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SBL Test 1 > Robbins: Chapter 25 Review > Flashcards

Robbins: Chapter 25 Review Flashcards

1
Q

Melanocytes are derived from ____ and migrate during embryogenesis to selected ______ sites (skin/CNS), but also eyes and ears.

A

NC cells

Ectodermal sites (skin/CNS) + eyes + ears

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2
Q

Freckles histology

A

Hyperpigmentation: ↑↑↑ production of melanin by basal keratinocytes

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3
Q

Disorders of pigmentation and melanocytes

A
  1. Freckles
  2. Lentigo (Lentigines)
  3. Nevi
  4. Melanoma
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4
Q

Benign Epithelial Tumors

A
  1. Seborrheic keratoses
  2. Acanthosis nigricans
  3. Fibroepithelial polyp
  4. Epithelial Inclusion Cyst
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5
Q

Adnexal Appendage Tumors

A
  1. Eccrine poroma
  2. Cylindroma
  3. Syringoma
  4. Sebaceous adenoma
  5. Pilomatricoma
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6
Q

Premalignant and malignant epidermal tumors

A
  1. Actinic keratoses
  2. Squamous cell carcinoma
  3. Basal cell carcinoma
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7
Q

Tumors of dermis

A
  1. Dermatofibroma (Benign fibrous histiocytoma)

2. DFSP (dermatofibrosarcoma protuberans)

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8
Q

Tumors of cellular migrants of skin (proliferative disorders of cells that arise everywhere, but home to skin)

A
  1. Mycosis Fungoides (Cutaneous T-cell lymphoma)

2. Mastocytosis (Uticaria pigmentosa)

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9
Q

Disorders of epidermal maturation

A

Ichythosis

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10
Q

Acute Inflammatory Dermatitis:

A
  1. Uticaria (Hives)/Wheals
  2. Acute eczematous dermatitis
  3. Erythema multiforme
  4. Psoriasis
  5. Seborrheic Dermatitis
  6. Lichen planus
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11
Q

Linear (non-nested) hyperplasia of hyperpigmented melanocytes in the basal layer of the epidermis

A

Lentigo (lentigines): hyperpigmentation is NOT due to sunlight

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12
Q

Melanocytic/ pigmented nevi aka “Mole” are more often acquired or congenital?

A

Acquired.

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13
Q

Mutations in acquired melanocytic nevi

A
  1. RAS signaling (most are due to activating mutations in RAS signaling): BRAF or NRAS
  2. Loss of CDKN2A (encodes p16/INK4a) => CDK4 activation
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14
Q

Types of acquired melanocytic nevi (moles)

A
  1. Junctional nevi (flat macule)
  2. Compound nevi (elevated papule)
  3. Intradermal nevi (elevated papule)
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15
Q

Specific histological findings in compound nevi

A
  1. Pseudohorn cyst

2. No inflammatory response

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16
Q

Spitz nevus

A

aka spindle/epitheloid nevus

Red-pink nodule, often confused hemangioma

Large, plump fusiform cells with pink-blue cytoplasm that undergo fasicular growth.

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17
Q

Blue Nevus

A

Painful black-blue nodules, often confused with melanoma

Non-nests in dermis
Highly dendritic
Very pigmented
Undergo fibrosis

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18
Q

What is a potential marker/ precursor of melanoma

A

Dysplastic nevus

Also: congenital nevus

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19
Q

What do dysplastic nevus look like

A
  • Flat macules/ slightly raised plaques with variable pigmentation and irregular borders
  • Larger than acquired and can be hundreds
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20
Q

Dysplastic nevus mutations

A

Same as melanocytic nevus

+ TERT

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21
Q

Do all melanomas begin as dysplastic nevus and vise verse

A

If multiple => ↑↑↑ risk of melanoma. However, majority do NOT become melanomas and not all melanomas are first dystplastic nevi.

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22
Q

Dysplastic nevus syndrome?

