Dermatology

Question 1

Childhood pigmented lesion 1-10mm. tan-brown macules that fades and is recurring dependent on sun-exposure. melanocytes density is normal. hyper pigmentation is based on overproduction of melanin what is this?

Answer 1

freckles (ephelis)

Question 2

cafe au lait spots larger than freckles, independent of sun-exposure and contain aggregated melanosomes) what is the classic condition that this could be?

Answer 2

neurofibromatosis type 1

Question 3

benign hyper pigmented macules (tan-brown) in infancy and children and involves mucous membrane independent of sun-exposure (does not get darker) characterized by hyper pigmented, non-basal melanocytes hyperplasia (restricted to cell layer immediately above the basement membrane) with rete ridges and thinning

what is this?

Answer 3

lentigo

lentiginous = describe similar proliferation just in the basal layer in melanocytic tumors

Question 4

well-demarcated, uniformly round tan-brown papules <6mm acquired mutation of BRAF, NRASm p16/INK4a (the RAS pathway)

three categories

junction nevi

compound nevi

dermal nevi

what condition am I describing and describe the three categories describe neurotization

the moles starts out flat, but then the papules with age

Answer 4

melanocytic nevus (nevi, mole)

junction nevi-nest of nevus cells at dermoepidemeral junction -earliest lesions

compound nevi- nest or cords of melanocytes that extend into the underlying dermis

intradermal nevi- the epidermal component is lost

neurotization- nevi cells that enter the dermis can mature (become smaller, nonpigmented and resembling neural tissue)

Question 5

moles that are larger than acquired moles (>5mm) flat macules to slight raise plaques with variegated pigmentation and irregular borders that occur in sun-exposed as well as protected skin can be in the hundreds (what is this syndrome called)

pathogenesis of the syndrome are mutation of the CDKN2A (normally encode p16 or CDK4) acquired mutation NRAS, BRAF, and TERT over-expression most are compound nevi with enlarged and fused nest of nevus cells, lentiginous melanocytes hyperplasia, linear papillary dermal fibrosis surround the rete ridges and pigment incontinence (release of melanin from dead melanocytes)

typically have shouldering (typical junction nevi extend 2 rete ridges from the nevi if it extends >2 rete ridges than we worry about dysplastic/melanoma

is there a risk for melanomas?

Answer 5

dysplasic nevi

the syndrome is dysplastic nevus syndrome half of the patients with this syndrome develop melanoma by age 60, but most are clinically stable and sporadic with low risk of malignant transformation

Question 6

malignant tumor most commonly arises from skin.

pathogenesis- sun-exposure, light skin dysplastic nevi syndrome, mutations that increase RAS and PI3K/AKT pathway (NRAS and BRAF),

mutations that reduces retinoblastoma protein activities or CDK inhibitors (CDKN2A, p16/INK2a, p14/ARF), TERT mutation

morphology: large cells with expanded irregular nuclei containing peripheral clumped chromatin and prominent eosinophilic nucleoli what is this lesion?

progress in radial pattern (describe it)

• lentigo meligna-indolent lesion on the face that may not progress for years
• superficial spreading- most common form of melanoma in sun-exposed spots
• acral ( pertaining to peripheral body parts, such as toes and fingers. Acral melanoma is a type of skin cancer that occurs on fingers, palms, soles, and nail beds. Acral distribution of a dermatosis means it affects distal portions of limbs (hand, foot) and head (ears, nose)) and mucosal lentiginous melanoma unrelated to skin exposure

vertical growth (describe it)

what are the favorable prognostic factors? what are the ABCDE signs?

