Week 1 - Derm Flashcards

1
Q

Vitiligo

A
  • Partial or complete LOSS of melanocytes
  • Due to autoimmune
    • T-cells attack melanocytes in skin and cause destruction of melanocytes resulting in hypopigmented skin

**Autoimmune lymphocyte mediated melanocyte destruction (normal enzyme)

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2
Q

Albinism

A
  • No melanin production/decreased production
  • Inherited defect in Tyrosinase enzyme
  • Normal number of melanocytes

***Congenital abscence of enzyme and melanin is not made/decreased.

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3
Q

What are three pigmented lesions due to excess melanin?

A
  1. Freckle
  2. Melasma
  3. Solar lentigo
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4
Q

What three pigmented lesions due to increased number of melanocytes?

A
  • Melanocyte hyperplasia
    • lentigo simplex
  • Melanocytic neoplasia
    • Nevi
    • Melanoma
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5
Q

Freckle

A
  • a.k.a Ephelis, Ephelides
  • small tan red macules arising in childhood
  • fade and reappear in cycle
  • Histology: increased pigment in basale melanocytes
    • overactive melanocytes due to sun exposure
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6
Q

Melasma

A
  • Mask-like facial hyperpigmentation
    • usually on cheeks, forehead, temples
    • bilateral cheeks of face in “butterfly” pattern
  • Melanocytes have enhanced pigment transfer to keratinocytes or macrophages
    • thought to be estrogen related (pregnancy, oral contraceptives, hydantoin)
    • resolves after pregnancy
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7
Q

Solar Lentigo

A
  • Hyperpigmentation of basale epidermis due to excess melanin production
  • Sun protective mechanism of melanocytes
    • too much sun exposure over a lifetime
    • Typical farmer (>70 years old)
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8
Q

Lentigo Simplex

A
  • Localized hyperplasia of melanocytes
  • Small brown macules
  • Not sun related
  • All ages

***Histopathology: Increased melanocytes, increased pigment in stratum corneum and basale epidermis, rete ridges elongated/thinned

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9
Q

What is neoplasia?

A

Genetically abnormal growth (irregular cell growth).

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10
Q

What is cancer?

A

Malignant neoplasm

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11
Q

Benign neoplasia

A
  • Neoplasm with no capability for metastasis
  • Can be destructive or symptomatic
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12
Q

Malignant neoplasia

A
  • Neoplasm with potential for metastasis and subsequently growth/proliferation at distant site
  • Often locally destructive, but may not be
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13
Q

Nevi

A
  • Benign neoplasms of melanocytes
  • Many Types:
    • Acquired/congenital = typical mole
    • Junctional (epidermal), Compound (epidermal/dermal), or Dermal
    • Spitz/spitzoid
    • Atypical (dysplastic)
    • Dermal variants
      • Blue nevus
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14
Q

Spitz nevi

A

Difficult to distinguish from melanoma under microscope occasionally.

ALL HAVE TO BE EXCISED.

  • don’t know how they will behave
  • difficult to judge malignant potential
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15
Q

Dysplastic Nevi (DPN)

A
  • Atypical nevi (mild, moderate, severe atypia)
  • Isolated dysplastic nevus = probably no risk or minimal risk of melanoma
  • Multiple dysplastic nevi = marker of increased risk of melanoma

***Should excise moderate/severe dysplastic nevi.

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16
Q

Malignant neoplasm

A
  • Malignant neoplasm of melanocytes
  • Most arise in skin (can arise in oral/anogenital mucosa, meninges, esophagus, eye)
  • Usually asymptomatic, may itch
  • Change in color or size of pre-existing lesion
  • RISK FACTORS: fair skin, sun exposre, many DPN
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17
Q

ABCD’s of Melanoma

A
  • Asymmetry
  • Border
  • Color
  • Diameter (>6 mm = penicl eraser)
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18
Q

Melanoma in situ

A

Localized to epidermis

(does not cross basement membrane)

***Benign, but likely to become malignant at some point

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19
Q

Breslow depth

A

How deep melanoma invades into the dermis.

  • Probability to metastasize is best predicted by depth of invasion
  • ***Best prognostic indicator***
  • measured in millimeters
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20
Q

Breslow depth and survival rates

A
  • <1mm: 5 year survival is 95-100%
  • 1-2mm: 5 year survival is 80-96%
  • 2.1-4mm: 5 year survival is 60-75%
  • >4mm: 5 year survival is 37-50%
21
Q

Other prognostic indicators

A
  • Ulceration (usually bad, rapidly growing)
  • Mitotic rate
  • Sentinel lymph node biopsy
  • Clark level (I-V)
  • Gregression
  • Inflammatory pattern
22
Q

Seborrheic keratosis

A
  • Most common epithelial neoplasm
    • sign of aging
    • benign epithelial proliferations
  • “Stuck on” brown velvety papules/plaques
    • exuberant keratin formation
    • variable melanin
    • sharply demarcated
23
Q

Fibroepithelial polyp/Acrochordon

A

Skin Tag

  • Soft flesh colored bag-like tumor with stalk
  • Inconsequential
  • very common
  • not neoplastic
  • may increase in pregnancy
  • may be increased in diabetes, obesity
24
Q

Epithelial Cyst

A
  • Down growth of epidermis which becomes cystic
  • Filled with keratin
  • Subcutaneous or dermal nodule
  • Rupture easily and become inflammed
  • Subtypes:
    • Epidermal
    • Pilar
    • Dermoid
    • Steatocystoma multiplex
25
Q

Actinic keratosis

A
  • Benign neoplasm of epidermis
    • may preced sqaumous cell carcinoma
  • Induced by sunlight, ionizing radiation, arsenicals, hydrocarbons
  • Rough spots on skin
  • Cytologic atypia of basale layer, hyperkeratotic
    • usually scaly and erythematous papules or plaques
26
Q

How do you treat actinic keratosis?

