Dermopathology - Dr. Martin Flashcards
Freckle
Pigmentation and melanocytes disorders (usually after sun exposure)
High melanin in basal keratinocytes (hyperpigmentation)
Changes with seasons
Lentigo
What is it
Benign usually in children / infancy and mucus membrane and skin
(Check oral)
5mm - 10mm oval tan-brown macule or patch (no darkening with sunlight)
Pigmentation and melanocytes disorders (hyperplasia, linear, restricted to right above BM)
Melanocytic nevus (mole)
Pigmentation and melanocytes disorders
P16/INK4a does not arrest
Dysplasitic Nevi
Risk for melanoma by age 60yo
AD
CDKN2A or CDK4 gene that get the NRAS and BRAF mutation
Biopsy of a skin things like nevi
Do the periphery of it since the middle are more dead cells
Melanoma
UV radiation damage High incidence (GI, GU, skin, eye, esophagus) TX: immune checkpoint inhibitor Sporadic mostly (sunburns you’ve had)
Melanoma risks
Equator
Outdoor hobbies
Blistering sunburns
Lights skin and eyes
Melanoma in blacks and Asians should be examined where to find sx
Soles of feet
Palms
Nails
Mucous membranes
HMB-45 +
Staining into a LN
To see which one has the cell that started everything
Seborrheic keratoses (Seb K)
In scalp….
Ducts in skin biopsy
Shows it comes from a gland
= Cylendroma
AK
Sun damaged skin and hyperkeratosis Sandpaper Squamous cell carcinoma Certain = pink color Elastosis= blue
Dermatofibroma
Legs, adults, women
Goes down when pressed (not squeezed) = Dimple sign
Injury and inflammation can casue this benign thing
No capsule and well circumsribed
Spindle shaped
DFSP
COL1A1 PDGFB
Very firm and dense
Honeycomb look
Looks like fish swimming in circles
Ichthyosis
Fish scales looking
Not very serious
Testing for psoriasis
Lift one of the silvery scales and it bleeds
Seborrheic dermatitis
Sebum production in sebaceous glands
Can be associated with HIBV and Parkinson’s
Blistering Bullous Disease
Pemphigus vulgaris
IgG
Oral cavity
Exortiation
Traumatic lesions breaking skin (deep scratch)
Lichenification
Thickened rough skin (from repeated rubbing)
Macule
Circumcised flat lesion 5mm or smaller
Patch
Flat and circumscribed that is bigger then 5mm
Onycholysis
Separation of nail bed from nail plate
Papule
Elevated dome shaped or flat topped lesion 5mm or smaller
Nodule
Elevated dome shaped or flat topped lesion greater then 5mm
If flat -topped = plaque
Pustule
Pus filed raised lesion
Scale
Dry horny, platelike, usually from cornification not done right
Vesicle
Fluid pilled raised lesion 5mm or smaller
Also called a blister
Bulla
Raised fluid filled lesion grater then 5mm
Also called a blister
Wheal
Itchy transient elevated lesion (skin colored or lighter in color), can be red demo dermal edema
Acanthosis
Diffuse epidermal hyperplasia
Dyskeratosis
Abnormal, premature keratinization in the stratum granulosum
Erosion
Discontinuity of skin from incomplete loss of epidermis
Exocytosis
Inflammatory cells going to epidermis
Hydropic swelling
Ballooning (ICF edema or keratinocytes) usually in viral infections
Hypergranulosis
Stratum granulosa hyperplasia
Usually from intense rubbing
Hyperkeratosis
Stratum corneum thickening
Lentiginous
Linear pattern of melanocyte proliferation in the BM
Papillomatosis
Surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae
Parakeratosis
Keratinization of the nuclei of stratum corneum (usually seen in mucous membranes)
Spongiosis
Incracellular edema of epidermis
Ulceration
Discontinuity of the skin complete loss of epidermis revealing dermis and subcutis
Vaculoization
Formation of vaculoes in cells or next to cells (usually in the BM basal side)
neurofibromitosis
Freckles if not from a sun exposed area = neurofibromitosis cafe au lait spots
Aggregated melanosomes in cytoplasm of melanocytes (macromelanosomes)
** see clump of macromelanosomes right above BM**
Lentigo
Histology and what it looks like
Linear melanocytic hyperplasia
= restricte to cell layer above BM and in linear way
= Lentiginous (is a melanocytic tumor that can also look like this and grow like this), however in the BM layer
Melanocytic nevus (mole)
Benign
Mutation in RAS or BRAF = proliferation
