Block 9 - L8, 9, 10 Flashcards

1
Q

What are the 3 layers of the skin (superficial to deep) and how do they appear on H&E stain?

A
  1. Epidermis (basophilic)
  2. Dermis (eosinophilic)
  3. Subcutaneous tissue (clear)
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2
Q

What are the 5 layers of the epidermis (superficial to deep)?

A
  1. Stratum corneum
  2. Stratum lucidum (in thick skin only)
  3. Stratum granulosum
  4. Stratum spinosum
  5. Stratum basale
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3
Q

Where are skin stem cells located?

A

Stratum basale

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4
Q

What makes up the stratum spinosum and what is its purpose?

A

Keratinocytes connected by desmosomes - strength

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5
Q

What makes up the stratum granulosum and what is its purpose?

A

Lipid envelope and keratohyalin granules - secrete substances that hold the corneum together

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6
Q

What is desquamatization?

A

Process of epidermal maturation; layers of the epidermis represent vertical maturation from undifferentiated basal cells to fully differentiated cornified cells

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7
Q

How long does it take for the skin to fully mature?

A

25 days

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8
Q

Disordered maturation causes ___ due to lack of desquamation.

A

Skin thickening

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9
Q

Shorter maturation periods are seen in ___ conditions.

A

Inflammatory

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10
Q

List the epithelial cell junctions of the skin.

A
  1. Tight junction
  2. Adherens junction
  3. Desmosome
  4. Gap junction
  5. Hemidesmosome
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11
Q

What is the role of tight junctions?

A

Seals the gap between epithelial cells, controls water and solutes

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12
Q

What is the role of adherens junctions?

A

Connects actin filament bundles in one cell with that in the next cell; strength

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13
Q

What is the role of desmosomes?

A

Connect intermediate filaments in one cell to those in the next; strength

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14
Q

What is the role of gap junctions?

A

Passage of small water solute molecules between cells; communication

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15
Q

What is the role of hemidesmosomes?

A

Anchor intermediate filaments to the ECM (basement membrane)

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16
Q

What are the three broad categories of skin pathology?

A
  1. Tumors
  2. Rashes
  3. Infection
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17
Q

What is ichthyosis?

A

Defective desquamatization leading to a build up of compacted scales (stratum corneum is retained and thickened)

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18
Q

What are the etiologies of ichthyosis?

A
  1. Ichthyosis vulgaris (AD)
  2. Congenital ichtyosiform erythroderma (AR)
  3. Lamellar icthyosis (AR)
  4. X-linked ichthyosis
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19
Q

X-linked ichthyosis involves a deficiency in ___.

A

Steroid sulfatase

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20
Q

How does ichthyosis vulgaris appear grossly?

A

Fish-like scales (orthokeratosis)

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21
Q

How does ichthyosis vulgaris appear microscopically?

A

Increase/thickening of the stratum corneum

Thinning or loss of the granular layer

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22
Q

List the benign epithelial neoplasms involving keratinocytes.

A
  1. Seborrheic keratosis
  2. Acanthosis nigricans
  3. Fibroepithelial polyp/acrochordon/skin tag
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23
Q

How does seborrheic keratosis appear grossly?

A

“Stuck-on” verrucous waxy brown papules or plaques

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24
Q

Where is seborrheic keratosis found on the body?

A

Anywhere on the skin except for the palms and soles

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25
Q

What population (age) gets seborrheic keratosis?

A

> 30 y/o (middle age and up)

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26
Q

How does seborrheic keratosis appear histologically?

A
  1. Hyperkeratosis
  2. Papillomatosis (undulating appearance - Bart Simpson hair sign)
  3. Acanthosis (thickening of the epidermis)
  4. Uniform small keratinocytes with a flat base (string sign)
  5. Keratin-filled horn cysts
  6. Frequent melanin pigment present
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27
Q

How does acanthosis nigricans appear grossly?

A

Poorly defined hyperpigmented verrucous plaques with velvety “scales”

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28
Q

Where is acanthosis nigricans found on the body?

A

Commonly in the creases of the axilla and neck

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29
Q

How does acanthosis nigricans appear histologically?

A
  1. Hyperkeratosis
  2. Papillomatosis
  3. Basal layer hyperpigmentation
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30
Q

What population (age) gets acanthosis nigricans - benign type and malignant type?

A

Benign type: childhood (associated with obesity, endocrine issues, also hereditary)

Malignant type: middle age and up

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31
Q

What is the Leser-Trelat sign?