A

Dysplastic nevus syndrome: AD => multiple dysplastic nevi and melanoma at many sites: >50% of getting melanoma by 60 YO

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23
Q

Histology of Dysplastic nevus

A
  1. Large and coalesced (fused) intraepidermal nests of melanocytes
  2. Cytologic atypia = irregularly shaped, dark staining nuclei.
  3. Lentiginous melanocyte hyperplasia: replacement of basal layer along DE junction
  4. Underlying dermis undergoes lamellar fibrosis.
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24
Q

Most deadly of all skin cancers

A

Melanoma

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25
Q

Marker and stain for melanoma

A

S100

HMB-45 (+)

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26
Q

Are most melanomas acquired or sporadic

A

sporadic due to UV damage

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27
Q

MC mutated gene in melanoma

A

TERT => activates telomerase

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28
Q

Driver mutations for melanoma

A
  1. Mutations that cause cell cycle to lose control:
    CDKN2A mutation  encodes CDK-I
    (p16/ INK4a) and decreases Rb
  2. Mutations that ↑↑↑ [RAS & PI3K/AKT] proliferation pathway:
    - BRAF activating mutation (40-50%
    melanomas);
    - NRAS activating mutation (15-
    20%)
  3. TERT activating mutation: activates telomerase = seen in 70% of
    tumors (most
    common mutated
    gene!!)
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29
Q

How do melanomas grow and which phase can metastatis occur?

A

Radial: spread along epidermis; do NOT metastasize

Vertical: Melanocytes lacking maturation (no neurotinzation) invade dermis => nodular melanoma (WORST type) that can metastasize

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30
Q

Types of Radial growing melanoma. Which has the best prognosis?

A

1) Superficial spreading = MC subtype (75% of melanomas) due to sunlight.
2) Lentigo maligna = Hutchinsons freckle (small, flat, dark spots) confined to epidermis that continue to grow slowlyyy. MC on face of older men. BEST prognosis
3) Acral/ mucosal lentiginous = MC type in dark-skinned patients (AZNs & AA) that grow on genitals*, palms, soles and under nails. C-kit mutation

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31
Q

Melanoma is associated with what disorder?

A

Xeroderma pigmentosum

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32
Q

RF for melanoma

A
  1. Sun exposure
  2. Dysplastic nevi (1/3 of melanomas arise from dysplastic nevi)
  3. Light skin, hair and eyes
  4. Hx of blistering, proximity to equator, indoor occupation, outdoor hobby
  5. FH of melanoma
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33
Q

Where are melanomas MC located?

A

Sun-exposed areas:

  1. BANL: Back, arms, neck and legs
  2. Females = back and legs
  3. Males = upper back
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34
Q

What determines the risk of a melanoma metastasizing?

A

↑↑↑ depth of thickness = ↑↑↑ risk of metastasis (Breslow thickness) =
distance from granular epidermis to the
deepest intradermal layer.

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35
Q

______ are inherently immunogenic, eliciting a T-cell response

A

Melanomas.

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36
Q

Melanomas metastasize to…

A

Regional LN (sentinel LN)

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37
Q

Favorable prognosis of melanoma

A
  1. Thinner depth of tumor (Breslow
    thickness) ,
  2. No mitosis (<1 mm),
  3. Brisk response of lymphocytes that infiltrate tumor
  4. NO tumor
  5. Regression
  6. NO ulceration
  7. No metastasis to sentinel LN
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38
Q

Poor prognosis of melanoma

A
  1. Sore that doesn’t heal
  2. Spread of pigment from border into surrounding skin
  3. Redn/ swelling @ border
  4. Itchiness/pain/ oozing
39
Q

Histology of melanoma

A
  1. Nests and single atypical melanocytes at the dermal-epidermal junction.
  2. Run on feet nests: nests merge
  3. Large cells with expanded, irregular nuclei + peripherally clumped chromatin + prominent eosinophilic nucleoli
  4. Mononuclear inflammatory infiltrate: because inherently immunogenic
  5. Stain with HMB-45
40
Q

Seborrheic Keratoses

A

Proliferation of immature keratinocytes that arise spontaneously on the trunk

MC in older people >50

41
Q

Seborrheic Keratoses can arise as a paraneoplastic syndrome due to..