p16/INK4a growth inhibitor problems also = melanoma
- Tan uniformed pigmentation, well defined boarders
- larger cells on the top (more melanin = nests) and gets smaller farther down beeper in tissue = cords or single cells
- deepest layer = Fusiform fascicles (looks like elongates cells or neural tissue
Junctional nevi
At dermoepidermal junction
Compound nevi
Into underlying dermis and epidermis
Intradermal Nevi
Only in dermis and usually older lesions
Dysplastic nevi
Risk of melanoma (50% by age 60yo)
CDKN2A and CDK4 gene causes this
* if NRAS + BRAF mutation it become melanoma
Dysplastic nevi histology
Greater then 5mm, and many of them
Variety of colors and irregular boarders
Nests can combine
- Lentiginous hyperplasia : linear growth along E-D junction
- Atypia : Ig nuclei , angulated nuclear contour, hyperchromasia
-Lymphocytic infilt : loosing melanin (melanin incontinence)
- Linear fibrosis : around epidermal rete ridges (see lymphocytes + bridging) —> shoulders
Shoulder region of nevi
Is the periphery of the mole (you don’t want to see the compound cells here, dermal nests)
The center is the compound potion
Melanoma is what and caused by what
UV radiation damaging DNA
Skin, oropharynx, GiGU, esophagus, meninges, uvea of eye
(Most is sporadic and not hereditary)
Lesions that are precursors to melanoma
Congenital or dysplastic nevi
Most common spots for melanoma
Upper back
Legs
Driver mutations for melanoma
- CDKN2A in 40% ——> p16, p15, ARF (mutation in these tumor suppressors)
- Increase RAS and P13K/AKT (from BRAF mutation)
- 70% sporadic is activating telomerase form the TERT**
What is a marker found in a LN that makes it the sentenial LN and shows melanoma
HMB-45+ (not always in every type of melanoma)
Radial growth phase
Macular areas (growing across skin)
= irregular nested single cell growth melanoma cells (inflammation in dermis also)
= cant metastasize
Vertical growth phase
Raised areas
= and nodular aggregates Of infiltrating cells
= growing downwards so can metastasize
= the deeper the invasion the more probability of metastasis
Specific histology of melanoma cell
Large nuclei, irregular contours, chromatin on periphery of nuclei , red eosinophilic nuclei
Breslow thickness
From the most superficial epidermal melanoma cell to the deepest intradermal tumor cell
EX of radial growth 3 of them
- Lentigo maligna : usually on face of elderly remaining radial for many years
- Superficial spreading : sun exposed areas (most common becoming melanoma)
- Acral / Mucosal Lentiginous : becomes melanoma not related to sun exposure
Worst prognosis points for melanoma
Tumor depth deep Many mitosis cells Regression of immune system Ulceration of skin Tumor in flirting lymphocytes in dermis Many LN involved (even 1 melanoma cell in a LN makes that LN completely involved)
Favorable prognosis of melanoma
Thinner tumor depth No regression of IS No ulcer Only some lymphocytes No mitosis
Seborrheic Keratosis (Seb K)
Spontaneous on head neck extremities, trunk (middle age and older)
= dark skinned
= waxy papules, coin -like , round flat**
= they are filled with keratin (not melanoma)**
= pseudo-horny cysts**
= Usually involved with FGFR-3 mutation (fibroblast GF)**
Lester Trélat sign
Paraneoplastic syndrome
Having spontaneous many Seborrheic Keratosis and it is associated with GI tract carcinoma
Seb K horny cyst are filled with
Keratin
Acnathosis Nigricans
Benign (80%) and malignant
= thickened hyperpigmentation + velvet like
= on skin fold areas
= obesity and diabetes, some AD inheritance
= mutation in FGFR3 causes malignancy
Acanthosis Nigricans that is malignant has what associations
Associated with GI adenocarcinoma
And FGFR3 mutation (like in Seb k)
DM2 causes hyperinsulinemia——> IFGR1 stimulation (insulin GF)
Acanthosis Nigricans histology
Enlarged dermal papillae (repeating peaks and valleys) + hyperkeratosis (no melanocytes), can also see hyperpigmentation
Fibroepithelial polyp
Skin tags = acrochordon (squamous papilloma)
= head neck trunk, face, skin folds
= obese, DM, intestinal polyps (Risks)
= soft and flesh colored, slender stalk
Fibroepithelial polyp histology
