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dermatology Flashcards

1
Q

what is a macule?

A

A flat, circumscribed region of skin with different color or texture (example: freckle)

completely flat!!! localized hyperpigmentation

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2
Q

what is a macule patch?

A

A large macule (> 1 cm) or a coalescence of macules (example: vitiligo)

still flat!

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3
Q

what are papule?

A

raised area, A palpable, circumscribed change in consistency or contour of the skin (example: acne vulgaris)

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4
Q

A papule larger than 1 cm in diameter

(example: neurofibroma)?????

A

Nodule

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5
Q

Plaque

A

a clump! larger raised area. A coalescence of papules (example: psoriasis)

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6
Q

Vesicle

A

A circumscribed, clear fluid filled lesion; a blister (example: Herpes simplex)

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7
Q

Bulla

A

A large vesicle (example: bullous

pemphigoid)

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8
Q

Pustule

A

A vesicle filled with inflammatory cells

(example: acne vulgaris)

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9
Q

Wheal

A

localized area of swelling…edema. A palpable, circumscribed, area of edema with central pallor and peripheral erythema (example: hives) that usually disappears relatively quickly.

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10
Q

Purpura

A

large area of bleeding into the skin…. Discoloration of the skin due to the presence of blood in the tissue, outside of blood vessels; will not blanch with pressure (example: vasculitis)

Petechiae A punctate region of purpura (tiny dots)

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11
Q

Comedo

A

plugged hair follicle… A plug within a hair follicle canal which is composed of keratin and sebum; a blackhead (example: acne vulgaris)

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12
Q

Milium

A

A white papule composed of whorls of keratinized epidermal cells beneath the skin surface (example: milia)

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13
Q

Burrow

A

A horizontal tunnel in the stratum corneum produced by a parasite (example: scabies)

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14
Q

Scaly

A

too much keratin produced. Characterized by exfoliation of surface keratin cells (example: psoriasis)

Hyperkeratotic Having very thick scale (example: icthyosis)

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15
Q

Eroded

A

Showing a superficial defect in the skin surface which does not penetrate through the epidermis (example: abrasion)

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16
Q

Ulcerated

A

Showing a skin defect which penetrates through the epidermis (example: diabetic foot ulcer)
looking at dermis

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17
Q

EXCORIATED

A

SCRATCHING THEMSELVES!!!!! Eroded or ulcerated, often in a linear fashion, due to scratching (example: dermatitis factitia)
LINIEAR

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18
Q

Erythematous

A

Reddened; due to vasodilation with increased blood flow. Blanches with pressure (example: viral exanthem)

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19
Q

*Hyperpigmented

A

Dark; due to increased

amount of melanin (example: nevus)

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20
Q

*Hypopigmented

A

Light; due to decreased amount of melanin (example: vitiligo)

Lose melanocytes (white)

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21
Q

Lichenified

A

Showing thickening with accentuation of the normal skin markings; usually a sign of chronicity associated with scratching or rubbing (example: atopic dermatitis)

elbows, knees due to constant pressure

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22
Q

Verrucous

A

usually a papule, scaly and hyperkeritotic Characterized by velvety or roughened wart-like change (example: verruca vulgaris

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23
Q

Telangiectatic

A

Showing dilated small arterioles or capillaries coursing parallel to the skin surface (example: spider telangiectasia)

PERMANENT, related to Erythematous

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24
Q

Atrophic

A

Emaciated or thinned (example: striae)