A

Leser- Trelat sign (HY): paraneoplastic syndrome associated with gastric adenocarcinoma, causing “explosive” onset of multiple itchy seborrheic keratoses lesions

42
Q

Seborrheic Keratoses gross morphology

A

waxy, tan-brown flat plaques (raise, but flat) that “stuck on lk a coin” and itchy.

can scrape off

43
Q

Seborrheic Keratoses histology

A
  1. Dark cells, similar to basal skin cells
  2. Horn cysts =keratin-filled cysts
  3. Invagination cysts = invaginations of keratin into the main mass
  4. NL dermis
44
Q

What is Acanthosis Nigricans

A

Diffuse epidermal hyperplasia due to stratum spinosum

45
Q

Is AN benign or malignant?

A

can be BOTH

Benign = childhood or puberty

Malignant = middle-age or older

Can be benign or malignant:
80% = Benign
• Acquired or inherited

20% = AN is a paraneoplastic syndrome associated with with malignancy (GI carcinoma)

46
Q

how can you acquire a benign AN?

A

(obesity, DB, pineal/pituitary tumor) or inherited (AD)

47
Q

AN histology

A
  1. Epidermal and dermal papillae undulate sharply to form many peaks and valleys
  2. Hyperkeratosis with prominent rete ridges and basal hyperpigmentation (W/O melanocyte hyperplasia)
48
Q

Fibroepitelial polyp is also called what?

A

skin tag, acrochrodon, squamous papilla

49
Q

Epithelial inclusion cyst is also called what?

What is it?

Complication

A

wen” or “sebaceous cyst”

Invagination and cystic expansion of epidermis or a hair follicle

Traumatic rupture can spill keratin into dermis, leading to painful granulomatous inflammation

50
Q

Syringoma

MC where
What are they?
Histology?

A
  1. MC = lower eyelid
  2. Multiple, small tan papule near lower eyelid
  3. BAsaloid epithelium with eccrine differentiation
51
Q

Actinic Keratosis

A

Proliferation of atypical keratinocytes in the epidermis due to UV radiation => premalignant skin lesion

52
Q

RF for actinic keratosis

A
  1. Light skin
  2. Ionizing radiation
  3. Hydrocarbons
  4. Arsenic
53
Q

Gross morphology of actinic keratosis

A
  1. <1cm tan/brown/red skin colored papule or plaques that feel like sand paper
  2. Cutaneous horns
54
Q

Histology of actinic keratosis

A
  1. Hyperkeratosis
  2. Parakaratosis: keratin with retained nuclei in stratum corneum
  3. Dyskeratosis (ABNL premature keratinization in cells below stratum granulosum) => pink cytoplasm
  4. Cytologic atypia of keratinocytes in basal layer: enlarged and hyperchromatic nuclei
  5. Intracellular bridges
  6. INTACT BM

Dermis

  1. Thick dermis
  2. Solar elastosis = blue-gray elastic fibers (collagen) in superficial dermis due to sun damage
55
Q

Squamous cell carcinoma

MC in and genetics

A

> 75YO M (rare before 45 YO)

  1. TP53 mutations * (especially in actinic keratosis in whites)  DNA damaged caused by UV is NOT repaired
  2. Xeroderma pigmentosum = AR inherited mutation of nucleotide excision repair pathway, needed to repair pyrimidine dimers => ↑↑↑ risk of cutaneous SCC and BCC
  3. Epidermodysplasia verruciformis: AD disorder assx with ↑↑↑ susceptibility to HPV and cutaneous SCC
56
Q

Epidermodysplasia verruciformis: AD disorder assx with ↑↑↑ susceptibility to

A

HPV

cutaneous SCC

57
Q

Xeroderma pigmentosum = AR inherited mutation of nucleotide excision repair pathway, needed to repair pyrimidine dimers => ↑↑↑ risk of

A

SCC and BCC

Melanoma

58
Q

RF for SCC

A
  1. BIGGEST = Lifetime exposure to sun ***
  2. Chronic immunosuppression (chemo or organ transplant): increase risk of infection by HPV 5/8
  3. Chronic skin inflammation (burns, chronic ulcers, draining sinus tracts)
  4. Arsenic exposure
59
Q

Do SCC metastasize/invade often?