A

Sudden onset of multiple seborrheic keratoses that may indicate a paraneoplastic syndrome (most common underlying neoplasm - GI)

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32
Q

How does an acrochordon appear grossly?

A

Soft, tan to-flash-colored PEDUNCULATED papule, 1-10 mm in size with a smooth or folded surface

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33
Q

Where is acrochordon found on the body?

A

Axilla, neck, inframammary region, inguinal region, eyelids (areas where there is rubbing)

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34
Q

How do acrochordons appear histologically?

A
  1. Polypoid with loose fibrovascular core
  2. Papillomatosis
    (Also acanthosis and hyperkeratosis)
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35
Q

List the pre-malignant and malignant epithelial neoplasms involving keratinocytes.

A
  1. Actinic keratosis
  2. Squamous cell carcinoma
  3. Basal cell carcinoma
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36
Q

What is actinic keratosis?

A

Common scaly erythematous patch located on sun-damaged skin; increasingly common with age; precursor of SqCC

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37
Q

How is actinic keratosis treated?

A

Cryotherapy or topical chemotherapeutics to prevent progression to SqCC

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38
Q

How does actinic keratosis appear grossly?

A

Ill-defined scaly erythematous macules

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39
Q

How does actinic keratosis appear microscopically?

A
  1. Basal layer atypia

2. Parakeratosis (epidermal involvement) alternating with orthoparakeratosis (uninvolved hair follicles) - flag sign

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40
Q

What defines squamous cell carcinoma in situ?

A

It is confined to the epidermis - no invasion into the dermis

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41
Q

What are the two clinical manifestations of squamous cell carcinoma in situ and how do they appear on histology and grossly?

A
  1. Bowen’s disease - single irregulary scaly erythematous plaque
  2. Bowenoid papulosis - multiple papules (frequently)

Atypia at all level of the epidermis

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42
Q

Where on the body is Bowen’s disease found?

A

Trunk, extremities, face

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43
Q

Where on the body is Bowenoid papulosis found and what causes it?

A

Genital area; HPV-induced

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44
Q

How does Bowen’s disease appear on histology?

A
  1. Full thickness epidermal atypia
  2. Hyperkeratosis
  3. Basal layer sparing (eyeliner sign)
  4. Involves follicles
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45
Q

How common is squamous cell carcinoma of the skin?

A

2nd most common skin tumor

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46
Q

What populations (age, gender) get squamous cell carcinoma of the skin?

A

Older individuals

M>F

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47
Q

What is the most common cause of squamous cell carcinoma of the skin?

A

Exposure to UV light, which leads to TP53 mutations at pyrimidine dimers

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48
Q

What are other genetic mutations seen in squamous cell carcinoma of the skin?

A
  1. Activating mutations in HRAS

2. Loss of function mutations in Notch receptors

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49
Q

What are some other causes of squamous cell carcinoma in the skin?

A
  1. Immunosuppression (HPV 5 and 8)
  2. Industrial
  3. Chronic wounds
  4. Burn scars
  5. Arsenic
  6. Ionizing radiation
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50
Q

What percent of squamous cell carcinoma of the skin metastasize?

A

5% (not frequently metastatic, but it is aggressive)

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51
Q

How does squamous cell carcinoma of the skin appear grossly?

A

Scaly, sometimes ulcerated and verrucous (rough surface) papules and nodules

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52
Q

How does squamous cell carcinoma of the skin appear microscopically?

A
  1. Hyperkeratotic acanthotic epidermis with papillomatosis comprised of atypical squamous cells (pinkish) extending from the epidermis invading into the dermis
  2. Islands with keratin pearls
  3. Uneven base
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53
Q

Compare AK, SCCis, and SCC with respect to keratinocyte atypia.

A

AK - yes, basal layer
SCCis - yes, full thickness
SCC - yes, dermis

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54
Q

Compare AK, SCCis, and SCC with respect to dermal invasion.

A

AK - no
SCCis - no
SCC - yes

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55
Q

Compare AK, SCCis, and SCC with respect to involvement of the hair follicle.

A

AK - no (flag sign)
SCCis - yes
SCC - yes

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56
Q

Compare AK, SCCis, and SCC with respect to involvement of the basal layer.

A

AK - yes
SCCis - no (sparing)
SCC - yes

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57
Q

What is the most common invasive cancer in humans?

A

Basal cell carcinoma

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58
Q

What populations get basal cell carcinoma?

A

Older individuals
Sun-exposed sites
Immunosuppressed
DNA mismatch repair syndromes (xeroderma pigmentosa)

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59
Q

What are common mutations seen in basal cell carcinoma?