Fibrovascualr center with benign squamous epithelium covering it
Birt-Hogg Dube syndrome
Rare polyps + perifollicular mesenchymal tumors (fibroblasts + hair bulb)
= associated with Fibroepithelial polyps
Epithelial or Follicular Inclusion Cyst (wen)
Invaginatino and cystic expansion of epidermis or hair follicle
= can rupture and care KERATIN inside to spill into dermis —> extensive painful granulomatous inflammatory response
Wen or Epithelial / Follicular inclusion cyst are filled with what
Keratin from hair follicle or epithelium
2 Adrenal Appendage tumors
- Cobden syndrome
- Cylidroma
- Eccrine Poroma
Annexation appendage tumors are what
Hundreds of neoplasticism differentiating to appendages
Benign
Flesh colored and many papules and nodules
Can be confused with basal cell carcinoma
Cowden syndrome
Many trichilemmomas=neoplastic cells differentiations forming benign tumor of the outer root sheath of sebaceous follicles
X PTEN
= risk for endometrial cancer and breast cancer
= will get hemartomas
Cyindroma
Ductal differention of eccrine or apocrine ducts = forehead and scalp
= turban tumor, jigsaw puzzle = looks like this and on histology slide
= CYLD tumor suppressor gene mutation (can also associate with Familial TRichoepithelioma and Brooke-Spiegler
Eccrine poroma
Palms and soles of feet have 3X more sweat glands
Histology of sebaceous adenoma
Many bubbles inside of the cells in the duct
Nevoid basal cell carcinoma
9q22, PTCH mutation
Many BCC and medulloblastoma, and jaw cysts
Familial melanoma syndrome
9q21 CDKN2 mutation ——I cell cycle arrest = melanoma, pancreatic carcinoma
Increase p53 also melanoma and pancreatic carcinoma
Muir- torre syndrome
2q22 3q21 MSH2, MLH1 mutations = neoplasm in sebaceous glands from NO DNA repair = colon and internal malignancies
Xerderma pigmentosum
9q22
XPA mutation
= NER repair mutation = melanoma and other skin cancers
= die young
Actinic Keratosis
Sun damaged skin/ arsenic / ionizing radiation =hyperkeratosis in these areas
= face, arm, dorsum of hands
= usually light skinned
= rough sandpaper like and has ( Cutaneous horns, Dyskeratosis)
= becomes SCC over time *
Cutaneous horns
Excessive keratin production causing this horn to grow outwards form skin
Dyskeratosis
Pinkcytoplasm intracellular bridges, blue-gray elastosis (from sun damaged fibroblasts)
Parakeratosis (basal cel dysplasia of keratin growth)
Actinic cheilitis
Actinic keratosis of the lips
Intracellular bridges is found in what
SCC and actinic keratosis (not BCC)
Top 2 common tumors from sun exposure in older people
BCC
SCC
SCC
5% or less Metz in regional LN, if Metz then deeply invasive in subQ
= proportional to lifetime sun exposure (UV light)
SCC risk factors after sun exposure
- Immunosuppressive ( HPV 5 + 8), chemo, transplant
- Epidermoysplasia verruciformis : from HPV, high risk
- Industrial carcinogens, chronic ulcers, tobacco, betel nut chewing
SCC mutations involved
- TP53 (acquired in AK leading to SCC) = no DNA repair in G1 phase
- RAS and NOTCH signaling mutations
Xeroderma pigmentosum mutation
XPA gene, NO NER, no Pyrimidine diners are repaired and high risk of SCC
SCC looks like what if it is in situ (local)
Sharply defined, red, scaling plaques (large and hyperchromatic), involving all levels of dermis
Invasive SCC looks like what
Nodular keratin lesions (hyperkeratosic =) can ulcerated
Dyskeratosis = Intracellular bridges
BCC
Slow growing and no Metz, sunexposure and immunosuppressive and XP can all give rise to this
BCC mutation
X SHH from PTCH gene mutation
BCC what do you see
- Nevoid Basal cell carcinoma syndrome (basalis cell nests)
- Gorlin syndrome
- Basla cell nevus : many BCC less then 20yo + medulloblastoma, ovarian fibromas, pits arms soles
- Pearly papules with visible telangiectasis vessels, rodent ulcers = peripheral palisade glands (lined up linearly and parallel(
Rodent ulcers
Basically eat off the face of the person and grows huge
SHH role in PTCH and BCC
Unregulated SHH binds to PTCH so it CANT ——I SMO activity
SMO = activated TFs
(Mutation in BCC causes the PTCH to be constantly bound to and SMO is active all the time = Gorlin syndrome and sporadic bcc