Answer 6

melanoma (majority are sporadic)

radial growth is non-metastatic horizontal growth at the dermoepidermal

junction vertical growth is metastatic potential growth invading the dermis with the probability of metastasis correlates with depth of invasion. breslow thickness is measured from the epidermal granular layer to the deepest intradermal tumor cells

favorable prognostic factors

• breslow thickness (thinner is better)
• number of mitoses (<1 per mm2) evidence of regression (absent)
• ulceration (absent)
• presence of tumbor infiltrating lymphocytes (many)
• gender (female)
• location (extremities)
• sentinel node micrometastasis (absent)

ABCDE -asymmetries, irregular borders, variegated color, increasing diameter, and evolution over time

xeroderma pigmentosum (nucleotide excision repair is mutated)

neurotization is absent unlike in melanocyte nevi

Question 7

gross: lesion are uniform, waxy, tan-brown, velvety or granular, round plaques most commonly on the trunk.

if a smaller facial lesion in non-whites are present then that is called dermatosis papulosa nigra

microscopic: lesion are sharply demarcated with exophytic with hyperplasia of pigmented basaloid cells and hyperkeratosis; keratin-filled horn cysts are common large number indicate paraneoplastic syndrome (leser-Trelat sign) due to elaboration of TNF alpha and FGFR3 (found in many seb K and drive growth factors)

also contains pore-like ostia impacted with keratin (differentiate from melanoma)

what is this condition?

Answer 7

seborrheic keratoses

Question 8

thick lesion with velvety hyperpigmented plaques in flexural areas

benign type arises in childhood-puberty, autosomal dominant, associated with FGFR3 mutation, obesity or diabetes

malignant type: middle age-older individuals associated with adenocarcinoma morphology: hyperkeratosis with prominent rete ridges and basal hyperpigmentation (without melanocyte hyperplasia)

what is this condition?

Answer 8

acanthosis nigricans

Question 9

known as acrohordon, squamous papilloma or skin tag found on neck, trunk, face, or intertriginous zones in middle age-older individuals described as soft fresh-colored tumors attached to slender fibrovascular stalk covered by benign epidermis associated with pregnancy, diabetes, or intestinal polyposis

what is the condition?

Answer 9

fibroepithelial polyp

Question 10

cyst commonly presented as well-circumscribed firm, subcutaneous nodules rupture can spill keratin into the dermis, leading often to painful granulomatous inflammation

what is this condition?

Answer 10

epithelial cyst (Wen)

Question 11

lesion on the scalp and forehead composing of islands of basaloid cells and apocrine or eccrine differentiation to form a hat-like growths (tubans tumor), mutation of CYLD tumor suppressor “jagsaw puzzle” C

multiple small tan papules near the lower eyelids composed of basaloid epithelium with eccrine differentiation S

lobar proliferation of sebocytes with frothy lipid filled cytoplasm associated with muir-Torre syndrome (subset of HNPCC), linked to germline deficit in DNA mismatch S

proliferation of basaloid cells that form hair follicles-like structures T

proliferation of basaloid cells that show hair-like differentiation associated with mutation of CTNNB1 gene encoding beta-catenin P

apocrine carcinomas occurring inthe axilla and scalp and exhibit ducal differentiation showing prominent apocrine secretion A

palm and sole where sweat glands are numerous E

Answer 11

cylindroma

syringoma

sebaceous adenomas

trichoepitheliomas

pilomatrixomas

apocrine carcinoma

eccrine poroma

Question 12

premalignant dysplastic lesion associated with chronic sun-exposure in light-skinned individuals

caused by sun exposure, ionizing radiation, industrial hydrocarbon, arensic

gross: <1cm tan-brown, red, flesh colored with rough sandpaper-like consistency that can form cutaneous horns
microscopic: hyperkeratosis and parakeratosis (parakeratosis have retained nuclei). dermis exhibits thickened blue-gray elastic (elastosis) due to aberrant synthesis by sun damaged fibroblasts

eosinophilic (pink cytoplasm) due to dyskeratosis, intracellular bridges

can progress to SCC if given enough time

can get actinic cheilitis

what is the condition?