A
  1. PTCH gene mutations (regulates Hedgehog pathway signaling) - 30%
  2. P53 mutations - 40-60%
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60
Q

What is Gorlin Syndrome (Nevoid Basal Cell Carcinoma Syndrome)?

A

AD disorder of multiple BCC before age 20 accompanied by medulloblastomas, ovarian fibromas, odontogenic keratocysts

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61
Q

What genetic mutation is associated with Gorlin Syndrome?

A

PTCH gene on chromosome 9q22.3 (born with 1 hit)

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62
Q

How does basal cell carcinoma appear grossly?

A

Pearly, pink papule with overlying telangiectasia

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63
Q

How does basal cell carcinoma appear on histology?

A
  1. Proliferation of basaloid cells (dark, scant cytoplasm, elongated hyperchromatic nuclei)
  2. Connection to overlying basal layer
  3. Peripheral palisading
  4. Peritumoral clefting (artifact)
  5. Mucinous alteration of surrounding stroma
  6. Prominent dermal telangiectasias
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64
Q

What is on the differential for basal cell carcinoma?

A

Metastatic cancer

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65
Q

What are melanocytes?

A

Clearish cells in the basal layer with dark nuclei that produce melanin

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66
Q

What is the normal ratio of melanocytes to keratinocytes?

A

1:10 (non-sun damaged skin - changes to 1:4 in sun damaged skin)

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67
Q

List the pigmented skin disorders of melanocytes.

A
  1. Vitiligo
  2. Albinism
  3. Melasma
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68
Q

How does vitiligo appear grossly?

A

Well-defined milky-white patches of skin

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69
Q

How does vitiligo appear histologically?

A

Loss of melanocytes seen on IHC stain

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70
Q

What is the etiology of vitiligo?

A

Autoimmune destruction of melanocytes

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71
Q

How does albinism appear grossly?

A

Dilution of the color of the hair, skin, and/or eyes

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72
Q

How does albinism appear on histology?

A

Loss of melanin PIGMENT on IHC stain

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73
Q

What is the etiology of albinism?

A

Decreased tyrosinase activity or defect transport

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74
Q

How does melasma appear grossly?

A

Hyperpigmentation of skin

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75
Q

How does melasma appear on histology?

A

Melanin deposited in basal and suprabasal keratinocytes, melanin in the dermis within melanophases, solar elastosis, elastic fiber fragmentation

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76
Q

What is the etiology of melasma?

A

Pregnancy or OCP use

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77
Q

List the neoplasms of melanocytes.

A
  1. Freckle (ephelis)
  2. Lentigo
  3. Melancoytic nevi
  4. Melanoma
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78
Q

How do freckles (ephelises) appear grossly?

A

Small, tan-red to light brown macules on sun-exposed areas; most common lesion of childhood

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79
Q

How do freckles appear histologically?

A

Increased melanin PIGMENT with basal keratinocytes; melanocytes may be enlarged, but normal density

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80
Q

How do lentigos appear grossly?

A

Small, oval tan-brown found at mucus membranes and at any age

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81
Q

How do lentigos appear on histology?

A

Non-confluent typical single cell melanocytic HYPERPLASIA along the basal layer

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82
Q

How do melnaocytic nevi (moles) appear grossly?

A

Tan to brown macules and papules

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83
Q

How do COMMON TYPE melanocytic nevi (moles) appear grossly?

A

Small, well-circumscribed, banal

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84
Q

How does melanoma appear grossly?

A

Most greater than 10 mm, changes in color, size, shape of previous lesions, etc.

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85
Q

How does melanoma appear histologically?

A

Confluent nests and single atypical melanocytes

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86
Q

Compare freckles and lentigos.

A

Freckles: increased MELANIN in keratincoytes

Lentigo: increased MELANOCYTES

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87
Q

What are the three different types of benign common nevi and how do they differ?

A
  1. Junctional (majority in the epidermis) - young people
  2. Compound (epidermal and dermal components) - middle age people
  3. Intradermal (only dermal) - older people
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88
Q

How do dysplastic nevi appear grossly?

A

Usually >5mm, flat to slightly raised macules in sun-exposed and protected areas

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89
Q

What are the histologic features of dysplastic nevi?

A
  1. Architectural atypia - melanocytic nests may be larger and fused (bridging) and junctional component extends past dermal components (shouldering)
  2. Lamellar fibroplasia
  3. Cytologic atypia (enlarged, angulated nuclear contours, hyperchromasia)
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90
Q

What is dysplastic nevus syndrome?