There can also be loss of function PTCH and it cant block SMO (UV damage not fixed)
Dermatofibroma (Benign Fibrous Histocytoma)
= BENIGN Adults, legs (middle age women)
= + dimple sign (press around the lesion towards it and it depressed down the skin (dos not squeeze down)**
= trauma, injury, inflammation response
= firm tan papules (flattens with time)
Dermatofibroma histology (what do I see in the slide)
Spindle shaped cells, non-encapsulated mass in dermis
Epithelium above it is hyperplasia
elongated rete ridges that are hyperpigmented = Pseudoepitheliomatous hyperplasia
= collagen + fibroblasts
Dermatofibrosarcoma Protuberans (DFSP)
Mutation causing this
What is it
Primary fibrosarcoma (hardening of soft tissue)
Slow aggressive localized,
COL1A1 + PDGFB (plt-derived factor B) mutation = tumor cell growth
= protuberant nodules usual in trunk, firm (can form plaque or ulcer)
Dermatofibrosacroma Protuberans TX
PDGF-B receptor Tyrosine Kinase inhibitor (lifetime)
Dermatofibrosarcoma Protuberans (DFSP) looks like what and histology
Close packed fibroblasts radially arranged, (storefront pattern like fish swimming in circles of spindle cells, and some Swiss cheese fats cells) = Honeycomb patterns on dermis and subQ fat
Epidermis above is thin
Mycosis Fungoides (Cutaneous T-Cell Lymphoma)
CD4+ localized lymphoma that later in life becomes systematic
Scaly red brown patch
Mycosis Fungoides stages
Patch —> plaque —> nodule
Eczema lesions in very early stage
Mycosis Fungoides can be confused with what
Psoriasis (raised scaling plaques that are seen)
Sezary syndrome
Erythroderma, scaling of entire body
Cerebriform cells
Band-like aggregates in dermis
Pautrier microabscesses : small cell clusters in epidermis
Sezary syndrome and MF TX how
UV light therapy, topical steroids, or chemo if needed
Mastocytosis
Urticaria Pigmentosa
Common in children
Mast cells fills up in lesions round oval red/brown papules or small plaques
Can for blister
= if popped can cause histamine release and cell degranulation
= you can write of skin
Mastocytosis
Darier sign
Dermatographism
Darier sign : dermal edema look like wheals when skin is rubbed
Dermatographism : dermal edema hives looking, when stroking ski with pinpointed instrument
Mastocytosis mutation
SX
KIT receptor tyrosine kinase = mast cell growth and survival
SX : pruritus and flushing from foods, temps, alcohol, rhinorrhea, bone pain
= can be associated with osteoporosis from excessive histamine release in BM
Stain how mastocytosis
Giemsa purple granulated in mast cell cytoplasm
Ichthyosis
X epidermal maturation, chronic keratin buildup
= fish like scales on skin
= X desquamation of skin (stratum corneum buildup)
Acute inflammatory lesions (Dermatosis) usually you see which cells
Lymphocytes and macrophages
Urticaria
What is it and SX
- Localized mast cell degranulation (from microvascular hyperpermeabulity)
Ab mediated release of histamines form Mast cells (IgE) - Wheals
- Angioedema : dermis and subQ fat edema
Urticaria usually happens from what
Body parts exposed to pressure
Ab-mediated release from mast cells (hives)= IgE dependent
Urticaria macro lesions
Small, pruretic papules to large edematous plaques
Urticaria (hives) macro lesions
Sparse superficial infiltrate of mononucleosis cells + N
What drug can cause urticaria
Aspirin form cause vasodilation
Histology of urticaria
Space between the collagen bundles
Acute Eczematous Dermatitis
External type and tx
External Ag or ingested food (some irritant like Urishiol in Poison IVY)
Corticosteroids
T-cell mediated inflammatory reaction eczema
Type 4 hypersensitivity
SX: red papulovesicular oozing and crusted (impetigo) lesions
= can cause acanthosis hyperkeratosis
Acute eczemstous dermatitis causes edema where
Edema in the instracellular space of other stratum spinosum
Erythema Multiforme
Happens when
Self- limited hypersensitivity to infections and drugs (Herpes, histoplasmosis/mycoplasma, typhoid, leprosy) (PCN, sulfa….) (SLE)
Erythema Multiforme is what
CD8+ injure keratinocytes (center of lesion)
CD 4 + M are in the periphery of lesion