Answer 12

actinic keratosis

Question 13

second most common tumor of sun-exposed skin of older individuals UV radiation inducing DNA damage and dampening the immune function of langerhan cells this increase of infection to HPV subtype 5 and 8 acquired or germline (xeroderma pigmentosum) p53 mutation allows rapid accumulation of mutation that increase RAS signaling or that decrease Notch signaling

gross: well-demarcated, red, scaling plaques; invasive lesions are nodular and prone to ulceration
microscopic: full-thickness epidermal atypia invasive tumors vary from well differentiated (with prominent keratinization) to highly anaplastic with necrosis

risk factor: industrial carcinogens (tars/oil) chronic ulcers and draining osteomyelitis, burn scar, ingestion of arsenicals, ionizing radiation, tobacco and betel nut

in situ: lesion appear as sharply defined, red, scaling plaques (enlarged & hyperchromatic nuclei)

invasive: lesions are nodular, keratin production (hyperkeratotic scale) may ulcerate
- anaplastic cells, dyskeratosis (single-cell keratinization)

Answer 13

squamous cell carcinoma

Question 14

most common invasive human cancer of the skin PTCH absence or PTCH and SMO mutation leading to SMO activation and development of BCC

slow growing , sun-exposed sites of lightly pigmented elderly adults, immunosuppression, xeroderma pigmentosum

most BCC mutation resulting in unfettered hedgehog signaling

gross: pearly papules with prominent telangiectatic (rodent ulcers), peripheral palisading
microscopic: monotonous basal cell proliferation either as multifocal superficial growths over large area of skin or as nodules extending deeply into the dermis

gorlin syndrom=nevoid basal cell carcinoma syndrome

-AD, mult BCC <20yo + medulloblastoma, ovarian fibromas, dontogenic keratocyts, pits in palms and soles

Answer 14

Basal cell carcinoma

Question 15

group of dermal fibroblasts and histiocytes occurring in adults and frequently in the legs of young women.

benign

gross: firm tan-brown occasionally tender papules, become flat over time and inward dimpling with lateral compression (dimple sign), hx of antecedent trauma due to abn response to injury

composed at least patially of factor XIIIa-positive dermal dendritic cells

microscopic: spindle-shaped fibroblast with well-defined middermal nonencapsulated mass many cases have overlying epidermal hyperplasia

Answer 15

benign fibrous histiocytoma

Question 16

1. cutaneous T-cell lymphoma (CTCL) -generalized LAD in individual over 40 and remain localized for year before evolving into systemic lymphoma

2. if there is seeding of the blood by malignant T cells accompanied by diffuse erythema and scaling (erythroderma) that is this condition called?

the proliferating cells are CD4+ with clonal T cell receptor gene rearrangements and CLA is responsible for cutaneous homing behavior

gross: Mycosis Funoides have early lesion resemble eczema in the trunk (also extremities, face, scalp), progressive scaly red-brown patches, scaling plaques (similar to psoriasis) or fungating nodules over various body surfaces correlate with systemic spread

microscopic: hall mark of the original condition is sezary cells-malignant CD4 + (T-helper) markedly folded nuclear membrane, hyperconvoluted or cerebriform- sezary cells

-pautrier microabscesses- small clusters of cells in epidermis could be seen

-band-like aggregates within superficial dermis

Answer 16

1. mycosis fungoides
2. sezary syndrome

Question 17

gross: skin lesions are multiple, round-oval, nonscaling, red-brown papules and plaques

microscopic: lesion exhibit dermal fibrosis, edema, eosinophils and numerous mast cells characterized by increased numbers of cutaneous mast cells, the histamine and heparin release causes _p_ruritus, flushing, rhinorrhea, or dermal edema and erythema wheal formation when lesional skin is rubbed is termed dariers sign; dermatographism what is the condition?

bone pain

1. osteoporosis in premenopausal women and men due to excessive histamine release in the BM

histology: spindle-shaped and stellate mast cells and few eosinophils

if this condition occur in children then what is it called?

in children, is it a good prognosis how about adults?

acquired point mutation what which receptor?

