, delay in dx d/t location Desmoplasmic melanoma- very uncommon, usu older adults & elderly, most arise from preexisting cases of lentigo melanoma, frequently a/w neurotropic pain Amelanotic melanoma- irregular erythematous nodule on skin- generally resembles a pyogenic granuloma |
|
|
|
Malignant Melanoma (variants)
|
Hereditary melanoma- AD, 1:10 pts w/ malignant melanoma has a 1st degree relative with melanoma. The CDKN2A area on 9p21 encodes p16& p14ARF proteins which function to suppress cellular growth. Hereditary melanoma probably d/t a mutation in p16 resulting in heterozygosity.
Melanoma-Astrocytoma syndrome- very rare, predisposition to both melanomas and astrocytomas Non-cutaneous melanoma- ocular melanoma, usu whites, usu older adults/elderly, unilateral decreased visual acuity, majority are metastatic d/t delay in diagnosis |
|
|
|
Cutaneous T Cell Lymphoma
|
EPID: 1:300,000, M:F 2:1, usu blacks, usu older adults or elderly
Path: malignant lymphoma characterized by clonal expansion of CD4 T cells that also manifest cutaneous lymphocyte antigen (CLA), malignant cells are dermatotropic and may metastisize Variants: Mycosis Fungoides 1:160,000 Path: epidermis exhibits atypical lymphocytes infiltrating as single cells or as Pautrier microabcesses Lesion: pruritic, variably colored (violaceous, pink, orange) patches, plaques, or nodules that manifest scaling Location: trunk, buttocks Course: lesions grow to become exophytic tumorous growths in the systemic, aggressive stage, hepatomegaly/lymphadenopathy common. Early diagnosis of localized lesion 98% 10YS, systemic involvement <1YS Sezary syndrome: any type of CTCL in which malignant cells infiltrate the entire skin surface w/ malignant T cells (Sezary cells) in peripheral blood |
|
|
|
Psoriasis Variants
|
Guttate Psoriasis- usu in children, a/w Group A strep infection, salmon pink, circumscribed, 5-6 mm papules w/ a fine scale
Pustular Psoriasis- increased #s of neutrophils in the plaques, acute onset with rapid evolution (48-72 hours), often systemic sx including fever Psoriasis Inversus- in skin folds, often mistaken for seborrheic dermatitis Psoriasis Annularis- healing at center of lesions producing a ring shaped lesion Psoriasis Diffusa- confluence of plaques very large plaques covering body Psoriasis Punctata- small papular lesions w/ an adherent white scale Palmar Psoriasis- involves the palmar surfaces of fingers and palms Erythrodermic Psoriasis- uncommon, painful pruritic lesions- broad areas of erythroderma followed shortly by desquamation, systemic sx common |
|
|
|
Shingles Variants
|
Herpes Zoster Oticus
EPID:1:50000, usu older adults&elder Path: reactivation of latent HZVdysfunct of CN VII & CN VIII C/S: unilateral earache; commonly a/w hearing loss & vertigo; maj. Manifest shingles in sensory distribution of CN VII Note: maj. of pt do NOT manifest facial n. shingles, only CN VII dysfunct Course: maj have perm paresis or paralysis Variant: Ramsay Hunt Syndrome EPID:1:8 pt w/ Herpes Oticus Path: d/t CN VII geniculate ganglion infection; ipsilateral peripheral CN VII palsy w/ pain & vesicles Course: CN VII paralysis Herpes Zoster Multiplex: >1 non-contiguous dermatorme w/ lesions |
|
|
|
Shingles Variants
|
Zoster Vasculopathy
EPID:adults& elder; in temporal proximity to symptomatic shingles; focal area of brain or multiple areas; vasculitis a/w multinuc. Giant cells & thrombosis ischemia C/S: cognitive changes; ataxia; seizures; hemiparesis Diagnosis: VZV Ab in CSF; PCR VZV assay (+) in CSF Zoster Sine Herpeticum: Dermatomal pain w/o skin lesions; peripheral n. palsy w/o skin lesions Zoster Keratitis: Inv. cornea d/t shingles in ophthalmic br of CN V; freq a/w lesions @ tip of nose Zoster Myelitis: Usu in immunodeficient; onset of sp cord symptoms w/i wks of shingles episode Disseminated Herpes Zoster Infection: uncommon; 3+ dermatomes or int. organ |