What happens in Erythema Multiforme
Many diverse types of lesions
Macule, papule, vesicle , bullae
1. Interface dermatitis : dermal edema, degenerative keratinocytes,
2. Steven-Johnson’s : children, oral, conjunctiva, genitals, skin lesions that can lead to sepsis if infected
3. Toxic epidermal necrolysis : necrosis and sloughing of cutaneous and oral epithelium (looks like extensive burns)
Erythema Multiforme looks like what
Target lesions with dark spot in middle followed by light then dark raised then halo around
Psoriasis what is it and tx
Autoimmune which brings CD8 and CD 4 cells in to local site on skin inducing cytokines soup
(Can be caused by trauma)
TNF and IL17 inhibitors
Psoriasis SX
Pink salmon plaque
Loose silver scale on top of skin
Nail changes with holes (pitting), yellow-brown discoloring
Oncolsis
Auspitz sign +
Munro microabscesses : aggregation of PMNs
Koebner phenomenal
When trauma induces psoriasis or Lichen Planus
Auspitz sign
Lifting the scale on top of skin and it causes bleeding
Psoriasis looks like what in histology
Elongated rete ridges test tube racks
Mitosis above Basal layer, high parakeratotic scale
9think layer of keratin)
Seborrheic dermatitis
In places with high sebaceous glands
(Ear, scalp, nasolabial folds)
Inflammation of epidermis (has nothing to do with sebaceous glands)
Sebaceous glands therefore make a lot of SEBUM from androgen stimulation = lesions of flaky skin
Seborrheic dermatitis can be found highly in what patient population
Parkinson’s since they make mire sebum from dopamine deficiency
TX : levodopa to lower oil
HIV patients also
Seborrheic dermatitis on histology and how it looks
Follicular lipping, N
Red-yellow greasy base with scaling and crusting skin, looks like Dandruff
Lichen Planus
SX
6Ps 1. Prurstic 2. Purple 3. Polygonal 4. Planar 5. Papules 6. Plaques Resolved spontaneous in 1-2 years (skin and mucosa)
After Lichen planus goes away what is left
Hyperpigmentation in that area
Lichen Planus what do you see histology and how it looks
- Itchy violet flat-topped papules (Wickham striae = papules with white net like on top leaving dark dots in middle) = lace like pattern**, may look dark brown on darker people
- Symmetrical lesions
- Oral white net-like lesions
- Sawtoothing :zigzag dermoepithelial interphase (pointed retes)
- Colloid / CIVATTE BODIES : anucleated necrotic basal cells in papillary dermis
Pemphigus
What is it
IgG Abs disrupting adhesion of epithelium = blister
IgG net like deposits
Acantholysis
Acantholysis
Dissolution on intracellular bridges connecting skin cells
Pemphigus Vulgaris what and histology
Most common
= mucosa and skin of face, scalp, axilla, groin, pressure points
= easily rupturing vesicles (crust and dried serum forms)
= above basal layer (suprabasilar blister) acantholytic blister
IgG——> Dsg1 and Dsg3
Histology : row tombstones
Pemphigus Vegetans (foliaceus -> miler one)
Large moist verrucous (wart-like), vegetating plaques with pustules (groin, axilla, flexural surface)
= stratum granulosum level (subcorneal blisters), more superficial and not as erosive as vulgaris
IgG——> Dsg1 only
Bullous pemphigold Ig and what
IgG ——> BGAG2
BM blister, subepidermal, doesn’t rupture easily
Elderly inner thighs + FLEXORS forearm, groin, axilla
Don’t rupture easily
Dermatitis herpetiformis Ig and what
IgA to fibrils causing blisters
Urticaria of grouped vesicles = microabscesses
bilateral + EXTENSOR forearm elbows, knees, upper back, butt
Dermatitis herpetiformis associated with what
Celiac disease
From IgA to gluten also attaching to reticulin = subepithelial blister
Epidermolysis Bullosa :
subepidermal Blisters at sites of rubbing, pressure, trauma(at or right after birth)
= no inflammation (flexural creases)
Porphyria
Inborn metabolic disturbance of porphyrins (pigments in Hgb, myoglobin cytochromes)
You get subepithelial blisters from sunlight
= no inflammation
= Rigid dermal papillae, abnormal superficial BVs
= Ig and glassy serum protein deposits in BVs
Rosacea
SX and who
Middle aged and older Females usually = Slap cheek redness (flushing) = persistent redness and telangiectasia = pustules + papules = Rhinophyma