Answer 17

mastocytosis

urticaria pigmentosa-good prognosis in kids

c-KIT receptor point mutation leading to mast cell proliferation and survival

Question 18

this is a spectrum disorder of epidermal maturation leading to chronic excessice keatin accumulation (hyperkeratosis) resembing fish scales x-linked recessive, autosomal dominant and autosomal recessive forms

primary defect in most forms is increased cell-cell adhesion resulting in abnormal (insufficiency) desquamation

the x-linked disease is caused by steroid sulfatase deficiency leading to increased amounts of proadhesive cholesterol sulfate in intercellular spaces and persistent adhesion in the stratum corneum

microscopically: compacted stratum corneum with minimal inflammation the thickness of the epidermis or granulosum is use to subclassify the disorder

Answer 18

ichthyosis

acquired form (ichthyosis vulgaris)

Question 19

hives

focal mast cell degranulation resulting in edema and pruritus (wheal formation) regress within hours what is the condition?

hereditary angioneurotic edema is caused by deficient C1 esterase inhibitor angioedema is distinguished by presence of both dermal and subcutaneous fat edema

gross: small pruritic papules to large edematous plaques (trunk, distal extremities, ears)
microscopic: sparse mononuclear perivascular infiltrate are associated with edema and occasional dermal eosinophils

Answer 19

urticaria

Question 20

delayed hypersensitive response driven by langerhans cell proliferation

gross: pruritic, red, papulovesicular to blistered, oozing and crusted, chronic exposure can evolve into psoriasis-like scaling plaques or form yellow crust (impetiginization)
microscopic: early spongiosis (particularly in stratum spinosum) progresses to frank fluid accumulation to form vesicles in chronic condition the vesicular phase is replaced by acanthosis and hyperkeratosis

external application of Ag (poison ivy) or igested food

-usuhiol in poison ivy/oak (Rhus toxicodendron)

Answer 20

acute eczematous dermatitis

Question 21

self-limited hypersensitivity reponse triggered by drugs, infections, malignancy.

keratinocyte injury mediated by CD8 cytotoxic T lymphocytes

steven-johnson syndrome- severe frbrile form in children. there is erosion and hemorrhagic crusting of the lips, oral mucosa, conjunctiva, urethra

toxic epidermal necrolysis- characterized by diffuse mucocutaneous epithelial necrosis and sloughing similar to third degree burns

pathogenesis have shared similarities with GVHD and allograft rejection) epithelial cells are injured by skin homing (CLA+) CD8+ CTL responding to uncharacterized antigens prominent in the central portion of the lesion CD4 and langerhans cells localized to raised erythematous periphery

gross: macules, papules, vesicles, and bullae red maculopapular lesion with central pallor (target lesion), symmetric involvement of the extremities is common
microscopic: early lesion show dermoepidermal and perivascular lymphocytic infiltrates with dermal edema and focal basal keratinocyte degeneration and necrosis, exocytosis associatd with epidermal necrosis, blistering and shallow erosion

Answer 21

erythema multiforme

Question 22

gross: salmon-pink plaques with silvery scaling

commonly effects elbows, knees, scalp, lumboscral, nail changes can be seen with yellow-brown discoloration (oncolysis)

microscopic: marked acanthosis with downward rete elongation and mitoses well above the basal layer

Koebner phenomenon- induce psoriatic lesion in suscepible pts with local trauma, start a self-perpetuating local inflammatory response

thin straum granulosum or absent with extensive overlying parakeratosis, dilated vessels in the underlying dermal papillae yield pinpoint bleeds when scales is removed

munro microabscesses: small PMN aggregates in parakeratotic stratum corneum

Auspitz sign- multiple, minute, bleeding points when the scales lifed from the plagues

Answer 22

psoriasis

Question 23

gross: marcular or papule lesion on greasy, yellow erythematous base often with scaling and crusting. dandruff common

microscopic: early lesion resemble spongiotic dermatitis and later lesion resemble acanthotic psoriasis high densities of sebaceous glands, but not a disease of sebaceous glands, this is an inflammatory disease

pathogenesis: increased sebum production in response to androgens or due to dopamine deficiency in PD patients