A

Tendency to develop multiple dysplastic nevi and melanoma; 50% have melanoma byage 60

91
Q

What genetic mutations are involved in dysplastic nevus syndrome?

A

(Autosomal dominant)

CDKN2A gene on chromosome 9p21

CDK4 on chromsome 12q14

92
Q

What % of dysplastic nevi turn into melanoma?

A

20-30% (same rate as ordinary nevi)

93
Q

Define shouldering.

A

Epidermal component extends at least 3 rete ridges beyond dermal component

94
Q

Define bridging.

A

Confluence of rete ridge nests

95
Q

What are the prognostic factors for melanoma?

A
  1. Depth (Breslow thickness)
  2. Number of mitotic figures (less important these days)
  3. Ulceration
  4. Lymph node involvement
  5. Regression
  6. Tumor infiltrating lymphocytes
  7. Gender
  8. Location
96
Q

What does a positive sentinel lymph node biopsy indicate?

A

Melanoma spreading

97
Q

What are the ABCDEs of melanoma?

A
  1. Asymmetrical
  2. Border (irregular, notched, blurred, uneven)
  3. Color (uneven, may see areas of regression)
  4. Diameter (usually larger in diameter than the size of a pencil eraser = 6 mm)
  5. Evolving (changes in size, shape, color, eelvation, new symptoms - bleeding, pruritis, pain)
98
Q

How does melanoma in-situ appear on histology?

A

Confluent proliferation of single and nested atypical melanocytes with upward pagetoid spread

99
Q

How does malignant melanoma appear on histology?

A

(Shoulder + bridging + atypia + lamellar fibroplasma + confluence + upward pagetoid spread) + invasion of atypical melanocytes into the dermis

100
Q

What are the different types of melanoma?

A
  1. Lentigo maligna (seen in the elderly, hands/face/neck, sun exposure, long radial growth phase)
  2. Superficial spreading (seen on the trunk)
  3. Acral lentiginous (seen on the hands, palms, and soles)
  4. Nodular (increased vertical phase - goes deep fast)

Each has an in situ and an invasive phase

101
Q

Which types of melanoma have a significant radial growth phase and why is this important?

A

LM, SS, AL - unlikely that it has metastasized (no vasculature in the epidermis)

102
Q

Which types of melanoma have a significant vertical growth phase?

A

Nodular and any type of invasive melanoma

103
Q

What are the two most important predisposing risk factors for melanoma?

A
  1. Sun exposure

2. Inherited genes

104
Q

How does melanoma vary between men and women and between light skin and dark skin?

A

M: upper back vs. F: posterior legs

Light skin&raquo_space; dark skin

105
Q

What are some of the genes involved in melanoma?

A
  1. CDKN2A - mutation that diminishes the activity of RB tumor suppressor proteins
  2. Increase in RAS and PI3K/AKT signaling, which promote cell growth and survival
  3. BRAF, NRAS, PTEN, C-KIT (study further if there is time)
106
Q

What is the most common mutation in sporadic melanoma?

A

BRAF

107
Q

What is the most common mutation in familial melanoma?

A

CDKN2A

108
Q

What is the best prognostic feature for melanoma?

A

Breslow thickness

109
Q

What are favorable prognostic factors for melanoma?

A
  1. Depth <1.7 mm
  2. No ulceration
  3. No mitoses
  4. Negative sentinel lymph nodes
  5. Brisk TIL response
  6. Absence of regression
  7. Female gender
  8. Location on extremity
110
Q

How is melanoma staged?

A

Stage 0 - MIS
Stage 1/2 - confined to skin with any depth
Stage 3 - nodal involvement
Stage 4 - distant skin or visceral metastasis

111
Q

Compare lentigo simplex, banal (ordinary nevus), dysplastic nevus, and melanoma with respect to the presence of melanocytes as single cells.

A

LS - yes
BN - yes
DN - yes
M - yes

112
Q

Compare lentigo simplex, banal (ordinary nevus), dysplastic nevus, and melanoma with respect to the presence of melanocytes as nests.

A

LS - no
BN - yes
DN - yes
M - yes

113
Q

Compare lentigo simplex, banal (ordinary nevus), dysplastic nevus, and melanoma with respect to the presence of shouldering, bridging, lamellar fibropasia, and cellular atypia.

A

LS - no
BN - no
DN - yes
M - yes

114
Q

Compare lentigo simplex, banal (ordinary nevus), dysplastic nevus, and melanoma with respect to the presence of confluence and pagetoid spread.

A

LS - no
BN - no
DN - no
M - yes

115
Q

List the dermal neoplasms arising from follicles.