in groin, seen when over use of steroid cream

25
Vitiligo
Partial or complete loss of melanocytes Well demarcated macules/patches Hand/wrist, axillae, perioral/periorbital, anogenital Pathogenesis: autoimmune
26
ALBINISM
No melanin produced (or decreased) Inherited defect in tyrosinase has normal melanocytes but cant do anything!!!
27
Vitiligo vs ALBINISM | HYPOPIGMINTATION
Vitiligo is autoimmune lymphocyte mediated melanocyte destruction – normal enzyme associated with other autoimmune disorders: pernicious anemia, thyroiditis LATER ON IMMUNE ATTACK Albinism is congenital absence of enzyme and melanin is not made or is decreased Enzyme loss of defect in transport to melanosomes
28
NEOPLASM
SOME MUTATION that regulates cell divison clonal population of cells that are abnormal. Originate from one cell, mole!!!
29
freckles
too much melanin
30
Melasma
normal mealnocytes and they are stimulated to make more melain. Pregnancy, oral contraceptives, hydantoin Mask like facial hyperpigmentation Cheeks, forehead, temples Sunlight makes it worse Melanocytes have enhanced pigment transfer to keratinocytes or macrophages Resolves after pregnancy over or drug discontinued
31
Solar Lentigo
not a mealanocytes issue. Hyperpigmentation of basal epidermis due to excess melanin production Sun protective mechanism of melanocytes
32
Lentigo simplex
Too many melanocytes (Melanocytic Hyperplasia) Localized hyperplasia of melanocytes All ages Not sun related (vs. solar lentigo) Small brown macules Histopathology: Increased melanocytes, increased pigment in stratum corneum and basal epidermis, rete ridges elongated/thinned
33
Neoplasia benign
Neoplasm with no capability for metastasis | Can be destructive or symptomatic – this does NOT define malignancy!
34
Neoplasia Malignant (Cancer)
Neoplasm with potential for metastasis and subsequently growth/proliferation at distant site Often locally destructive but may not be!
35
Melanocytic Neoplasms benign
``` Nevi, in situ, ex. mole Junctional, compound, dermal Spitz/spitzoid Atypical (dysplastic) Dermal variants Blue nevus Many others Melanoma ```
36
``` Types of Nevi/Moles common congenital blue spitz halo dysplastic/atypical ```
Common: Acquired or congenital Congenital: Large ones have increased risk of melanoma Blue: confused with melanoma clinically Spitz: difficult to distinguish from melanoma under microscope occasionally Halo: immune reaction to nevus cells Dysplastic/Atypical: potential precursor of melanoma
37
Most common pigmented lesion Most start life within the epidermis As they grow will start to populate the dermis
Nevi – Common (acquired) and Congenital. Melanocytes grow in nests along junction (junctional nevus) and in time enter dermis (compound nevus) after aging become intradermal only ABCD Not in the genetic make up to be malignant. Can cross the basement membrane and enter the dermis
38
Blue nevi
Dark blue/brown papules Often clinically concerning for melanoma Benign Deep blue color due to deep pigmentation Tyndall effect – light scatter properties Entirely dermal proliferation of spindled melanocytes with many melanophages can be in the dermis too, wont metasize
39
Dysplastic Nevi
Multiple dysplastic nevi = marker of increased risk of melanoma Isolated dysplastic nevus = probably no or only minimal risk of melanoma Usually graded by pathologist Mild, moderate, severe atypia Can excise mild depending on clinical circumstances, should excise mod/severe All Benign!!!
40
Malignant Melanoma
Malignant neoplasm of melanocytes Used to be uniformly deadly Most arise in skin Other sites: oral/anogenital mucosa meninges, esophagus, eye Risk factors: fair skin, sun exposure, many DPN Usually asymptomatic, may itch Change in color or size of pre-existing lesion
41
CLASSIC teaching is the ABCD’s:
Asymmetry Border Color Diameter (>6mm or pencil eraser)
42
Melanoma in situ
Radial growth (in situ) Superficial, epidermis Cannot metastasize Treat aggresively
43
Melanoma vertical growth
Vertical growth Dermal invasion Formation of nodule Potential to metastasize
44
Breslow’s depth
Probability to metastasize is best predicted by depth of invasion Measured in **millimeters** ***Breslow depth is best*** for prognosis Beyond 1mm worst survival
45
Seborrheic keratosis
``` Common epithelial neoplasm Trunk, head, neck are typical “stuck on” Brown and velvety papules/plaques Leser-Trelat Sign – paraneoplastic, rapid growth of numerous seborrheic keratoses Increases with age Beingin ``` Sharply demarcated Variable melanin/histologically overlap with lentigo Exuberant keratin formation Horn cysts
