Dermatopathology (Martin) Flashcards
1
Q
- macroscopic lesion
- Traumatic lesion breaking the epidermis and causing a raw linear area (i.e., deep scratch); often self-induced
A
excoriation
2
Q
- macroscopic lesion
- Thickened, rough skin (similar to a lichen on a rock); usually the result of repeated rubbing
A
lichenification
3
Q
- macroscopic lesion
- Circumscribed, flat lesion distinguished from surrounding skin by color. Macules are 5 mm in diameter or less, patches are greater than 5 mm
A
macule, patch
4
Q
- macroscopic lesion
- Separation of nail plate from nail bed
A
onycholysis
5
Q
- macroscopic lesion
- Elevated dome-shaped or flat-topped lesion. Papules are 5 mm or less across, while nodules are greater than 5 mm in size.
A
papule, nodule
6
Q
- macroscopic lesion
- Elevated flat-topped lesion, usually greater than 5 mm across (may be caused by coalescent papules)
A
plaque
7
Q
- macroscopic lesion
- Discrete, pus-filled, raised lesion
A
pustule
8
Q
- macroscopic lesion
- Dry, horny, platelike excrescence; usually the result of imperfect cornification
A
scale
9
Q
- macroscopic lesion
- Fluid-filled raised lesion 5 mm or less across (vesicle) or greater than 5 mm across (bulla). Blister is the common term for either.
A
vesicle, bulla, blister
10
Q
- macroscopic lesion
- Itchy, transient, elevated lesion with variable blanching and erythema formed as the result of dermal edema
A
wheal
11
Q
- microscopic lesion
- Diffuse epidermal hyperplasia
A
acanthosis
12
Q
- microscopic lesion
- Abnormal, premature keratinization within cells below the stratum granulosum
A
dyskeratosis
13
Q
- microscopic lesion
- Discontinuity of the skin showing incomplete loss of the epidermis
A
erosion
14
Q
- microscopic lesion
- Infiltration of the epidermis by inflammatory cells
A
exocytosis
15
Q
- microscopic lesion
- Intracellular edema of keratinocytes, often seen in viral infections
A
hydropic swelling (ballooning)
16
Q
- microscopic lesion
- Hyperplasia of the stratum granulosum, often due to intense rubbing
A
hypergranulosis
17
Q
- microscopic lesion
- Thickening of the stratum corneum, often associated with a qualitative abnormality of the keratin
A
hyperkeratosis
18
Q
- microscopic swelling
- A linear pattern of melanocyte proliferation within the epidermal basal cell layer
A
lentiginous
19
Q
- microscopic swelling
- Surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae
A
papillomatosis
20
Q
- microscopic swelling
- Keratinization with retained nuclei in the stratum corneum. On mucous membranes, parakeratosis is normal.
A
parakeratosis
21
Q
- microscopic lesion
- Intercellular edema of the epidermis
A
spongiosis
22
Q
- microscopic swelling
- Discontinuity of the skin showing complete loss of the epidermis revealing dermis or subcutis
A
ulceration
23
Q
- microscopic swelling
- Formation of vacuoles within or adjacent to cells; often refers to basal cell-basement membrane zone area
A
vacuolization
24
Q
- “disordered growth”
- loss in uniformity of individual cells and architectural orientation
- pleomorphism
- hyperchromatic
- increased mitoses (nml and abnml)
A
dysplasia
25
Q
Disorders of pigmentation and melanocytes:
A
- freckle
- lentigo
- melanocytic nevus
- dysplastic nevi
- melanoma
26
Q
- most common pigmented lesion of childhood
- 1 mm to several mm, tan-red or light brown macules
- appear after sun exposure
- fade/darken cyclically w/ season changes: hyperpigmentation > increased melanin in basal keratinocytes
A
freckle
(ephelis)
27
Q
- occur in neurofibromatosis
- similar in histology to freckles
- larger, arise independently of sun exposure
- contain aggregated melanosomes (macromelanosomes) in cytoplasm of melanocytes
A
cafe au lait spots
28
Q
- benign localized hyperplasia of melanocytes (no sex or racial predilection, unknown cause)
- initiated in infancy and childhood, occurs at all ages
- mucous membranes and skin
- 5-10 mm, oval, tan-brown macules or patches
- do not darken w/ sun exposure
- histo: linear (nonnested) melanocytic hyperplasia (restricted to cell layer immediately above BM, elongation and thinning of rete ridges common)
A
lentigo
(lentiginous = describe similar proliferations in basal cell layer in melanocytic tumors (i.e. acral lentiginous melanoma, lentigo maligna))
29
Q
- benign, usually acquired by activating mutations in components of RAS or BRAF signaling pathway (limited period of proliferation): p16/INKa inhibitors of CDK4 and CDK6 cause permanent growth arrest (disrupted in melanoma)
- usually < 6 mm, tan-brown, uniformly pigmented
- flat macules or elevated papules, well-defined rounded borders
- different types: junctional nevi, compound nevi, intradermal nevi
- benign histo: superficial (nests, large-round cells, increased melanin), deeper (cords or single cells, smaller cells, decreased pigment), deepest (fusiform, fascicles resembling neural tissue)
- histo helpful in differentiating these lesions from melanoma
A
melanocytic nevus (mole)
30
Q
What are the different types of melanocytic nevi?