Answer 23

seborrheic dermatitis

Question 24

gross: pruritic, purple, polygonal planar papules that turns into plaques.

itchy, violaceous, flat-topped papules that coalesce-often highlighted by white dots or lines in darkly pigmented people (wickham striae) multiple and symmetrically on wrist and elbows and glans penis, oral mucosal lesions are generally white and netlike

microscopic: SCC noted to occur

koebner phenomenon seen

-wickham striae: papules highlighted with white dots, created by areas of hypergranulosis in darkly pigmented individuals

dense cutaneous infiltrate of lymphs, along dermoepidermal junct (interface dermatitis)

• saw toothing of dermoepidermal interface
• colloid or civatte bodies: anucleate, necrotic basal cell incorpated into inflamed papillary dermis

Answer 24

lichen planus (self-limiting)

Question 25

autoimmune blistering affecting 30-40 patients- autoantibodies dissolution of intracellular attachement within epidermis and mucosal epithelium and can be fatal with tx multiple variant: **-most common _oral mucosa, scalp, face, interiginous zone, trunk, and pressure points._ lesions are superifical easily ruptured blisters that leave _shallow, crusted erosion_. can be fatal if untreated, what is it?** **--suprabasal split** **-rare large moist verrucous plaques (wart-like), studded with pustules, typically flexural and interitriginous zones** **-more benign form occurring epidemically in south america (Brazil) mainly on _face, scalp, and upper trunk_. bullae are extremely superficial, leaving slight erythema and _crusting_ after rupture** **--subcorneal split** **-localized milder variant of pemphigus foliaceus involving only _malar distribution_** **-blistering disorder _associated with non-hodgkin lymphoma_** all variants have characterized acantholysis with intercellular clefting and intraepithelial blister

Answer 25

pemphigus vulgaris pemphigus vegetans pemphigus foliaceus pemphigus erythematosus paraneoplastic pemphigus

Question 26

describe the separation of pemphigus vulgaris and vegetans and foliaceus

Answer 26

separation occurs immediately above the basal layer (suprabasal blister leaving an intact layer of tombstone like basal cells in the **vegetans variant.** in the **foliaceus variant**, only the **stratum granulosum** is involved and anti-Ig or anti-complement immunofluorescence, netlike reticular staining may be seen in epidermis, outlining each keratinocytes

Question 27

**autoimmune blistering disease** of skin and mucosa typically affecting elderly individuals it does not rupture easily as pemphigus there are **antibodies against the hemidesmosome proteins** (bullous pemphigoid antigens, **BPAG**) that attach to the epidermal cells to the basal membrane. only antibodies against **BPAG2 causes blistering.** bound autoantibodies cause injury via complement activation and granulocyte recruitment gross: bullae containing **clear fluid, inner thighs, forearm flexor surfaces, lower abdomen and intertriginous zones are common** microscopic: subepidermal **nonacantholytic blister** with linear dermoepidermal junction staining for Ig and complement.

Answer 27

bullous pemphigoid

Question 28

**_gross_**: plaques and **_grouped vesicles bilaterally and symmetric involveing the extensor surfacesm upper back, buttocks_** microscopic: **neurophils and fibrin accumulate int he tips of dermal papillae** (microabscesses) with overlying **basal vacuolization** that comes together to a large **_subepidermal blisters_** imunofluorescence **shows granular IgA deposits on dermal papillae tips, intense pruritic urticaria** and **grouped vesicles** typically occurring in young men (3-4 decade) associated with **_celiac disease_ and responds to gluten-free diet** **pathogenesis:** either by immune complex deposition in the skin or by **gliadin (gluten protein)** and antibodies cross-react with junction-anchoring components (**reticulin**)--\> subepidermal blister