46
Epithelial Cyst
Down growth of epidermis which becomes cystic Filled with keratin Subcutaneous or dermal nodule Rupture easily and become inflamed Subtypes: epidermal, pilar, dermoid, steatocystoma multiplex
47
Actinic keratosis | Benign form
Benign neoplasm of epidermis (may precede squamous cell carcinoma) Induced by sunlight (most common), ionizing radiation, arsenicals, hydrocarbons Rough spots on skin (less than 1 cm) Sun exposed skin Cytologic atypia of basal layer, hyperkeratosis abnormal stratium cornia Some will progress to squamous cell carcinoma (malignant) if untreated (most likely 1%) Treated by liquid nitrogen, curettage, topical chemotherapy
48
Squamous cell carcinoma counter to actinic keratosis....
Common neoplasm on sun exposed skin in older people Risk factors sun (#1), carcinogens, chronic ulcer, old burn scar, Also xeroderma pigmentosum, chemotherapy or organ transplant In situ: contained above the basement membrane (full thickness atypia) Invasive: invades basement membrane and dermis Less than 5% will metastasize
49
Basal cell carcinoma
``` Most common human malignancy Slow growing, usually older adults Rarely metastasize Risk factors: sun exposure, light pigment, XP Pearly papule with telangiectasia ``` Resemble basal cell layer of epidermis Arise from base of epidermis, possibly hair follicle derived (controversial) Clefts are common between base of neoplasm and dermis
50
Adnexal neoplasms can be a clue to internal pathology
Cowden’s syndrome Muir Torre syndrome
51
Cowden’s syndrome
Hereditary condition prone to multiple hamartomas and malignancy Skin: multiple trichilemmomas (face), benign keratoses on acral skin Mucosal papules, cobblestoning tongue Internal: breast, endometrial and thyroid carcinoma Cerebellar lesions Mutation in PTEN (tumor suppressor gene) if many!!
52
Sebaceous hyperplasia
Acquired, localized increase in sebaceous glands, not neoplastic Glands larger than normal Common on the face Yellow papule
53
Sebaceous adenoma
Benign neoplasm | Lobular circumscribed proliferation of sebocytes and the peripheral basaloid epithelial cells
54
Sebaceous carcinoma
Malignant neoplasm Most are periocular (inner/outer lid) A periocular sebaceous neoplasm is most likely carcinoma, not adenoma or hyperplasia Extraocular forms less common but more likely to occur in Muir Torre syndrome Metastasis common, death in 20%
55
Muir-Torre Syndrome
related to sebaceous carcinoma and adenoma Hereditary syndrome Germline mutations in DNA mismatch repair proteins: (MLH1, MSH2), MSH6, PMS2 These repair errors in base pairing during replication, especially in 1-2 bp repeats (microsatellites) Skin: Sebaceous adenoma and carcinoma, keratoacanthomas Internal carcinomas: Colon/rectal, endometrial, ovarian Represents subset of hereditary non-polyposis colorectal carcinoma syndrome (HNPCC) Young/adult patient with sebaceous adenoma or carcinoma, test for MTS Immunohistochemistry Fast, relatively inexpensive Highly sensitive If loss of staining (indicating loss of DNA mismatch repair protein), genetic testing for confirmation
56
Dermatofibroma
Very common Dermal proliferation of histiocytes and fibroblasts Commonly on legs Tan brown firm papules Etiology unknown – many are clearly reactive hyperplasia (After bug bite) and resolve, others uncertain ``` pinch test Spindled fibroblasts Foamy histiocytes Multinucleated giant cells Collagen trapping Epidermal hyperplasia ``` ``` Well differentiated fibrosarcoma of skin Rarely metastasize/locally aggressive Protuberant nodule within a firm plaque Often nodular in kids Storiform bland spindled cells Honeycomb infiltration of fat ```
57
Capillary hemangioma
Well formed vascular spaces in dermis | Clinically must separate from malignant vascular neoplasms (Kaposi’s sarcoma, angiosarcoma)
58
Where to biopsy? | for rash and lesions
For rashes – non-ulcerated/intact skin, usually sample center and edge, next to the ulcer Discrete lesions Needs to be representative in horizontal AND vertical axis Think about depth
59
To shave or punch…???
Shave: use for superficial (epidermis) lesions (many BCC, AK, SCC in situ, pigmented macules) Better cosmetics, no sutures, electrocautery Punch: use for neoplasms involving the dermis (nodular BCC, SCC, melanoma, etc.) and most rashes Requires sutures Various sizes 1.5 mm – 8 mm

Skin/Musculoskeletal Medicine (10 decks)

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