A

5% metastasize to regional N; RARELY metastasize beyond LN.

If invasive, they are usually found when small and resectable :)

60
Q

Gross morphology of SCC

A

In-situ (no post dermoepidermoid junction): Red, scaly plaques with sharp borders

Invasive (more advanced): Nodular, hyperkeratotic and may ulcerate/undergo necrosis

61
Q

Histology of SCC

A

In-situ lesion:
• Keratinocytes in ALL of epidermis has cytologic atypia (enlarged and hyperchromic nuclei)

Invasive lesion
•	Diff amounts of hyperkeratosis
•	Dyskeratosis (single-cell keratinization)
•	Infiltrate BM
•	Highly anaplastic
62
Q

How do SCC differ from actinic keratosis?

A

Cytologic atypia (enlarged and hyperchromic nuclei) is seen in ALL levels of epidermis

63
Q

MC skin cancer BUT LOWEST potential for recurrence or metastasis

A

Basal Cell carcinoma: Slow growing, locally aggressive skin cancer that RARELY metastasizes, often in sun-exposed areas.

64
Q

Basal cell carcinoma

Genetics

A
  1. LOF PTCH mutation on Chr 9q22.3:  PTCH associates with SMO transmembrane protein forming a receptor for SHH. W/o PTCH, SMO (+) without SHH binding  constitutive (+) of GLI1 uncontrolled SHH signaling
65
Q

BCC is associated with what disorders?

A
  1. Xeroderma pigmentosum
2. NBCCS (Nevoid BCC syndrome) /Gorlin syndrome / Basal Cell Nevus Syndrome: AD LOF mutation of PTCH on Chr 9q22 =>
A.  many BCC in pts < 20YO + 
B. Medulloblastomas
C.  + ovarian fibromas 
D. + odontogenic keratocysts 
E. + pits of palms and soles
66
Q

Clinical presentation of BCC

How do they present if aggressive?

A
  1. Pearly papules with telangiectasias (dilated BV in dermis)

2 If aggressive => Rodent Ulcer= may ulcerate and extend into bone or facial sinuses

67
Q

Histology of BCC

A
  1. Nests of basaloid dark cells that extend into dermis surrounded by clear halo (artifact)
  2. Hyperchromatic nuclei
  3. Palisading nuclei: cells at periphery of nests whose nuclei line up in parallel.
68
Q

What is a Dermatofibroma (Benign fibrous histiocytoma)

A

Benign tumor of fibroblasts + histiocytes (Factor 13a -positive dendritic cells) in dermis that most commonly occurs after trauma, suggesting ABNL injury and inflammation response.

69
Q

Dermatofibroma (Benign fibrous histiocytoma) is MC in who

A

young/middle aged F

70
Q

Dermatofibroma presentation

A

Tender, asymptomatic firm, tan brown papule MC on LEGS

Dimple sign: lateral pressure causes dimpling

71
Q

Dermatofibroma histology

A
  1. Well-defined non encapsulated mass made up of benign spindle-shaped fibroblasts in mid-dermis
  2. Overlying epidermal hyperplasia
  3. Pseudoepthielium hyperplasia: hyper pigmented elongated rete ridges
72
Q

DFSP mutation

A

Translocation of collagen 1A1 (COL1A1) and PDGFB  ↑↑↑ secretion of PDGF-B  tumor grows via autocrine loop

73
Q

DFSP presenation

A

trunk
Firm (indurated) plaque that can ulcerate

slow growing

locally aggressive

RARELY metastasizes

74
Q

DFSP histology

A
  1. Storiform pattern of fibroblasts = fibroblasts arranged in pinwheel
  2. Honeycomb appearance: = extends into SUBQ fat
75
Q

Osteoporosis in a pre-menopausal W or M is a clue of dx of what?