A
  1. Epidermal inclusion cysts (follicular cyst)

2. Trichilemmoma

116
Q

List the dermal neoplasms arising from histiocytes.

A
  1. Dermatofibroma
  2. Keloid
  3. Dermatofibroma sarcoma protuberans
117
Q

List the dermal neoplasms arising from eccrine/aprocrine glands.

A
  1. Cylindroma
118
Q

List the dermal neoplasms arising from sebaceous glands.

A
  1. Sebaceous adenoma
119
Q

List the dermal neoplasms arising from vasculature.

A
  1. Pyogenic granuloma
  2. Bacillary angiomatosis
  3. Cherry hemangioma
  4. Cystic hygroma
  5. Glomus tumor
  6. Strawberry hemangioma
  7. Kaposi sarcoma
  8. Angiosarcoma
120
Q

List the dermal neoplasms arising from smooth muscle.

A
  1. Leiomyoma
121
Q

How does an epidermal inclusion cyst appear grossly?

A

Nodule under the skin

122
Q

How does an epidermal inclusion cyst appear on histology?

A

Epithelial-lined cyst with keratin debris and a granular layer lining the epithelium

123
Q

How do trichilemmomas appear grossly?

A

Multiple flesh-colored papules, usually around the nose and mouth

124
Q

What are trichilemmomas associated with?

A

PTEN mutations

Cowden’s syndrome (AD) - increased risk for breast, endometrial, and thyroid cancers

125
Q

How do trichilemmomas appear on histology?

A

Endophytic growth of ordinary clear cells

Palisading and pushing border

126
Q

How do dermatofibromas appear grossly?

A

Pink to brown papule or nodule most common on lower extremities, dimples when pushed together

127
Q

How do dermatofibromas appear on histology?

A
  1. Dermal proliferation of boomerang-shaped fibrohistiocytes
  2. Collagen trapping**
  3. Overlying tabling of rete ridges
  4. Basal layer hyperpigmentation
128
Q

How do dermatofibrosarcoma protuberans appear grossly?

A

Large nodule with multiple protuberances; most common on the trunk of young to middle-aged adults

129
Q

How do dermatofibrosarcoma protuberans appear on histology?

A
  1. Dense proliferation of spindle cells in the dermis

2. Storiform (irregulary whorled) pattern of fibroblasts

130
Q

How does a keloid scar appear grossly?

A

Firm, smooth, hard growths

131
Q

How does a keloid scar appear on histology?

A
  1. Dermal proliferation of spindle cells

2. Fibroblasts and myofibroblasts with wide bands of collagen with large, brightly eosinophilic, glassy fibers

132
Q

How does a cylindroma appear grossly?

A

Solitary or multiple small papules and/or large dome-shaped nodules on the scalp, face, or extremities (occasionally); “turban tumor”

133
Q

How does a cylindroma appear on histology?

A
  1. Non-encapsulated tumor nodule arising in the dermis formed by multiple irregular tumor islands (jigsaw pattern)
  2. Thick hyaline deposit surrounds the tumor island; also seen in discrete droplets within the nodules
  3. Two populations of cells: smaller cells with a hyperchromatic nucleus tending to the periphery, larger cells with open nuclei throughout the center of the nodule
134
Q

How does a sebaceous adenoma appear grossly?

A

Yellowish papule or small nodule

135
Q

What are sebaceous adenomas associated with?

A

Lynch Syndrome/Muir Torre syndrome (MLH1, MSH2, MSH6), especially if multiple or cystic

136
Q

How does a sebaceous adenoma appear on histology?

A

Relatively well-circumscribed lobulated tumor consisting of lobules of sebaceous cells (bubbly cytoplasm) lined by basaloid cells

137
Q

How do pyogenic granulomas appear grossly?

A

Single papules that are ulcerated (upper extremities, especially fingers)

138
Q

How do pyogenic granulomas appear on histology?

A

Lobular capillary proliferation, mixed inflammatory infiltrate, often ulcerated and crushed

139
Q

How does bacillary angiomatosis appear grossly?

A

Single or multiple papules

140
Q

What causes bacillary angiomatosis and what is it associated with?

A

Caused by infection Bartonella Henselae; associated with AIDs

141
Q

How does bacillary angiomatosis appear on histology?

A

Resembles PG and KS, but has neutrophils and positive staining with Warthin Starry

142
Q

How does a cherry hemangioma appear grossly and on histology?

A

Single or multiple papules; benign proliferation of capillaries (frequency increases with age)

143
Q

How does a strawberry hemangioma appear grossly and on histology?