A
- junctional nevi: nests at dermoepidermal junction
- compound nevi: nests or cords grow into underlying dermins (nest in epidermis and dermis)
- intradermal nevi: no epidermal nests, usually older lesions
31
Q
- +/- precursors of melanoma, multiple of these may increase risk of melanoma
- familial atypical mole and melanoma syndrome: AD, >50% chance of developing melanoma by 60 y/o, CDKN2A or CDK4 gene
- not all of these types of lesions develop into melanoma, and not all melanoma are derived from these types of lesions
- majority of these lesions are stable and never progress to melanoma
- these lesions often acquire activating mutations in NRAS and BRAF genes
A
dysplastic nevi
32
Q
- familial atypical mole and melanoma syndrome
- autosomal dominant inheritance
- >50% chance of developing melanoma by 60 y/o
- individuals may develop several melanomas at multiple sites
- CDKN2A or CDK4 gene
A
dysplastic nevus syndrome
33
Q
Dysplastic nevus histology:
A
- large than acquired nevi, >5 mm, can be hundreds
- variegated pigmentation, irregular borders of lesions
- enlarged epidermal nests that may coalesce w/ other nests
- lentiginous hyperplasia: single nevus cells replace basal cells along E-D junction
- atypia: Ig nuclei, irregular angulated nuclear contour, hyperchromasia
- lymphocytic infiltration of superficial dermis, melanin incontinence (loose melanin)
- linear fibrosis surrounds epidermal rete ridges
*refer to image*
34
Q
A
35
Q
Describe how dysplatic nevi can progress to melanoma:
A
a) lentiginous melanocytic hyperplasia develops
b) lentiginous junctional nevus develops
c) lentiginous compound nevus w/ abnml architectural and cytologic features (dysplatic nevus)
d) early melanoma (radial growth phase) w/ large dark cells in epidermis
e) advanced melanoma (vertical growth phase) w/ malignant spread into dermis and vessels
36
Q
- most deadly of all skin cancers, strongly linked to acquired mutations caused by exposure to UV radiation in sunlight (DNA damage)
- skin, oropharynx, GI/GU tracts, esophagus, meninges, and uvea of eye
- most cured surgically
- increased incidence: >100,000 cases and >6,800 deaths expected in US in 2020 (lol? it’s 2021 babes)
- despite increased incidence there is decreased death rates in past several years, may reflect effectiveness of immune checkpoint inhibitor therapy
- 10-15% inherited AD w/ variable penetrance
- majority sporadic due to single factor (UV radiation), periodic severe sunburns early in life are an important risk factor
- since melanomas sometimes occur in dark-skinned individuals and at body sites that are not sun-exposed, sunlight is not always an essential predisposing factor, and other environmental factors may also contribute to risk
A
melanoma
37
Q
Risk factors for melanoma:
A
- light complexion, hair, eyes
- hx of blistering subburns
- proximity to the equator
- indoor occupation, outdoor hobies
- fmhx of melanoma or dysplastic nevi
- precursor lesions (congenital or dysplastic nevi)
- xeroderma pigmentosum
38
Q
Most common melanoma sites in white ppl:
A
- upper back (esp men)
- legs (esp women)
39
Q
Most common melanoma sites in blacks and asians:
A
- soles of feet
- mucous membranes
- palms
- nail beds
(among African Americans, avg lifetime risk of melanoma is about 15x lower than in white population)
40
Q
Clinical features of melanoma (ABCDE’s mnemonic):
A
- A: asymmetry
- B: irregular borders
- C: variegated color
- D: increasing diameter
- E: evolution/change over time (esp rapid)
- any pigmented lesion w/ diameter >6mm, any change, itching or pain
41
Q
What are the main drivers/gene mutations in melanoma?
A
- disruption of cell cycle control genes: CDKN2A in 40% AD familial melanomas and 10% sporadic melanomas; encodes 3 tumor suppressor genes (p15, p16, ARF)
- activation of pro-growth signaling pathways: increase RAS and PI-3K/AKT signaling (drug tx target), mutations in BRAF occur in 40-50% of melanomas
- activation of telomerase: TERT in 70% of tumors (most commonly mutated gene in melanoma)
- non-sun-exposed sites: rarely have BRAF or RAS mutations; more likely to have activating mutations in receptor tyrosine kinase, KIT, which sits upstream of both RAS and PI-3K/AKT; PTEN is also silenced in 20% of melanomas arising from non-sun-exposed sites
42
Q
- melanocytic marker
- monoclonal Ab that reacts against an intrinsic antigen known as Pmel-17
- can be detected in only 50-70% of melanomas
- does not react well against intradermal nevi, nml adult melanocytes, spindle cell melanomas, and desmoplastic melanomas
- nonreactive w/ almost all non-melanoma human malignancies, w/ the exception of rare tumors showing evidence of melanogenesis (e.g. pigmented schwannoma, clear cell sarcoma) or tumors a/w tuberous sclerosis complex (angiomyolipoma and lymphangiomyoma)
A
HMB-45
(human melanoma black)
43
Q
How will melanoma cells appear histologically?
A
- usually larger than nml melanocytes or cells found in melanocytic nevi
- have large nuclei w/ irregular contours, chromatin that is clumped at periphery of the nuclear membrane, and prominent red (eosinophilic) nucleoli
44
Q
- horizontal spread of melanoma within the epidermis and superficial dermis
- tumor cells seem to lack the capacity to metastasize
- lentigo maligna: usually an indolent lesion on the face of older men, may remain in this type of growth phase for several decades
- superficial spreading: most common type of melanoma, usually involving sun-exposed skin
- acral/mucosal lentiginous: melanoma that is unrelated to sun-exposure
A
radial growth phase
45
Q
- tumor cells that invade downward into the deeper dermal layers as an expansile mass, after a variable (and unpredictable) period of time following radial phase
- this growth phase is often heralded by the appearance of a nodule and correlates w/ the emergence of a tumor subclone w/ metastatic potential
- unlike melanocytic nevi, “neurotization” is absent
- the probability of metastasis in such lesions correlates w/ the depth of invasion, which by convention is the distance from the superficial epidermal granular cell layer to the deepest intradermal tumor cells, this is known as Breslow thickness
A
vertical growth phase
46
Q
- measurement of the depth of invasion of a melanoma
- distance from the superficial epidermal granular cell layer to the deepest intradermal tumor cells
A
Breslow thickness
47
Q
Factors to consider for melanoma prognosis:
A
- tumor depth (Breslow thickness)
- # of mitoses
- evidence of regression (host immune response)
- ulceration of overlying skin
- presence and # of tumor infiltrating lymphocytes
- gender
- location (central body or extremity)
48
Q
Favorable melanoma prognosis:
A
- thinner tumor depth
- no mitosis (<1 per mm^2)
- brisk tumor infiltrating lymphocyte response
- no regression
- lack of ulceration
49
Q
Poor melanoma prognosis:
A
- deep tumor depth
- mitosis present
- regression present
- ulceration present
- metastases, even micrometastases
- # and degree of LN involvement correlates well w/ overall survival
50
Q
4 common types of benign epithelial tumors:
A
- seborrheic keratoses
- acanthosis nigricans
- fibroepithelial polyp
- epithelial or follicular inclusion cyst (Wen)
51
Q
- occurs typically in middle age or older individual
- arises spontaneously, primarily in trunk but also in extremities, head, and neck
- dermatosis papulosa nigra: people of color, multiple small lesions on face (35% of AA adults)
- round, flat, coin-like, waxy papules, tan-dark brown; velvety or granular suface; pore-like ostia impacted w/ kertain (helps DDx of melanoma); sharply dermacated sheets of small cells resemble nml basal cells; hyperkeratosis, horn cysts (keratin filled cysts)
- activating mutations in fibroblast growth factor receptor-3 (FGFR-3), found in many of these sporadic lesions, thought to drive growth of tumor
- Leser-Trelat sign: paraneoplastic syndrome, sudden appearance of large numbers of Seb K’s, a/w carcinomas of GI tract
A
seborrheic keratoses
52
Q
- subtype of seb k lesion seen in ppl of color
- multiple small lesions on face
- occurs in 35% of AA adults
- Morgan Freeman lesions
A
dermatosis papulosa nigra
53
Q
Seb k mutation:
A
fibroblast growth factor receptor-3 (FGFR-3)
54
Q
- paraneoplastic syndrome
- sudden appearance of large numbers of seb k’s
- a/w carcinomas of GI tract
A
Leser-Trelat sign
55
Q
- cutaneous sign of several underlying benign and malignant conditions
- thickened, hyperpigmented, skin w/ velvet-like texture in flexural/intertriginous areas (two skin surfaces that rub together)
- 80% benign condition that develops gradually during childhood or puberty: AD w/ variable penetrance, a/w obesity/endocrine abnmalities (obesity/diabetes most common), several rare congenital disorders
- remaining cases a/w cancers, commonly GI adenocarcinomas in middle age or older individuals (d/t paraneoplastic process, aka growth factors released from tumors)
- pathogenesis: increased growth factor receptor signaling in skin; familial form (FGFR-3) same as seb k; DM2/hyperinsulinemia believed to increase stimulation of insulin-like growth factor receptor-1 (IGFR-1)
- histo: epidermis and underlying enlarged dermal papillae undulate sharply > numerous repeating peaks/valleys; variable hyperplasia may be seen w/ hyperkeratosis and slight basal cell layer hyperpigmentation (no melanocytic hyperplasia)
A
acanthosis nigricans
56
Q
What cancer is a/w acanthosis nigricans?
