Derm I, II, III Flashcards

Question

Seborrheic Keratosis (SK) Where are they located/ where are they NOT seen? General population you can see SK in? Histologically what can be seen? Any important associations?

Answer 1

epidermal papillomatosis, acathosis and horn cyst formation "stuck- on" waxy appearaning brown papules or plaques anywhere on the skin EXCEPT PALMS and SOLES Generally patients \> 30 y/o *growth of aging; seldom in young pts* _Histo_: hyperkeratosis, epidermal acanthosis (thickening of S. spinosis), composed of uniform small keratinocytes with a FLAT BASE "**string sign**" and keratin filled "**horn cells**" -- frequent melanin pigment present \*string sign lets us know its benign\* **Leser-Trelat Sign-** multiple (hundreds) may be seen as part of a paraneopastic syndrome in patients with metastatic cancer

Answer 2

Clinically presents as a velvety, papillomatous, hyperpigmented plaques Common on the back of the neck or axilla Could be seen in all age pateints _Histo_: lots of papillomatosis, hyperkeratosis, **NO acanthosis, NO horn cyst** (in comaprision to SK) Associated with insulin resistance and malignancy

Answer 3

SK: Roudish, flat, coin-like waxy plaques with velvety surface. Appears everywhere except palms and soles. Usually seen in middle age people and above - aging. Histologically, acathotic hyperkeratosis, horn cysts, increased melanin. Associated with leser-trelat sign, paraneoplastic syndrome / malignancy AN: Velvety patches that could be seen everywhere but most prominent on the back of the neck and axilla. See in any age. Histologically - epidermal papillomatosis, with increased melanin but NO acanthosis and NO horn cells. Associated with obesity, endocrine issue or hereditary in children and bening. In middle age and above, could be malignant

Answer 4

Skin tag or acrochordon BENIGN polypoid growths most common at sites of RUBBING/FRICTION Composed of **fibroblasts** and **collagen** with **vessels** covered with *_normal or acanthotic epidermis_* *_Inside the polp - adipose tissue and vessels creating the pulp_*

Answer 5

NOT an epidermal neoplasm Follicular cysts composed of hte infundibular portion of the hair follicle which is similar to epidermis, with the exception of a LOSS of RETE PEGS. Makes keratin (like epidermis) and thus appears as a kertain filled cystic structure lined by epidermis. Most do NOT communicate with the epidermis and are therefore DERMAL based nodules

Answer 6

Actinic Keratosis (AK) Squamous Cell Carcinoma (SCC) Basal Cell Carcinoma (BCC)

Answer 7

**_Actinic Keratosis:_** * Clinical presenation:***scaly erythematous papule/plaque** located on *_sun-damaged skin_*; **poorly demarcated**, and esp located on face, balding scalp, posterior neck and dorsal upper extremity. Feel rough and "gritty" and may be difficult to see * Typical patient:* increasingly _common with age_, esp with sun-damaged skin What causes AKs? **UV** radiation but ionizing radiation, arsenic or polycyclic hydrocarbon exposure could also cause them **PRECURSOR OF SCC, third most comon dermatological dx** **Histo:** basal layer ATYPIA with overlying parakeratosis alternating with orthoparakeratosis = FLAG SIGN (alternating pink/blue), SOLAR elastosis _Tx_? **Cryotherapy** or **topical chemotherapeutics** to prevent progression to SCC

Answer 8

Clinical Pres: Generally erythematous, scaly papules / plaques with ill-defined borders (may be confused with AKs) Population: sun-exposed sites (head and neck) region of older individuals, esp MALES. Hyperkeratosis, ulceration or crustin gmay be found on its surface, and sx such as itching, pain and bleeding may also be seen Microscopic Pres: SCC show proliferation of pleomorphic keratinocytes confied to the epidermis (SCC in situ) or extending into the dermis (invasive) Causes- AK is a precursor of SCC although it can develop de novo. Most common cause is exposure to **UV light** with **TP53** mutations, often see at **pyrimidine dimers** (=driving force behind SCC via two hit hypothesis). Xeroderma pigmentosum, extra susceptible. Activating mutations n HRAS, loss of function mutations in Notch receptors, immunosupression (specifically HPV 5 and 8), industrial, chronic wounds, burn scars, arsenic, ionizing radiation