A
  • Liquid nitrogen
  • curettage
  • topical chemotherapy
27
Q

Types of Squamous cell carcinoma

A
  • In situ: contained above the basement membrane
  • Invasive: invades basement membrane and dermis (malignant)
28
Q

Clinical presentation of Squamous Cell Carcinoma

A
  • Usually very scaly, red, raised
  • common on sun exposed skin in older people
  • Risk factors: sun, carcinogens, chronic ulcer, old burn scar
  • Less than 5% will metastasize
29
Q

Basal cell carcinoma

A
  • Most common human malignancy
    • slow growing, usually older adults
  • Appearance: pearly papule with telangiectasia (small dilated blood vessels near the surface)
    • arise from base of epidermis
  • Risk factors: sun exposure, light pigment, xeroderma pigmentosum
30
Q

Gorlin Syndrome

A
  • Basal cell Nevus syndrome
  • Dominant inheritance (rare)
    • tumor suppressor gene is mutated
  • BCC at early age with abnormalities of bone, nervous system, eyes, and reproductive organs
31
Q

Cowden’s syndrome

A
  • Hereditary condition prone to multiple hamartomas and malignancy
    • Skin: multiple trichilemmomas (benign proliferation of hair follicle epithelium), benign keratoses on acral skin
    • Mucosal papules, cobblestoning tongue
    • Internal: breast, endometrial, and thyroid carcinoma
    • cerebellar lesions
  • Mutation in PTEN tumor suppressor gene
32
Q

Sebaceous hyperplasia

A
  • Acquired, localized increase in sebaceous glands
  • Non-neoplastic
  • Glands larger than normal
  • Common on the face
  • yellow papule
33
Q

Sebaceous adenoma

A
  • Benign neoplasm
  • Lobular circumscribed proliferation of sebocytes and the peripheral basaloid epithelial cells
34
Q

Sebaceous carcinoma

A
  • Malignant neoplasm (cancer)
  • Most are periocular (inner/outer eye lid)
    • A periocular sebaceous neoplasm is most likely carcinoma, not adenoma or hyperplasia
  • Extraocular forms are less common, but more likely to occur in Muir Torre syndrome
  • Metastasis common (death in 20%)
35
Q

Muir-Torre Syndrome

A
  • Hereditary syndrome
  • Germline mutation is DNA mismatch repair proteins
    • **MLH1, **MSH2, MSH6, PMS2
    • repair errors in base pairing during replication, especially in 1-2 bp repeats
  • Skin: sebaceous adenoma and carcinoma, keratoacanthomas
  • Internal: carinomas of the colon/rectum, endometrium, ovarian
  • subset of hereditary non-polypsis colorectal carcinoma syndrome (HNPCC)
36
Q

Who do you test for Muir Torre Syndrome (MTS)?

A

Young/adult patients with sebaceous adenoma or carcinoma.

37
Q

Merkel Cell Carcinoma

A
  • very aggressive epithelial neoplasm
    • highly fatal due to metastasis
  • most caused by polyomavirus
38
Q

Dermatofibroma

A
  • a.k.a. benign fibrous histiocytoma
  • very common dermal proliferation of histiocytes and fibroblasts
  • extremely firm, tan/brown papules
  • commonly on legs
39
Q

Dermatofibrosarcoma Protuberans (DFSP)

A
  • Malignant form of a spindle cell stromal neoplasm
  • locally aggressive
    • rarely metastasize
  • Protuberant nodule with a firm plauq
    • honeycomb infiltration of fat
40
Q

Hemangioma

A
  • Benign vascular neoplasm
  • well formed vascular spaces in dermis
41
Q

Angiosarcoma

A
  • Malignant
  • Very aggressive in skin and internally
  • usually fatal
    • hard to treat/cure
42
Q

Cutaneous T-cell lymphoma

A
  • T-cells arise in marrow and travel to skin
  • Usually very slowly progressive disease
  • Age: >40 years
  • Looks like psoriasis, eczema, etc. in early stage
    • nodules come later
43
Q

Mycosis Fungoides

A
  • Most common type of Cutaneous T-cell Lymphoma
  • Neoplastic CD4+ cells
    • Infiltrate the epidermis and form clusters
    • T-cells invade the epidermis
  • Patchy, circular rashes
44
Q

Cutaneous B-cell Lymphoma

A
  • Less common than T-cell lymphoma
  • Usually solitary of few nodules rather than patches/plaques
  • Usually good prognosis
  • Must exclude secondary cutaneous involvement by nodal lymphoma
45
Q

Mastocytosis

A
  • Mast cells originate in the marrow and travel to the skin
  • Classified by cutaneous vs. systemic
  • Urticaria pigmentosa: localized to skin
    • Darier’s sign (histamine)
  • Systemic mastocytosis: organ involvement
    • Pruritis, flushing, runny nose, bleeding (heparin)
46
Q

When do you do a shave biopsy?

A

**Superficial lesions**

  • BCC, AK, SCC in situ, pigmented macules
  • Better cosmetics
  • No sutures
  • Electrocautery
47
Q

When do you do a punch biopsy?

A

Neoplasms involving the dermis.

  • Nodular BCC
  • SCC
  • Melanoma
  • Most RASHES
  • Requires sutures
  • Various sizes 4mm-8mm
48
Q

What biopsy should a doc perform if they do not know what type of neoplasm?

A

***IF YOU DON’T KNOW,

DO A PUNCH BIOPSY!!!

49
Q
A