A
- most commonly GI adenocarcinomas in middle aged/older individuals
- d/t paraneoplastic process (growth factors released from tumors)
- recall 80% of acanthosis nigricans are benign
57
Q
- aka acrochordon, squamous papilloma, or skin tag
- occurs on head, neck, trunk, face, and intertriginous areas typically in middle aged/elderly
- a/w diabetes, obestity, and intestinal polyposis
- Birt-Hogg-Dubé syndrome: rare, polyps and perifollicular mesenchymal tumors (fibroblasts a/w hair bulb)
- soft, flesh-colored, bad-like tumors often attached by slender stalk
- histo: fibrovascular cores covered by benign squamous epithelium
- torsion > ischemic necrosis > removal
A
fibroepithelial polyp
58
Q
- invagination and cystic expansion of the epidermis or hair follicle
- subject to traumatic rupture, spill keratin into dermis > extensive and painful granulomatous inflammatory response
A
epithelial or follicular inclusion cyst (Wen)
59
Q
- hundreds of neoplasms arising from or showing differentiation toward cutaneous appendages, benign tumors may be confused w/ basal cell carcinoma
- nondescript, flesh-colored, solitary or multiple papules and nodules
- types: Cowden syndrome (trichilemmomas), cylindromas, eccrine poromas, syringomas, sebaceous adenomas, pilomatricomas
A
adnexal (appendage) tumors
60
Q
- a type of adnexal tumor
- inheritance: AD
- chromosomal location: 10q23
- gene/protein: PTEN/PTEN
- multiple trichilemmomas d/t loss of function in PTEN
- increased risk for endometrial cancer, breast cancer, etc
A
Cowden syndrome
61
Q
- a type of adnexal tumor
- ductal differentiation, forehead or scalp, “jigsaw puzzle”
- turban tumor: coalesce, hat-like growth d/t CYLD (tumor suppressor gene)
- CYLD* associated genetic syndromes: familial trichoepithelioma and Brooke-Spiegler
A
cylindroma
62
Q
- a type of adnexal tumor
- occurs on palms and soles, where there is increased sweat glands
A
eccrine poroma
63
Q
- a type of adnexal tumor
- eccrine differentiation, small tan papules, lower eyelids
A
syringoma
64
Q
- a type of adnexal tumor
- Muir-Torre syndrome (internal malignancies)
- hereditary nonpolyposis colorectal carcinoma syndrome (Lynch syndrome)
- DNA mismtach repair proteins
- histo: shows a lobular proliferation of sebocytes with increased peripheral basaloid cells and more mature sebocytes in the central portion that have frothy or bubbly cytoplasm due to the presence of lipid vesicles
A
sebaceous adenoma
65
Q
- inheritance: AD
- chromosomal location: 9q22
- gene/protein: PTCH/PTCH
- mutation in developmental patterning gene, promotes multiple basal cell carcinomas, medulloblastoma, and jaw cysts
A
nevoid basal cell carcinoma syndrome
66
Q
- inheritance: AD
- chromosomal location: 9p21
- CDKN2/p16/INK4; CDKN2/p14/ARF
- (CDKN2/p16/INK4) inhibits CDK4/6 phosphorylation of RB, promoting cell cycle arrest; (CDKN2/p14/ARF) binds MDM2, promoting p53 function; both mutations promote melanoma and pancreatic carcinoma
A
familial melanoma syndrome
67
Q
- inheritance: AD
- chromosomal location: 2p22, 3p21
- gene/protein: (2p22) MSH2/MSH2; (3p21) MLH1/MLH1
- (MSH2) involved in DNA mismatch repair, promotes sebaceous neoplasia; (MLH1) internal malignancy (colon and others)
A
Muir-Torre syndrome
68
Q
- inheritance: AR
- chromosomal location: 9q22 and others
- gene/protein: XPA/XPA and others
- mutation in nucleotide excision repair, promotes melanoma and nonmelanoma skin cancers
A
xeroderma pigmentosum
69
Q
3 most common types of premalignant and malignant epidermal tumors:
A
- actinic keratosis
- squamous cell carcinoma
- basal cell carcinoma
70
Q
- occurs predominantly on sun damaged skin w/ hyperkeratosis (face, arms, dorsum of hands)
- risks: light skin individuals, ionizing radiation exposure, industrial hydrocarbons, arsenic
- given enough time progressively worsens > squamous cell carcinoma
- appearance: <1cm, tan-brown, red or skin colored, rough sandpaper-like consistency; cutaneous horn (excessive keratin prod); dyskeratosis (pink cytoplasm), intracellular bridges, blue-gray elastosis (sun damage), parakeratosis
- actinic cheilitis: similar lesions of the lips
A
actinic keratosis
71
Q
- second most common tumor arising in sun exposed sites in older ppl, (basal cell carcinoma is first)
- M > W, except on lower legs W > M
- <5% metz to regional LN’s; if metz occurs it’s usually deeply invasive into subQ
- pathogenesis: lifetime sun exposure; immunosuppression, chemotox, organ transplantation; epidermodysplasia verruciformis; environmental exposures
- mutations: acquired (TP53 and RAS signaling), xeroderma pigmentosum (XPA gene mutation)
A
squamous cell carcinoma
72
Q
Describe the pathogenesis of SCC:
A
- DNA damage by UV light: incidence proportional to degree of lifetime sun exposure
- immunosuppression, chemotx, organ transplantation: decreases host surveillance, increases risk infection by oncogenic virus esp HPV 5 and 8
- epidermodysplasia verruciformis: AR, HPV implicated, increases risk of cutaneous SCC
- environmental exposures: industrial carcinogens (tars/oils), chronic ulcers and draining osteomyelitis, old burn scars, ingestion of arsenicals, ionizing radiation, tobacco and betel nut chewing (oral cavity)
73
Q
What are the mutations a/w SCC?