|
|
|
HPV Variants
|
Plantar Wart (PW)
EPID: 1:15 in US; M:F=1:2; usu children & adolescents ROI: ft direct virus contact Lesion: round, hyperkeratotic, cauliflower-like w/dark petechiae; 5-10mm dia; ext pressure pushes wart into skin Location: anywhere on plantar ft surface; most common on plantar surface of toes, heel, or ball of ft C/S: commonly painful when walking or to lateral pressure Course: inc of autoinoculation; inc of Epithelioma Cuiculatum; majority undergo spontaneous remission Variants: Mosiac PW (confluent PW forming lg complex wart); Giant PW (very rare; MC in immunosuppressed; 2+cm) |
|
|
|
dysplastic Nevis Nosologies
|
Sporadic Dysplastic Nevis
EPID: range 1:10 to 1:2 in US C/S: risk of malignant melanoma Familial Dysplastic Nevus Syndrome “B-K Moles” EPID: rare Genetics: autosomal dominant w/ variable penetrance; CMM2 gene on 9p21 encodes CDK inhibitor 2A mutation C/S: fam Hx of multiple nevi or melanoma; onset during childhood/birth; majority of nevi are lg (6-10mm); nevi manifest dysplasia Course: inc nevus transform to melanoma, Non-Nevus- related melanoma, risk retinal melanoma, non-nevus related BCC, non-nevus related cutaneus SCC; solid organ malignancy of pancreas, breast, lung, CNS |
|
|
|
Mucocutaneous Herpes Simplex
Acquired childhood, adolescent & adult mucocutaneous |
Path: direct contact: HSV1-saliva or weeping lesions, HSV2-genitalia;cytolytic to epidermal cells celllular necrosis & vesicles; nuclear viral inclusions in cells; latent infection in nerves
Histo: (+) Tzanck smear, multinucleated giant cells & epithelial cells w/ eosinophilic intranuclear inclusion bodies, (+) herpes culture, (+) immunofluorescent or DNA PCR C/S: any skin via contact, cluster 1-2mm vesicles on erythematous area, progress to ulcer, painful for few days & form honey-colored crust, heal w/I 3 wks Course:can disseminate resulting in herpes encephalitis; autoinoculation occurs, spontaneous resoln in few wks, recurrences are common Herpes Labialis “cold sore”: caused by HSV1, confined to lip, grp of vesicles that rupture causing ulcer Mucocutaneo |
|
|
|
Porphyria Cutanea Tarda Type 1 and 2
|
Type 1
EPID: 1:75000-1:38000 in US; very common in Bantu of South Africa; 1:5 cases of PCT; AD; caused by mut in UROD gene Path: inherited enzyme defect is manifested only in liver & NOT in erythropoietic cells of bone marrow Histo: heptatic & erythrocyte uroporphyrinogen decarboxylase activity C/S: homozygotes-symptoms onset @ childhood; heterzygotes-symptoms delated to adulthood or asymptomatic Type 2 EPID: MC type of PCT; MC type of acquired porphyria Path: chronic liver injury leads to porphyrin production & accumulation of excessive iron stores Histo: heptatic uroporphyrinogen decarboxylase activity & normal erythrocyte uroporphyrinogen decarboxylase activity |
|
|
|
Vasculitis types
|
Septic Vasculitis: acute & abrupt onset commonly w/ fever
Meningococcemia Virulence: pili that facilitate bacterial adhesion to mucosal epithelial cells; polysaccharide capsule; endotoxin shed causing endothelial cells, monocytes, & macrophages to release TNF alpha, IL1, IL6, IFN gamma; immunoglobulin A1protease EPID: 1:100,000; MC in lower socioeconomic grp; black>white; M>F ROI: aerosol, human respiratory tract is ONLY known reservoir; by late adolescence, over 90% of pop manifest circulating anti-Neisseria Abs Path: attach to nasopharyngeal epithelia then enter bloodstream |
|