Answer 28

dermatitis herpetiformis

Question 29

group o**f noninflammatory disorders that have blistering** at pressure sites or trauma due to **defect in structural proteins forming the dermoepidermal junction.** **simplex type**-mutation of keratin 5 or 14 leading to structural defects in epidermal basal cell layer **junctional type**: defect in either BPAG2 or laminin, the latter is protein that links hemidesmosomes and anchoring fibrils; the resulting is blistering at the lamina lucida in otherwise normal skin **dystrophic type:** blistering beneath the lamina densa due to to type 7 collagen mutations this form typically leads to cutaneous scarring NOTE: blisters at site of pressure, rubbing, trauma electron microscopy can differentiate the various types

Answer 29

epidermolysis bullosa

Question 30

group of inborn or acquired disturbances of porphyrin metabolism **porphyrin are ring structures that bind metal in hemoglobin, myoglobin, cytochromes,** cutaneous lesions consist of urticaria and scarring that exacerbated by **sun exposure** histology: subepidermal vesicles with marked thickening of the walls of the superficial dermal vessels

Answer 30

porphyria

Question 31

**common chronic lesion of hair follicles** (particularly the sebaceous glands that occur in the mid-late teens and in males more than females. associated with hormonal changes and alter hair follicle maturation induced by sex hormones, corticosteroids, occupational exposure (coal tars) or occlusive conditions (heavy clothes) **Gross**: noninflammatory acne is characterized by **open comedones**- follicular papules with central black keratin plugs (color is due to oxidized melanin) **closed comedones**- follicular papules with central plugs trapped beneath the epidermis. -this one of the 2 can rupture and cause inflammation **microscopic**: comedones are composed of expanding masses of lipid and keratin at midportion of hair follicles pathogenesis: acne likely involves **propionibacterium acne** causing **lipase degeneration of sebaceous oils to form highly irritating fatty acids**. the keratinization of the follicle and development of keratin plug blocks serum outflow **tetracyclines and vitamin A can be used for treatment**

Answer 31

acne vugaris

Question 32

middle aged women, inappropriate activation of innate immune system characterized by increased **cathelicidin production** is implicated gross: disorder has four characteristic stages: 1 **flushing,** 2) **persistent erythema and telangiectasia,** 3) **pustules and papules** and 4) **rhinophyma**- permanent thickening of nasal skin by confluent papules and follicles microscopic: nonspecific perifollicular lymphocyte infiltrate with dermal edema and telangiectasia

Answer 32

rosacea

Question 33

**most common panniculitis** (inflammation of subcutaneous fat), associated with **beta-hemolytic streptococcus and TB,** sarcoidosis, IBD, visceral malignancy deep wedge biopsy shows **early septal widening** and lymphohistiocytic infiltration o**ccasionally with giant cells and eosinophils without vasculitis** readily palpated than seen over week, the lesion will flatten and becom bruise-like, no residual scars consider delayed hypersensitivity to microbials and drug related

Answer 33

erythema nodosum

Question 34

uncommon panniculitis affecting **adolescents and menopausal women.** may **represent with vasculitis of subcutaneous fat with necrosis of adipose tissue.** tender nodule that eventually ulcerate and scars early lesions show necrotizing vasculitis in small to medium size vessels in deep dermis **subcutis weber-christian disease** (relapsing febrile nodular panniculitis) is a rare lobar form present as crops of erythematous plaques or nodules (mainly legs) **factitial panniculitits (**self-administered foregin substances) deep mycotic infections in immunocompromised hosts, and lupus can mimic clinical and histologic appearance ofprimary panniculitis

Answer 34

erythema induratum

Question 35

**1. common spontaneously regressing lesion seen in _children and adolescent caused by HPV classification_** **2. most common, typically found on hand dorsum, lesions are _gray-white to tan, flat to convex \<1cm papules with rough surface_** **3. on face or hand dorsum as _flat smooth, tan papules smaller than verruca vulgaris_** **4. rough, scaly _1- 2 cm lesions_ and can be confused with _callus_** **5. (anogenital and venereal (**relating to sexual desire or sexual intercourse) **warts)-_soft, tan, cauliflower-like masses_ measuring up to many centimeters in diameter** **HPV 6 and 11** are predominant for **anogenital warts HPV 16** is associated with lesion dysplasia and **in-situ squamous cell carcinoma**