A
- acquired defects in precursor actinic keratosis, TP53 mutations high in whites: suggests p53 dysfunction is an early event > improper repair of UV damage, also mutations in RAS signaling and decrease in Notch signaling
- xeroderma pigmentosum: AR, XPA gene, mutation in nucleotide excision repair pathway, inhibiting accurate repair of pyrimidine dimers, increased SCC risk
74
Q
Describe the histology presentation of SCC:
A
- in situ: lesions are sharply defined, red, scaling plaques; atypical (enlarged & hypochromatic) nuclei involve all levels of epidermis
- invasive: lesions are nodular, keratin production (hyperkeratotic scale), may ulcerate; anaplastic cells w/ dyskeratosis (single-cell keratinization)
75
Q
- most common invasive cancer, 1 million cases/yr in US
- slow growing, rarely mets, cured by local excision, <0.5% locally aggressive
- risks: sun exposed sites of light skin elderly adults, immunosuppression, xeroderma pigmentosum
- mutation: unbridled Hedgehog signaling, PTCH gene
- nevoid BCC syndrome = Gorlin syndrome = BC nevus syndrome: AD, mult BCC <20 y/o, medulloblastoma, ovarian fibromas, odontogenic keratocytes, pits of palms/soles
- appearance: pearly papules, telangiectasias, rodent ulcers; basophilic/basaloid cells, hyperchromatic nuclei, peripheral palisading (arranged radially w/ long axes in parallel alignment); artificial clefts separate stroma from tumor
A
basal cell carcinoma
76
Q
Describe the role of PTCH mutation in BCC:
A
- Mutations in PTCH , and less often in SMO, allow SMO to signal without SHH binding and produce constitutive activation of GLI1
- GLI signaling is a characteristic feature of sporadic basal cell carcinomas and tumors associated with the nevoid basal cell carcinoma (Gorlin) syndrome
- Mutations that activate Hedgehog signaling are also prevalent in sporadic basal cell carcinomas
- Loss-of-function PTCH mutations are common, and about one-third of these mutations consist of C→T transitions that are hallmarks of UV damage. This insight has paved the way for the development and clinical implementation of small molecule inhibitors of the Hedgehog pathway
77
Q
2 most common tumors of the dermis:
A
- benign fibrous histiocytoma (dermatofibroma)
- dermatofibrosarcoma protuberans
78
Q
- benign dermal neoplasm of uncertain origin
- most common in adults, esp legs of young to middle aged women
- the lesions may be asx or tender, +/- size change over time, indolent
- dimple sign: lateral pressure on the skin produces a depression
- many individuals have hx of antecendent trauma, the lesions are abnml response to injury/inflammation
- appearance: firm, tan-brown papules, <1cm, become flattened w/ time
- histo: benign spindle-shaped cells, well defined, non-encapsulated mass in mid dermis; overlying epidermal hyperplasia, downward elongation of hyperpigmented rete ridges (pseudoepitheliomatous hyperplasia)
A
benign fibrous histiocytoma (dermatofibroma)
79
Q
- well differentiated fibrosarcoma of the skin
- slow growing, locally aggressive, can recur, rarely mets (more likely if more cytological atypia)
- mutation: translocation collagen 1A1 (COL1A1) and PDGFB, promoting tumor cell growth
- appearance: “protuberant” nodule, usually on the trunk, firm indurated plaque +/- ulceration
- histo: closely packed fibroblasts arranged radially (i.e. blades of a pinwheel = storiform); rare mitoses, overlying epidermis is thinned (opposite of dermatofibroma); honeycomb pattern = deep extension from dermis into subQ fat
A
dermatofibrosarcoma protuberans (DFSP)
80
Q
2 most common tumors of cellular migrants to skin:
A
- mycosis fungoides (cutaneous T-cell lymphoma)
- mastocytosis
81
Q
- CD4+ helper T-cells in the skin
- remains localized for many years, may eventually evolve into systemic lymphoma
- individuals are usually >40 y/o, w/ truncal lesions (also can present on extremities, face, and scalp)
- appearance: scaly, red-brown patches; raised scaling plaques can be confused w/ psoriasis; fungating nodules
- prognosis: determined by % of body surface involved and progression from patch > plaque > nodule; eczema-like lesions = early stages, multiple tumor nodules = systemic spread
- when the lymphocytes move to the blood, this is Sézary syndrome
- tx: topical steroids or UV light for early skin lesions; more aggressive systemic chemo indicated or advanced dz
A
mycoides fungoides
(cutaneous T-cell lymphoma, CTCL)
82
Q
- cutaneous T-cell lymphoma where the T-cells have moved into the blood
- appearance: erythroderma, diffuse erythema and scaling of entire body surface
- histo: markedly folded nuclear membrane, hyperconvoluted or cerebriform contour; band-like aggregates within superficial dermis; Pautrier microabscesses are small clusters of cells in epidermis
A
Sézary syndrome
(it is unknown whether this is an advanced from of mycosis fungoides or a separate dz)
83
Q
- urticaria pigmentosa (cutaneous form in children) accounts for >50% of all cases: multiple, widely distributed lesions, round-oval, red-brown, nonscaling papula and small plaques
- adults: usually multiple cutaneous lesions, ~10% have systemic dz w/ mast cells infiltrating organs
- solitary mastocytoma: usually seen in young children, pink-tan brown nodule, +/- pruritic or blister formation
- histamine and heparin are released when mast cells degranulate
- Darier sign: localized are of dermal edema and erythema (wheal) when skin is rubbed
- dermatographism: area of dermal edema resembling a hive, result of local stroking of skin w/ pointed instrument
- systemic sx: pruritus/flushing; triggered by certain foods, temp changes, alcohol, drugs (morphine, codeine, aspirin); rhinorrhea; rarely GI or nasal bleeding (anticoagulant effect of heparin); bone pain (mast cell infiltration or osteoporosis); osteoporosis in premenopausal women/men d/t excessive histamine release in BM
- mutation: point mutations in KIT receptor tyrosine kinase > mast cell growth/survival
- histo: spindle-shaped and stellate mast cells, fibrosis, edema, few eosinophils; metachromatic stain (toluidine blue or Giemsa), IHC for mast cell tryptase and KIT
A
mastocytoma
84
Q
- impaired epidermal maturation leading to chronic keratin buildup (hyperkeratosis) that results in clinically fish-like scales
- defective desquamation leads to retention of abnormally formed scale
- buildup of compacted stratum corneum, a/w loss of normal basketweave pattern, generally no inflammation present
- there are multiple different forms of this condition w/ differing inheritance patterns
A
ichthyosis
85
Q
What are the different forms of ichthyosis?