A

Benign proliferation of capillaries appearing in the first few weeks of life, regresses by age 5-8; histology same as cherry angioma

144
Q

How does a cystic hygroma appear grossly?

A

Cavenous lymphangioma of the neck

145
Q

What is cystic hygroma associated with?

A

Turner syndrome (female partly or completely missing an X-chromosome, presentation: short, webbed neck, low-set ears, low hairline, short stature, swollen hands and feet at birth)

146
Q

How does a glomus tumor appear grossly?

A

Benign, painful red-blue tumor commonly under the fingernails

147
Q

Glomus tumors arise from ___ cells of the ___ body.

A

Smooth muscle; thermoregulatory glomus

148
Q

Compare PG/hemangioma to GT.

A

PG/hemangioma: more vessels than cells

GT: more cells than vessels

149
Q

What is a kaposi sarcoma?

A

Malignant vascular tumor of the skin, mouth, GI tract, respiratory system; common on the feet

150
Q

What is kaposi sarcoma associated with?

A

HHV-8 and HIV

151
Q

How does kaposi sarcoma appear on histology?

A

Lymphocytic infiltrate, proliferation of spindle cells, extravasated blood cells; HHV8+ stain

152
Q

What is an angiosarcoma?

A

Malignant vascular tumor in the head, neck, and breast areas occurring in the elderly, sun-exposed, radiation, lymphedema

153
Q

Hepatic angiosarcoma is associated with exposure to what substances?

A

Vinyl chloride and arsenic

154
Q

COMPLETE TABLE - SLIDE 75

A

Do it.

155
Q

How does a pilar type leiomyoma appear on histology?

A

Small fascicles of bland, eosinophilic spindle cells in the mid-dermis; cigar-shaped nuclei, bubbles

156
Q

How doe a pilar type leiomyoma appear grossly?

A

Flesh-colored nodule of the skin

157
Q

List the patterns of inflammatory dermatosis.

A
  1. Lichenoid
  2. Psoriasiform
  3. Spongiotic
  4. Bullous
158
Q

Describe lichenoid dermatitis.

A

Band of inflammation at the DEJ

159
Q

List the types of lichenoid dermatitis.

A
  1. Lichen planus
  2. Erythema multiforme
  3. SJS/TENS
  4. Cutaneous T cell lymphoma (mycosis fungoides)
160
Q

What are the 5 P’s of lichen planus?

A

Pruritic, purple, polygonol, papules, plaques (also Wickham striae, common oral involvement)

161
Q

How does lichen planus appear on histology?

A
  1. Lichenoid lymphocytic infiltrate with epidermal hyperplasia, hypergranulosis
  2. Sawtooth rete ridges
  3. Colloid bodies (CD) - dead keratinocytes - on the basal layer
162
Q

How does EM, SJS, and TEN appear on histology?

A

Lichenoid dermatitis with necrotic keratinocytes (Civatte bodies), prominent or confluent (full thickness - not just the basal layer)

163
Q

What causes EM?

A

Infections, most commonly HSV; self-resolving

164
Q

What causes SJS/TENs?

A

Drug-induced

165
Q

What defines SJS/TENS?

A

Mucosal involvement, body surface involvement >30%

166
Q

How does EM appear grossly?

A

Characteristic target

167
Q

How does EM appear on histology?

A

More sparse lichenoid infiltrate, plentiful necrotic keratinocytes high in the epidermis

168
Q

How does TEN appear on histology?

A

Necrotic keratinocytes at all levels of epidermis (full thickness necrosis); no epidermis

169
Q

How does cutaneous T cell lymphoma appear grossly?

A

Patches/plaques on the trunk (older people)

170
Q

How does cutaneous T cell lymphoma appear on histology?

A
  1. Atypical lymphocytes along the DEJ (look like soldiers); band-like pattern
  2. Pautrier’s microabscess (collection of atypicaly lymphocytes within the dermis)
  3. Cerebriform nuclei
171
Q

Describe psoriasiform dermatitis.

A

Regular acanthosis (thickening of the epidermis)

172
Q

What is psoriasis associated with?

A

Arthritis, myopathy, enteropathy, spondylitic joint disease, acquired immunodeficiency

173
Q

What are genetic and environmental factors of psoriasis?

A

2/3 affected have HLA-C, but only 10% of HLA-C people have psoriasis

CD4+ and CD8+ cells accumulate, Ag unknown

174
Q

How does psoriasis appear grossly?