Answer 35

1. verrucae (warts) 2. verruca vulgaris 3. verruca plana (flat warts) 4. verruca planaris (soles) or plamaris (palms) 5. condyloma acuminatum all have epidermal hyperplasia and superficial **keratinocyte perinuclear vacuolization (koilocytosis)** electron microscopy reveals numerous intranuclear viral particules **_HPV 16_** associated with **in-situ SCC of the genitalia** and with **bowenoid papulosis** (genital lesions of young adults with histologic appearance of carcinoma in-situ, but regresses spontaneously) **the relationship of HPV 5 and 8** to SCC and especially in individiaul with **epidermodysplasia veruciformis-**develop multiple flat warts, some progress to carcinoma

Question 36

self-limiting **_poxvirus_** infection transmitted by direct contact **_gross_**: **firm, pruritic, pink to skin -colored, umbilicated papules** seen on **trunk or anogenital regions**; cheesy material containing diagnostic **molluscum bodies** can be **expressed on central umbilication** **_microscopic:_** lesion exhibit cuplike verrucous epidermal hyperplasa with pathognompnic **molluscum bodies- eosinophilic cyptoplasmic inclusion in stratum granulosum or stratum corneum**

Answer 36

molluscum contagiosum

Question 37

**staphylococcus aureus** is the most common agent, although **beta-hemolytic streptococci** can cause lesion especially on the face and hands mainly affect **kids** **_pathogenesis:_** epidermal bacterial infection provoke a destructive innate immune response with a serous exudate. blister formation is driven by bacterial production of the **toxin** that **cleaves DsIg (desmoglein 1)** **_morphology:_** **_gross:_** erythematous macules that progress to small pustules and eventually to **shallow erosion with honey-colored crust** **_microscopically_**: **characteristic _subcorneal pustules filled with neutrophils and gram-positive cocci_** accompanied by non-specific dermal inflammation

Answer 37

impetigo

Question 38

superficial fungal infection confined to nonviable **stratum corneum** caused by **dermtophytes derived from soil or animal contact** 1. typically in **children** causing asymptomatic **hairless patches on scalp**, associated with mild **erythema** **crusting and scale** 2. affects **beard area** in adult men 3. **common superficial dermatophytosis of body, especially _children_**. predisposing factors are **excessive heat or humidity, exposure to infected animals and chronic foot or nail dermatophytosis.** typically presents with **expanding erythematous plaque with** **elevated scaling border** 4. typically found in **inguinal area, obesity, heat, friction, and maceration (**Maceration is caused by excessive amounts of fluid remaining in contact with the skin or the surface of a wound for extended periods.) **are predisposing factors**. presents as **_moist_ red patches with raised scaling borders** 5. **athlete's foot** characterized **_erythema and scaling,_ beginning with the webbed spaces between digits**. most the inflammation is due secondary bacterial superinfection 6. due to **malassezia furfur infection** presenting on the **upper trunk** as groups of various-sized hyperpigmented or hypopigmented macules with **peripheral scale** 7. **nail dermatophytosis** characterized by **discoloration, thickening and deformity** of the nail plates **_morphology_**: histology depends on the organism that infected the host, but lesion have characteristically exhibit reactive epidermal changes **similar to mild eczematous dermatitis**

Answer 38

these are superficial fungal infections 1. tinea capitis 2. tinea barbae 3. tinea corporis 4. tinea cruris 5. tinea pedis 6. tinea versicolor 7. onychomycosis

Question 39

what are some histology features to note when looking for melanomas?

Answer 39

Question 40

describe

Question 41

Answer 41

Question 42

primary fibrosarcoma of the skin slow growing, locally aggressive translocation of collagen 1A1 (COL1A1) and PDGFB protuberant nodules usually trunk, firm plaque closely packed fibroblastthat looks like blades of a pinwheel-storiform honeycomb pattern-deep extension from the dermis into the subQ fat

Answer 42

dermatofibrosarcoma protuberans (DFSP looks like a school of fish