A
- ichthyosis vulgaris: AD or acquired
- congenital ichthyosiform erythroderma: AR
- lamellar ichthyosis: AR
- X-linked ichthyosis
(most ichthyoses become apparent either at or around time of birth; acquired variants also exist; one such variant (ichthyosiss vulgaris) may be a/w lymphoid and visceral malignancies)
86
Q
3 most common types of acute inflammatory dermatoses:
A
- urticaria
- acute eczematous dermatitis
- erythema multiforme
87
Q
- acute lesions last from days to weeks and are characterized by inflammatory infiltrates (usually composed of lymphocytes and macrophages rather than neutrophils), edema and variable degrees of epidermal, vascular, or subQ injury
- chronic lesions persist for months to years and are often a/w changes in epidermal growth (atrophy or hyperplasia) or dermal fibrosis
A
acute inflammatory dermatoses
88
Q
- localized mast cell degranulation > dermal microvascular hyperpermeability (antigen-induced release of vasoactive mediators from mast cells)
- wheals: pruritic edematous plaques
- angioedema: edema of the deeper dermis and subQ fat
- occurs predominantly in 20-40 y/o, usually <24 hrs, sites exposed to pressure (trunk, distal extremities, ears), persistent episodes may herald an underlying dz (e.g. collagen vascular disorders, Hodgkin lymphoma), but usually no underlying case found
- appearance: small, pruritic papules to large edematous plaques; individual lesions may coalesce to form annular, linear, or arciform configurations
- histo: sparse superficial perivenular infiltrate of mononuclear cells and rare neutrophils, +/- eosinophils; collagen bundes more widely spaced than nml skin d/t edema; dermal lymphatics may be dilated d/t absorption of edema fluid
A
urticaria (hives)
89
Q
What are the various forms of urticaria classified based on their dependence of IgE Ab’s and mast cells?
A
- mast cell-dependent, IgE-dependent: exposure to antigens (pollens, foods, drugs, insect venom) and is example of localized immediate hypersensitivity rxn (type I) triggered by binding of antigen to IgE Ab’s that are attached to mast cells through Fc receptors
- mast cell-dependent, IgE-independent: results from substances that directly incite degranulation of mast cells, such as opiates, certain antibiotics, and radiographic contrast media
- mast cell-independent, IgE-independent: triggered by local factors that increase vasc permeability; one form is initiated by exposure to chemicals/drugs, such as aspirin, that inhibit cyclooxygenase and arachidonic acid prod; second form is hereditary angioneurotic edema caused by inherited def of C1 inhibitor that results in excessive activation of early components of complement system and prod of vasoactive mediators
90
Q
- literally means “to boil over”, one of the most common skin conditions
- T-cell mediated inflammatory rxn (type IV hypersensitivity)
- external application of Ag (poison ivy) or ingested food/drug (5 different types)
- appearance: red, papulovesicular, oozing/crusted (impetiginization) lesions; if persists, can develop acanthosis and hyperkeratosis > raised scaling plaques; spongiosis (edema in intracellular spaces, splaying them apart, particularly in stratum spinosum)
- tx: no cure, palliative w/ topical steroids
A
acute eczematous dermatitis
91
Q
What are the 5 subtypes of acute eczematous dermatitis?
A
- allergic contact dermatitis
- atopic dermatitis
- drug-related eczematous dermatitis
- photoeczematous dermatitis
- primary irritant dermatitis
- the pattern/composition of infiltrate (on histo) may provide clues to underlying cause
- eczema resulting from certain ingested drugs is marked by perivascular infiltrates that often contain eosinophils in the superficial and deep dermis
- eczema resulting from contact antigens tends to prod a mononuclear inflammatory rxn w/o eosinophils that preferentially affects the superficial dermis
92
Q
- uncommon, self-limited hypersensitivity rxn to certain infections/drugs (infections, drugs, cancer, collagen vascular dz)
- keratinocyte injury mediated CD8+ cytotoxic T-lymphocytes: CD8+ cytotoxic T-cells in center of lesion, CD4+ helper T-cells and Langerhans cells in the periphery; similar to acute graft vs host dz, skin allograft rejection, and fixed drug eruptions
- diverse array of lesions: targetoid lesions, interface dermatitis, Stevens-Johnson condition, toxic epidermal necrolysis
A
erythema multiforme
93
Q
Infections a/w erythema multiforme:
A
- herpes simplex
- mycoplasm
- histoplasmosis
- coccidiodomycosis
- typhoid
- leprosy
94
Q
Drugs a/w erythema multiforme:
A
- sulfonamides
- PCN
- barbiturates
- salicylates
- hydantoins
- antimalarials
95
Q
Cancers a/w erythema multiforme:
A
- carcinomas
- lymphomas
96
Q
Collagen vascular dz’s a/w erythema multiforme:
A
- SLE
- dermatomyositis
- polyarteritis nodosa
97
Q
Diverse lesions a/w erythema multiforme:
A
- targetoid lesions, macules, papules, vesicles, and bullae
- interface dermatitis: dermal edema, lymphocyte infiltration along dermoepidermal junction, a/w dermal edema and degenerating keratinocytes
- Stevens-Johnson: predominantly in children, extensive skin involvement plus oral mucosa, conjunctiva, urethra/genital/perianal areas, secondary infections lead to life-threatening sepsis
- toxic epidermal necrolysis: diffuse necrosis/sloughing of cutaneous and mucosal epithelia, resembles extensive burns
98
Q
3 most common types of chronic inflammatory dermatoses:
A
- psoriasis
- seborrheic dermatitis
- lichen planus
99
Q
- chronic inflammatory dermatosis, autoimmune basis
- 1-2% ppl in US, ~15% develop assoc arthritis; may also be a/w myopathy, enteropathy, and AIDS