Rhinophyma
Thickening of the nasal skin
Rosacea is associated with what
Cathelicidin (anti-microbial peptide) high amounts
= something cause in the micro bacterial effects causes this
Erythema nodosum
HX of sarcodosis , pannicultis , painful nodule deep lesions
Acne vulgaris
What is it, who, and 2 types
Universal in teens and all races except Asians milder
Induced by testosterone, corticosteroids, androgens, contraceptives, heavy clot IgM tropical climate
1. Open comedomes : central is black(oxidized melanin) keratin plug
2. Closed comedomes : keratin plug is beneath epidermis (can cause follicular rupture/ inflammation
What causes acne vulgaris to happen in puberty
- Hypertrophy of sebaceous glands
- Propionibacterium acne’s colonize the hair follicle causing inflammation
- Androgens involved
Acne conglobate
Severe variant of acne vulgaris and you have sinus tract formation and dermal scarring
Panniculitis is what and found in what
Inflammmation in Sub Q fat, usually in lower legs
- Erythema nodosum
- Erythema induratum
Erythema nodosum is what and what happens
CT septae separate from edema and fibrin/N exudate
Later the Lymphocytes and histocytes come
Erythema nodosum SX
Very tender red plaque and nodules, ropy when palpated or seen
= over weeks it becomes flat and bruise like
Reason erythema nodosum happens
Delayed hypersensitivity to microbiota or drug (** B-hemolytic strep, TB, histoplasmosis, leprosy, coccidiomycosis) (Sulfa, contraceptives)
Or a disease (sarcoidosis, IBD)
Erythema Induratum
Who and what happens
Adolescents + menopause women’s
Primary vasculitis of deep vessels to fat ——> fat necrosis and inflammation
Erythema induratum SX
Slightly tender nodule however usually ulcerated
Necrotizing vasculitis in deep dermis and subQ
Granulomatous inflammation (as seen in TB) = caseous necrosis
Weber-Christian disease
Relapsing Febrile nodular panniculitis, red plaques and nodules on Lower extremities mostly + foamy M, L, N, giant cells
Factitial panniculitis
Secondary panniculitis from sled-inflicted trauma or injection on something
What can look like panniculitis
T- cell lymphoma (causing fat necrosis and superimposed inflammation)
What can be associated with panniculitis
SLE (also causing inflammation of sub Q)
Verrucae is also a
Wart
Verrucea is what
Who
Squamous cell proliferation form HPV
Direct contact
Regress spontaneous is 6mo-2yrs
Verrucae anogenital is caused by
Anogenital : HPV 6 and 11
Verrucae HPV 16 does what
In situ SCC of genitals and Bowenoid papulosis (regresses usually)
Verrucae HPV 5 and 8
Related to SCC and especially epidermodysplasia verruciformis (many flat warts that some progress to SCC)
How does HPV cause warts
Interferes with NOTCH signaling = no maturation on keratinocytes = epidermal hyperplasia
How does HPV cause cancer
When it produces E6 proteins that block p53 = no G1 arrest
Verruca plana`
Warts on dorsal side of hands or face, smaller then verruca vulgaris
Verruca planteris
Verruca Palmeris
Soles of feet and palms of hands
Condylomata acuminatum (venereal wart)
Penis, GU areas, soft tan, cauliflower like can get big
Verruca vulgaris
Epidermal hyperplasia , keratohyaline granules, koilocytosis (vacuole in cytoplasm)
Molluscum contagiosum
Is what and looks like what inhistology
Pox infection causing Trunk and GU firm, pruritic, umbilicated papules= dimple down in center of papule
Molluscum bodies in stratum granulosum and stratum corneum in BS (cytoplasmic inclusion, ellipsoid)
Pox virus looks like what
Brick shaped, dumbbell shaped DNA inside
Stain for Tinea corporis (dermophyte fungus)
Periodic acid-Schaffer stain (PAS) = red hyphae in stratum cornuem
Impetigo
Superficial bacteria infection of STAPH AUREUS on skin , very contagious,
= honey colored crust should be cleaned immediately (red macule forming and breaking)
the toxin in staph aureus does what
toxin cleaves desmoglein 1 which injures the epithelium
Tinea versicolor
Upper trunk fungal infection
Malassezia furfur (yeast) , not dermophyte
Many macule of different sizes and colors with fine peripheral scale