A

Mastocytosis (urticaria pigmentosa)

76
Q

Signs of Uticaria pigmentosa1

A
  1. Darrier Sign => when rub=> produces area of dermal edema and erythema (wheal)
  2. Dermatographism
  3. If systemic = purititis and flushing triggered by food, temp changed and alcohol
77
Q

What is ichythosis

A

Inherited defect in epidermal maturation (defective desquamation => inc cell-cell adhesion) => hyperkeratosis and kids are born with fish-like scales

78
Q

Ichythosis could be a paraneoplastic syndrome d/t

A

lymphoid or visceral malignancy

79
Q

Histology of ichythosis

A
  1. Buildup and compaction of statum corneum

2. No inflammation

80
Q

Acute inflammatory dermatitis disorders

A
  1. Uticaria (hives)/wheals
  2. Acute eczematous dermatitis
  3. Erythema Multiforme
81
Q

Charactersitsics of Acute inflammatory dermatitis disorders

A
  1. Days - weeks
  2. Inflammatory infiltrates (usually lymphocytes and MO, rather than neutrophils
  3. Edema
  4. Different degrees of epidermal, vascular or subQ injury
82
Q

Histology of Uticaria/hives

A
  1. Superficial perivenular infiltration of mononuclear cells and MO sparsely infiltrate superficial perivenular
  2. Collagen bundles are more widely spaced apart due to edema
  3. Dermal edema (angioedema)

Lasts only a few hours

83
Q

what type of HS reaction is Acute eczematous dermatitis

A

Type 4 hypersensitivity reaction that is T-cell mediated

84
Q

Morphology of rash in Acute eczematous dermatitis

A

red, papulovesicular rash (blistering) that oozes and crusts

If persists => reactive acanthises and hyperkeratosis => red, scaly plaque

85
Q

Histology of Acute eczematous dermatitis

A
  1. Spongiosis => intracellular edema in epidermis, particular in stratum spinosum
  2. Intracellular bridges = desmosomes that are pulled apart due to edema (spongiosis)
  3. If spongiosis is severe enough  acantholysis
86
Q

Erythema Multiforme histology

A
  1. Interface dermatitis = lymphocytes along DE junction

2. Degenerating and necrotic keratinocytes

87
Q

Psoriasis histology

A
  1. Acanthosis = epidermal thickening  Elongation of rete ridges (test-tubes in rack)
  2. Papillomatosis
  3. Parakeratotic scaling
  4. Stratum spinosum = inc size
  5. Stratum granulosum = thin/absent
  6. Neutrophils superficial dermis. If go to the stratum corner => Munro microabscesses
88
Q

Psoriasis is MC in who

A

HLA-C; (HLA Cw*0602)

89
Q

Seborrheic Dermatitis

histology

A
  1. Spongiotic dermatitis = edema
  2. Acanthosis
  3. Mounds of parakeratosis + acute inflammatory cells at ostia hair follicles.
90
Q

Lichen Planus

associated with =

histology =

A
  1. HepC
  2. Acanthosis = saw-tooth pattern of rete ridges
  3. Hyperkeratosis
  4. Hypergranulosis
  5. Lymphocytes at D-E junction
91
Q

Lichen planus in oral mucosa can evolve into what

A

SCC

92
Q

Lichen planus is MC where

A

MC= ankle and wrists

*Self-limited: goes away 1-2 years after onset, but leaves a post-inflammatory hyperpigmentation. Oral lesions, however can persist for years

93
Q

Wickham straie = white dots/lines caused by Hypergranulosis that is best seen on oral lesions is MC in what

A

lichen planus

SBL Test 1 (15 decks)

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