- Koebner phenomenon: induced psoriatic lesions in susceptible pts by local trauma, starts self-perpetuating local inflammatory response
- appearance/histo: pink to salmon colored plaque covered by loosely adherent silver scale present on elbows, knees, scalp, lumbosacral region, intergluteal clef, and glans penis; nail changes; MKD acanthosis; Munro microabscesses; Auspitz sign; erythroderma
- tx: excellent clinical responses are observed in patients tx w/ TNF & IL-17 inhibitors
A
psoriasis
100
Q
- condition where local trauma induces psoriatic or lichen planus lesions in susceptible patients
- starts a self-perpetuating local inflammatory reponse
A
Koebner phenomenon
101
Q
Describe the pathogenesis of psoriasis:
A
- believed to be the product of environmental and genetic factors, including particular HLA gene variants
- culprit antigens remain elusive, but it appears that sensitized populations of CD4+ Th1 and Th17 cells and activated CD8+ cytotoxic effector T cells enter the skin and accumulate in the epidermis
- these T cells may create an abnormal microenvironment by stimulating the secretion of cytokines and growth factors that induce keratinocyte proliferation, resulting in the characteristic lesions
- interactions between CD4+ T cells, CD8+ T cells, dendritic cells, and keratinocytes give rise to a cytokine “soup” dominated by Th1-type and Th17-type cytokines such as IL-12, interferon-γ, tumor necrosis factor (TNF), and IL-17
- the importance of these factors is highlighted by the generally excellent clinical responses that are observed in patients treated with TNF inhibitors
102
Q
Describe psoriasis gross appearance and histo:
A
appearance
- pink to salmon colored plaque covered by loosely adherent silver scale
- early lesions: dominated by inflammation, marked by presence of small pustules/erythema
- chronic lesions: erythematous and covered by characteristic silver-white scale
- present on elbows, knees, scalp, lumbosacral region, intergluteal cleft, and glans penis
- 30% w/ nail changes: pitting, dimpling, yellow-brown discoloration (oil slick), oncolysis (separation of nail plate from underlying nail bed), thickening, crumbling
- erythroderma: psoriasis one cause of total body erythema/scaling
- Auspitz sign: mult, minute, bleeding points when scale lifted from plaque
histo
- Mkd acanthosis, regular downward elongation of rete ridges “test tubes in rack”
- mitoses above basal cell layer, stratum granulosum thin or absent, extensive parakeratotic scale
- Munro microabscesses: small PMN (polymorphonuclear leukocytes) aggregates in parakeratotic stratum corneum
103
Q
- occurs in 5% of population, more common than psoriasis
- occurs in bodily regions w/ increased sebaceous glands: scalp, forehead, external auditory canal, retroauricular area, nasolabial folds, presternal area
- inflammation of epidermis, not a dz of sebaceous gland
- increased seb prod in response to androgens is a possible contributory factor
- Parkinson’s dz: increased sebum prod secondary to dopamine def, leads to this condition, tx is levodopa which decreases oil prod
- a severe form of this condition that is difficult to tx was once common in individuals w/ HIV w/ low CD4 counts, but its incidence has fallen w/ advent of antiviral therapy
A
seborrheic dermatitis
104
Q
Describe the gross appearance and histo of seborrheic dermatitis:
A
appearance
- individual lesions are macules and papules on an erythematous-yellow, often greay base, typically a/w extensive scaling/crusting
- fissure may also be present, partically behind the ears
- dandruff is common clinical expression of seborrheic derm of scalp
histo
- mounds of parakeratosis containing neutrophils and serum are present at ostia of hair follicles = follicular lipping
105
Q
What neurologic dz is a/w development of seborrheic dermatitis?
A
- Parkinson’s dz
- increases sebum prod secondary to dopamine def, leading to seborrheic dermatitis
- tx: levodopa which decreases oil
106
Q
- 6 P’s: pruritic, purple, polygonal, planar, papules, plaques
- self limited dz of skin/mucosa, resolving spontaneously in 1-2 yrs
- postinflammatory hyperpigmentation left after resolution
- squamous cell carcinoma noted to occur in chronic mucosal and paramucosal lesions of this kind (possibly carcinogenesis in setting of chronic inflammation)
- Koebner phenomenon: also seen in psoriasis
- appearance: itchy violaceous, flat-topped papules that may coalesce, Wickham striae; lesions may be dark brown in darker individuals; 70% of cases have white oral mucosal lesions
- histo: interface dermatitis, sawtoothing, Civatte bodies
A
lichen planus
107
Q
Describe the appearance and histo of lichen planus:
A
appearance
- itchy violaceous, flat-topped papules, that may coalesce
- Wickham striae: pink-purple polygonal papules highlighted w/ lacelike pattern of white lines, created by areas of hypergranulosis
- darker individuals may develop lesions w/ dark brown color d/t release of melanin into dermis as basal cell layer is destroyed
- multiple, symmetrical lesions esp on extremities, wrist, elbows, and glans penis
- 70% of cases have oral mucosal lesions w/ white, reticulated or net-like appearance
histo
- dense cutaneous infiltrate of lymphs, along dermoepidermal junct (interface dermatitis)
- sawtoothing: angulated zigzag contour of dermoepidermal interface
- colloid or Civatte bodies: anucleate, necrotic basal cells incorporated into inflamed papillary dermis
108
Q
What skin cancer is a/w lichen planus?
A
squamous cell carcinoma
109
Q
What are the different types of inflammatory and noninflammatory blistering diseases?