A
  1. Well-demarcated plaques with adherent silver/white scales

2. 30% have nail changes - yellow-brown discoloration with pitting, onycholysis (splitting apart)

175
Q

Where is psoriasis found on the body?

A

Elbows, kness, scalp, lumbosacral, intergluteal cleft, glans penis

176
Q

How does psoriasis appear on histology?

A
  1. Psoriasiform hyperplasia with parakeratotic “wafer-like” scales containing neutrophils
  2. Acanthosis
  3. Munroe microabscesses (filled with neutrophils)
  4. Spongiform pustules in the epidermis
  5. Thinning of the suprapapillary plates with dilated papillary vessels (Auspitz sign)
  6. Loss of granular layer, increased epidermal mitotic figures
177
Q

Describe spongiotic dermatitis.

A

Irregular acanthosis with edema in the epidermis

178
Q

What is a common form of spongiotic dermatitis?

A

Eczema

179
Q

What is seen on histology in eczema?

A

Irregular acanthosis, vesicle formation, eosinophils

180
Q

What is allergic contact dermatitis?

A

Inflammatory disorder initiated by contact with an allergen to which the person has been previously sensitized

181
Q

How does allergic contact dermatitis appear grossly?

A

Erythematous papules, small vesicles, or weeping plaques, very pruritic, glove-like distribution; occurs 12-48 hours after exposure to allergen (delayed hypersensitivity rxn)

182
Q

Describe bullous dermatitis.

A

Vesicles or bullae caused by splits in the epidermis or by the DEJ

183
Q

List the types of bullous dermatitis.

A
  1. Bullous pemphigoid
  2. Pemphigus vulgaris
  3. Dermatitis herpetiformis
184
Q

How is bullous dermatitis diagnosed?

A

Direct IF

185
Q

Diagnosis of bullous dermatitis depends on what three features?

A
  1. Anatomic level of split
  2. Underlying mechanism of the split
  3. Nature of the inflammatory infiltrate
186
Q

Discuss the features of bullous pemphigoid.

A
  1. Occurs in older individuals
  2. Tense bullae on the inner aspects of thighs, flexor surfaces of forearms, axillae, groin, and lower abdomen
  3. Subepidermal blister with eosinophils
  4. IgG Ab to hemidesomsomes - linear pattern at the BM
  5. Split is at the DEJ

Ag - BPAG1 and 2

187
Q

Discuss the features of pemphigus vulgaris.

A
  1. Superficial vesicles and bullae that rupture easily, leaving shallow, crusted erosions
  2. Acanthloysis results in suprabasilar clefting (tombstoning)
  3. Dissolution due to IgG Ab against desmoglein
  4. Net-like IgG and C3 on direct immunoflorescence
  5. Suprabasilar split
188
Q

Discuss the features of dermatitis herpetiformis.

A
  1. Pruritic papules/vesicles on erythematous base (elbows, buttocks)
  2. Associated with celiac (Ab to gliadin)
  3. Granular IgA deposits on direct immunofluorescence
  4. DEJ split
  5. Neutrophils
189
Q

What causes verruca?

A

HPV

190
Q

What are the different types of verruca?

A
  1. Verruca vulgaris - common type (warts)
  2. Verruca plana - face and dorsal hands
  3. Verruca plantaris/palmaris
  4. Condyloma acuminatum (HPV 6, 11)
191
Q

How does verruca vulgaris appear on histology?

A
  1. Hyperkeratosis
  2. Hypergranulosis (dark purple)
  3. Papillomatosis
  4. Koilocytes - vacuolated keratinocytes with raisin-like nuclei
192
Q

How does molluscum contagiosum appear on histology?

A
  1. Crater produced by epidermal hyperplasia
  2. Henderson-Patterson (molluscum) bodies in the crater - intracytoplasm inclusions that push the nucleus and keratohyaline granules aside

Very common in childhood

193
Q

Compare HSV 1 and 2 with Varicella Zoster virus (VZV)

A
  1. Both part of human herpes virus family
  2. Both double stranded DNA virus with similar mechanisms for infection
  3. Both have the ability to cause primary and latent infection
  4. Both cause a vesicular viral exanthem (maculopapular rash with vesicles on top)
  5. Positive Tzanck or DFA of blister contents, positive viral culture
194
Q

The first infection with HSV1/2 is often asymptomatic. How do primary or latent infections present?

A

Vesicles or erosions

195
Q

HSV1 more commonly causes infection in what location? HSV2?

A

Oral - more commonly HSV1

Genital - more commonly HSV2

196
Q

What are the 3 M’s of HSV?

