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