Answer 9

Islands of atypical squamous cells (pinkish)/atypical keratinocytes extending from epidermins into the dermins (if invading) with an uneven base Individual cells have a glassy eosinophlic cytoplasm, with large nuclei. MItotic figures and kertain pearls are also seen (with retained nucelus Normal spinous layer is increased various degrees of differentiation could be seen; increasing malignancy show less demarcation btw the tumor masses and teh stroma, greater atypia, less keratinization and loss of intraceullar bridges other histologic variants include acatholytic, adenosquamous, spindle cell, verrucous and desmoplastic SCC

Answer 10

SCC _in situ -- confied to the epidermis (NO invasion to dermis)_ Histology: **full thickness atypia**, basal layer sparing (EYELINER SIGN), may show skip areas but involved follicles (in contrast to AKs), NO invasion into the dermis (in contrast to SCC) - no blebbing -- no atyoical signs in the lower levesl; otherwise, atypical full thickness, disorganization across layers Clincally a plaque like lesion Won't regress, needs to be excised

Answer 11

**SCC IN SITU** Similar histological appearance as bowen's disease **HPV induced**, located on the **genitals**! *esp HPV 5 and 8* Frequently multiple papules May spontaneous regress or progress Major difference is that this is HPV driven and CAN REGRESS

Answer 12

_Appearance_: Pearly, pink papule with overlying telangiectasia _Risk Factors:_ older individuals at sun exposed sites, fair skin, men (2:1), family history of skin cancer, immunsuppressed, radiation therapy, genetic syndromes - DNA mismatch repair sydromes (xeroderma pigmentosa, nevoid BCC syndrome) **_PTCH_** gene mutations - 30%, regulates the hedgehog pathway, could be genetically acquired (Gorlin Syndrome) **P53** mutations 40-60% Epidemiology: Most COMMON invasive cancer in humans

Answer 13

Nevoid Basal Cell Carcinoma **Autosomal Dominant** *_Multiple BCC before the age of 20_* accompanied by medulloblastomas, meningioma, ovarian fibromas, odontogenic keratocyts, skeletal defects (macrocephaly, hypertelorism, frontalparieta bossing, spina bifida or rib abnormality...) **PTCH** gene on chromosome **9q22.3** **"2 hit" hypothesis**

Answer 14

Comes from the basal layer Blue tumor **peripheral palisading**"picket fence" **Retraction artifact** (due to how the neoplasm separates from the rest of the layers) *_Nodular type - islands of basaloid cells in the dermis_*

Answer 15

Only 5% are malignant; most are excised 1) excision for low risk SCC (less than 2 cm in diameter, well differentiated) 2) Mohs micographic surgery 3) Radiation therapy (in combi with other modalities for aggressive, recurrent or large inoperable tumors) 4) Cryotherapy (for small, superficial or low-risk lesions)

Answer 16

Lentigos Melanocytic Nevi Melanoma

Answer 17

FALSE! Melanocytes are clearish cells in the BASAL layer with dark nuclei @ a ratio of 1:10 Derived from neuroectoderm Fxn: make melanin pigment using enz tyrosinase They are smaller hyperchromatic with clearish cells - they don't hold their pigment but pass it to their neighbor, agulated nuclei on the basal layer * Dark skin indviduals don't have more melanocytes but rather the melanocytes are just more active thus make more melanin.* * Albinism is a disease in which melanocytes are unable to produce melainin because they lake the enzyme tyrosinase and thus have very high rates of skin cancer (don't have melanin to protect from the UV radiation)*

Answer 18

Lentigos and nevi **Lentigo** = small, oval tan-brown, located in mucous membranes at any age; flat lesion melanocytic hyperplasia along basal layer (difficult to appreciate) _Two types:_ solar lentigines (liver spots, age spots) and simple lentigines **_Melanocytic Nevi:_** tan to bronw macules and papules. ***Common type:*** junctional (epidermal), compound (both epi and derma), and intradermal (dermal) - **nests** of melanocytes ***Dysplastic Nevi**:* single and cytologically atypical melanocyte, in addition to nests with architectural atypia

Derm I, II, III Flashcards

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