A
inflammatory
- pemphigus
- bullous pemphigoid
- dermatitis herpetiformis
noninflammatory
- epidermolysis bullosa and porphyria
*blistering (bullous) dz’s prod dramatic lesions which can be fatal if untx*
*blisters occur at different levels of the skin, histologic assessment is essential for accurate dz*
110
Q
- type of inflammatory blistering/bullous dz
- IgG autoantibodies dissolution of intracellular attachments within the epidermis and mucosal epithelium lead to these blisters, may be fatal w/o tx
- net-like pattern of intercellular IgG deposits: vulgaris = all levels; foliaceus = superficial
- occurs predominantly in 40-60 y/o’s, equally affecting sexes
- histo: acantholysis (dissolution of intercellular bridges connecting squamous epithelial cells, these cells become rounded)
- types: vulgaris (most common), vegetans, foliaceus, erythromatosus, paraneoplastic
- tx: immunosuppressives
A
pemphigus
111
Q
- most common type of pemphigus, >80% of cases worldwide
- occurs in mucosa and skin of scalp, face, axilla, groin, trunk and pressure points
- superficial vesicles rupture easily > shallow erosions w/ dried serum/crust
- histo: deposition of immunoglobulin along the plasma membranes of keratinocytes in a reticular or fishnet-like pattern accompanied by suprabasalar loss of cell-to-cell adhesion (acantholysis); single layer of intact basal cells that forms the blister base has been likened to a row of tombstones
A
pemphigus vulgaris
112
Q
- subtype of pemphigus
- rare
- large moist verrucous (wart-like) vegetating plaques studded w/ pustules
- occurs in groin, axilla, and flexural surfaces
A
pemphigus vegetans
113
Q
- benign subtype of pemphigus
- endemic to Brazil
- occurs on scalp, face, chest, back
- erythema and crusting lesions; delicate superficial (subcorneal) blisters are much less erosive than those seen in pemphigus vulgaris
- histo: subcorneal separation of the epithelium is seen; the immunoglobulin deposits and acantholysis are more superficial
A
pemphigus foliaceus
114
Q
- subtype of pemphigus that is a localized, less severe form of foliaceous
- occurs on the malar area of the face in a SLE-like fashion
A
pemphigus erythromatosus
115
Q
- a subtype of pemphigus
- a/w malignances: NHL, lymphoid neoplasms
A
paraneoplastic pemphigus
116
Q
- a type of inflammatory blistering/bullous dz
- occurs in elderly on inner aspect of thighs, flexor surfaces of forearms, axilla, groin, and lower abd; 10-15% are oral lesions
- antibody (IgG) linear deposits at dermoepidermal junction; BPAG’s (antigens a/w dz, components of demidesmosomes)
- do not rupture easily d/t subepidermal nature (nonacantholytic blisters)
- ulcers form when blisters rupture, however they usually heal w/o scarring unless they become secondarily infected
A
bullous pemphigoid
117
Q
- type of inflammatory blistering/bullous dz
- urticarial and grouped vesicles that typically occur in men in their 30-40’s
- bilateral, symmetric, grouped lesions on extensor surfaces of elbows, knees, upper back, and buttocks
- a/w celiac dz d/t IgA Ab’s to gluten (Ab’s cross react w/ reticulin > subepidermal blister)
- histo: granular deposits of IgA at the tips of dermal papillae, a/w acccumulation of neutrophils (microabscesses) at tips of dermal papillae
- tx: some individuals respond to gluten-free diet
A
dermatitis herpetiformis
118
Q
- a type of non-inflammatory blistering/bullous dz
- groups of disorders that are inherited defects in structural proteins
- blisters at sites of pressure, rubbing, or trauma at (or soon after) birth
- electron microscopy differentiates the various types
A
epidermolysis bullosa
119
Q
- a type of non-inflammatory blistering/bullous dz
- group of inborn or acquired disturbances in porphyrin metabolism
- porphyrins: pigments normally present in Hgb, myoglobin, and cytochromes
- sx: urticaria and subepidermal vesicles a/w scarring, exacerbated by sunlight
- histo: rigid dermal papillae at the base that contain abnml superficial vessels; subepidermal vesicles w/ adjacent dermis that contains vessels w/ walls that are thickened by glassy deposits of serum proteins (Ig’s)
A
porphyria
120
Q
2 most common disorders of epidermal appendages:
A
- acne vulgaris
- rosacea
121
Q
- occurs in middle aged and older individuals, 3% of US, predominantly women
- 4 stages: flushing, persistent erythema/telangiectasia, pustules/papules, rhinophyma (permanent thickening of nasal skin)
- a/w high cutaneous levels of antimicrobial peptide cathelicidin
- several microbial triggers have been proposed, but none are proven
A
rosacea
122
Q
4 stages of rosacea:
A
- flushing
- persistent erythema and telangiectasia
- pustules and papules
- rhinophyma: permanent thickening of nasal skin; confluent erythematous papules and prominent follicles
123
Q
Elevated levels of what antimicrobial peptide is a/w rosacea?
A
cathelicidin
124
Q
- virtually universal in middle-late teens, affects genders equally, more severe dz in men
- occurs in all races, however Asians usually have milder dz
- induced/exacerbated by: corticosteroids, adrenocorticotropic hormone, testosterone, gonadotropins, contraceptives, trimethadione, iodides, bromides; occupational exposure (heaving clothing, cosmetics, tropical climate (blocks sebaceous glands))
- open comedones: central black (oxidation of melanin, not dirt) keratin plug
- closed comedones: keratin plug trapped beneath epidermal surface, potential for follicular rupture and inflammation
- multifactorial dz due to keratin block, puberty, bacteria (Propionibacterium acnes), and inflammation
- acne conglobate: severe variant, sinus tract formation and dermal scarring
- tx: abx for P. acnes, 13-cis-retinoic acid (isoretinoin) for antisebaceous action
A
acne vulgaris
125
Q
What factors induce/exacerbate acne?
A
hormonal
- corticosteroids
- adrenocorticotropic hormone
- testosterone
- gonadotropins
- contraceptives
- trimethadione
- iodides
- bromides
occupational exposure
- heaving clothing
- cosmetics
- tropical climate (blocks sebaceous glands)
126
Q
Why is development/progression of acne vulgaris multifactorial?
A
- keratin plug blocks outflow of sebum
- hypertrophy of sebaceous glands (puberty)
- Propionibacterium acnes colonizes hair follicles
- secondary inflammation of follicles occurs
127
Q
How is acne tx?
A
- P. acnes: abx
- antisebaceous action: 13-cis-retinoic acid (isoretinoin)
128
Q
- a subtype of panniculitis
- most common form of subacute presentation
- poorly defined, exquisitely tender erythematous plaques and nodules, more readily palpated (ropy) than seen
- over weeks, lesions flatten and become bruise-like, no residual scars
- considered delayed hypersensitivity rxn to microbial or drug related antigens: infectious β-hemolytic streptococcal infection, TB, or less commonly coccidiodomycosis, histoplasmosis, and leprosy; drugs including sulfonamides and oral contraceptives; and inflammatory dz’s including sarcoidosis, inflammatory bowel dz, and certain malignant neoplasms
- histo: in early lesions, the CT septae are widened by edema, fibrin exudation, and neutrophilic infiltration; later, infiltration by lymphocytes, histiocytes, multinucleated giant cells, and eosinophils is a/w septal fibrosis
A
erythema nodosum
129
Q
What are the microbes or drugs that can induce erythema nodosum?