A

Molding, multinucleated, marginated chromatin

197
Q

What is a primary VZV infection and how does it present?

A

Chicken pox; vesicles on a red base/papules/crusted erosion; transmitted by respiratory secretions and cutaneous lesions

198
Q

What is a reactivation of VZV infection and how does it present?

A

Shingles; focal unilateral/dermatomal distribution (unless disseminated); painful/pruritic vesicles most commonly on the trunk; increased in patients over 50 or in people who are immunocompromised

199
Q

What is the Hutchinson sign?

A

HSV involvement of the nose, which alerts the physician to the possibility of ocular involvement (which can lead to vision impairment)

200
Q

What causes bullous impetigo?

A

Most common - Staph
Also GAS

Specifically exfoliative toxicns A and B from Phage II Group 71 Staph attack the epidermis, resulting in subcorneal splitting

201
Q

Bullous impetigo is most common in ___ - how does it present?

A

Children; flaccid blisters that collapse easily resulting in honey-colored crust

202
Q

How is bullous impetigo treated?

A

MRSA mupirocin

203
Q

How does bullous impetigo appear on histology?

A

Subcorneal blister with neutrophils +/- bacteria

204
Q

What causes scalded skin syndrome?

A

Exotoxin from S. Aureus destroys keratinocyte desmosomes, leading to fever and generalized erythematous rash with sloughing of the upper layers of the epidermis

Seen in newborns, children, and adults with renal insufficiency

205
Q

Compare TENS, BI, and SSSS with respect to site of epidermal split.

A

TENS - DEJ
BI - Sub-epidermis
SSSS - Sub-epidermis

206
Q

Compare TENS, BI, and SSSS with respect to organisms present.

A

TENS - no
BI - yes
SSSS - no

207
Q

Compare TENS, BI, and SSSS with respect to systemic symptoms.

A

TENS - yes
BI - no
SSSS - yes

208
Q

Compare TENS, BI, and SSSS with respect to culture.

A

TENS - n/a
BI - yes (skin)
SSSS - yes (not skin)

209
Q

What is erysipelas?

A

Infection involving the superficial dermis and lymphatics caused by S. pyogenes; well-defined demarcation between infected and normal skin; dermal edema

210
Q

What is cellulitis?

A

Acute, painful spreading infection of deeper dermis and subcutaneous tissue caused by S. pyogenes or S. Aureus; starts with break from trauma or other infection

211
Q

What is necrotizing fasciitis?

A

Infection involving deep subcutaneous tissue/fascia caused by S. pyogenes; crepitus, pain out of proportion to clinical findings

212
Q

What are dermatophytes and what are the most common genera?

A

Fungus that live on keratin; Microsporum, Trichophyton, Epidermophyton

213
Q

How do are dermatophytes imaged in the lab?

A

Hyphae on KOH prep, in corneal layer using PAS stain

214
Q

What are the 4 types of dermatophyte infections?

A
  1. Tinea pedis - foot
  2. Tinea corpora - body
  3. Tinea cruris - inguinal folds
  4. Tinea capitis - scalp
215
Q

What is onychomycosis?

A

Dermatophyte infection of the nail

216
Q

How does tinea versicolor appear grossly?

A

Macules and patches of hypo/hyperpigmentation on the trunk

217
Q

How does tinea versicolor appear on histology?

A

Spaghetti and meatball appearance of hyphae and yeast forms (Malassezia globosa organisms) - can visualize with Wood’s lamp as well

218
Q

How does tinea nigra appear grossly?

A

Tan-brown patches on palms or soles

219
Q

What causes scabies?

A

Sarcoptes scabiei mite; overcrowding, poor hygiene, sexual contact

220
Q

How does scabies appear grossly?

A

Papulovesicular, persistent nodules, Norwegian (crusted forms), often seen in webbed spaces between fingers

221
Q

How does cutaneous infection with blastomycosis appear histologically?

A
  1. Epidermal acanthosis
  2. Dermal necrosis
  3. Histiocytes

Broad based budding yeast form

222
Q

How does cutaneous infection with coccidiomycosis appear histologically?

A

Large spherule with little spherules inside (bigger than blast)

223
Q

How does cutaneous infection with cryptococcus neoformans appear grossly and histologically?

A

Gross - nodules with central area of umbilication

Histology - large, intracellular or free yeast-like organisms, mucin stains thick capsule; very small

224
Q

How does cutaneous infection with histoplasm capsulatum appear histologically?

A

Very small intracytoplasmic organisms with surroudning clear halo, PAS and GMS +, often within histiocytes