A
- microbes: infectious β-hemolytic streptococcal infection, TB, or less commonly coccidiodomycosis, histoplasmosis, and leprosy
- drugs: sulfonamides and oral contraceptives
- inflammatory dz’s: sarcoidosis, inflammatory bowel dz, and certain malignant neoplasms
130
Q
- uncommon type of panniculitis
- occurs in adolescents and menopausal females
- once considered hypersensitivity rxn to TB, but not a/w any dz currently
- sx: primary vasculitis of deep vessels suppling fat lobules of subQ (necrotizing vasculitis) > fat (caseous) necrosis and inflammation > erythematous, slightly tender nodule that usually ulcerates
A
erythema induratum
131
Q
- relapsing febrile nodular panniculitis
- rare form of lobular, nonvasculitis panniculitis in children and adults
- crops of erythematous plaques or nodules, predominantly over lower extremities
- created by deep-seeded foci of inflammation containing aggregates of foamy macrophages w/ lymphocytes, neutrophils, and giant cells
A
Weber-Christian disease
132
Q
form of secondary panniculitis caused by self-inflicted trauma or injection of foreign/toxic substances
A
factitial panniculitis
133
Q
T-cells move to fat lobules, producing fat necrosis and superimposed inflammation that mimics panniculitis
A
T-cell lymphoma
134
Q
autoimmune dz that may occasionally cause inflammation of subcutis and associated panniculitis
A
systemic lupus erythematosus
135
Q
- squamoproliferative lesions caused by HPV infection
- anogenital: HPV types 6 and 11
- HPV 16: a/w in site SCC of genitalia and bowenoid papulosis (genital lesions of young adults w/ histologic appearance of carcinoma in situ, but usually regresses spontaeously)
- HPV 5 and 8: related to SCC, esp individuals w/ epidermodysplasia verruciformis, develop mult flat warts w/ some that progress to carcinoma
- children/adolescents: direct contact or autoinnoculation; generally self-limited, regressing spontanesouly in 6mo-2yrs
A
verrucae (warts)
136
Q
HPV types for anogenital warts:
A
HPV types 6 and 11
137
Q
HPV type a/w in situ SCC of genitalia and bowenoid papulosis (genital lesions of young adults w/ histologic appearance of carcinoma in situ, but usually regresses spontaeously)
A
HPV 16
138
Q
HPV types related to SCC, esp individuals w/ epidermodysplasia verruciformis, develop mult flat warts w/ some that progress to carcinoma
A
HPV types 5 and 8
139
Q
Why is it believed HPV causes warts?
A
- HPVs that are a/w a high risk of cancer produce E6 proteins that abolish p53 function
- the E6 proteins of low-risk HPVs interfere with Notch signaling, which is required for the normal maturation of keratinocytes; this effect likely contributes to the epidermal hyperplasia that characterizes warts
140
Q
Histology of verrucae (warts):
A
lesions show papillomatous epidermal hyperplasia and cytopathic alterations, including nuclear pallor and prominent keratohyaline granules
141
Q
- common, self-limited poxvirus infection (virus is brick shaped, w/ dumbbell shaped DNA core)
- spread through direct contact, within children and young adults
- occurs in trunk and anogenital regions
- appearance: firm, pruritic, pink-skin colored umbilicated papules; curd-like material can be expressed from umbilication (smear shows molluscum bodies)
- histo: (Giemsa or H&E) molluscum bodies = ellipsoid, homogenous, cytoplasmic inclusions
A
molluscum contagiosum
142
Q
- common superficial bacterial infection of skin
- highly contagious, occurs in otherwise healthy children and occasionally in adults w/ poor health
- occurs on exposed skin of face/hands
- Staphylococcus aureus > toxin causing epidermal injury (toxin cleaves desmoglein 1)
- appearance: erythematous macule initially, then mult small pustules which break > shallow erosions > honey colored crust (drying serum, if not removed new lesions form around periphery and extensive epidermal damage may occur)
- two forms: contagiosa and bullosa (differ based on size of pustules)
- tx: eliminate bacteria and lesion heals
A
impetigo
143
Q
- usually occurs in children, rarely seen in infants & adults
- dermatophytosis of the scalp; asymptomatic, often hairless patches of skin with mild erythema, crust formation, and scaling
A
tinea capitis
144
Q
dermatophyte infection of the beard; adult men; relatively uncommon disorder
A
tinea barbae
145
Q
- common superficial fungal infection of the body surface; occurs in all ages, but esp children
- predisposing factors: excessive heat and humidity, exposure to infected animals, and chronic dermatophytosis of the feet or nails
- most common appearance: expanding, round, slightly erythematous plaque with elevated scaling border
- histo: routine histo shows mild eczematous (spongiotic) dermatitis and focal neutrophilic abscesses, periodic acid–Schiff stain (PAS) reveals deep red hyphae within the stratum corneum
A
tinea corporis
146
Q
- occurs in inguinal areas of obese men during warm weather
- heat, friction, and maceration all predispose to its development
- infection usually first appears on the upper inner thighs as moist, red patches with raised scaly borders
A
tinea cruris
147
Q
- affects 30-40% of the population at some time in their lives
- diffuse erythema and scaling, often initially localized to the web spaces
- most of reaction due to bacterial superinfection and is not directly related to the primary dermatophytosis
- spread to (or primary infection of the nails) is referred to as onychomycosis > discoloration, thickening, & deformity of the nail plate
A
tinea pedis
148
Q
- occurs on upper trunk, highly distinctive in appearance
- caused by Malassezia furfur (a yeast, not a dermatophyte)
- the lesions consist of groups of macules of varied size and color with a fine peripheral scale
A
tinea versicolor
149
Q
*FYI*
Five potentially life-threatening disorders that have skin rash as a primary feature:
A
- Pemphigus vulgaris (PV)
- Stevens-Johnson syndrome (SJS)
- Toxic epidermal necrolysis (TEN)
- Toxic shock syndrome (TSS)
- Staphylococcal scalded skin syndrome (SSS)
*These diseases tend to have certain signs and symptoms (see previous slide) and generally affect the entire body, or most of it – the skin and mucous membranes. Blistering or vesicobullous lesions may be (and is in PV) a feature*
*The above is certainly not a definitive list. Consider other conditions, e.g. meningococcemia that typically is life threatening, or Rocky Mountain Spotted Fever that can be severe and deadly in certain cases*
