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23 General Pathology > 7 - Skin > Flashcards

7 - Skin Flashcards

1
Q

what structures of the skin are not present in the oral cavity

A

sweat glands and sebaceous glands

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2
Q

what is a highly sophisticated sensory organ

A

skin

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3
Q

skin plays a role in the synthesis of what

A

vitamin D

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4
Q

what is the first line of defense against potentially harmful infectious physical agents

A

skin

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5
Q

what has nerve endings to sense hot, cold, etc.

A

skin

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6
Q

what are the cell types of the skin

A
  1. squamous epithelial cells (keratinocytes)
  2. melanocytes
  3. dendritic cells (Langerhans cells)
  4. lymphocytes
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7
Q

squamous epi cells are glued together by what

A

desmosomes

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8
Q

squamous epi cells produce an abundant amount of what

A

keratin protein

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9
Q

what do squamous epi cells secrete

A

soluble molecues (e.g., cytokines and defensins that augment and regulate immune responses)

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10
Q

how do squamous epi attach to basement mem

A

hemidesmosomes

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11
Q

what is within the epidermis and is responsible for producing melanin

A

melanocytes

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12
Q

what processes microbial and nonmicrobial agents that the skin is exposed to

A

dendritic cells (langerhans)

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13
Q

what protects the skin against cutaneous inflammatory and infectious diseases

A

T and B lymphocytes

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14
Q

what is responsible for feelings of touch, vibration, itchiness, cold, and heat in the skin

A

AFFERENT NERVE FIBERS and diverse set of associated structures called NEURAL END ORGANS

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15
Q

what guard against deletrious variations in body temp

A

sweat glands

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16
Q

what manufacture hair shafts and have protects niches harboring epi stem cells capable of regenerating superficial epi skin structures following disruption by trauma, burns, and other types of injuries

A

hair follicles

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17
Q

what are the disorders of melanocytes and nevus cells

A
  1. Freckle (ephelis)
  2. Lentigo
  3. Melanocytic nevus
  4. Dysplastic nevus
  5. Melanoma
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18
Q

about how many keratinocytes equal one melanocyte

A

10-20

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19
Q

what is the maturation sequence of nevi

A

normal skin shows scattered dendritic melanocytes within epidermal basal cell layerh

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20
Q

what are aggregates of round nevus cells that brow along dermoepidermal junction

A

junctional nevus

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21
Q

what are nevus cells seen in epidermis and dermis

A

compound nevus

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22
Q

what are nevus cells only in the dermis

A

intradermal nevus

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23
Q

what are the most common pigmented lesions of childhood in lightly pigmented individuals

A

freckle (ephelis)

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24
Q

what are small (one to several mm), tan-red to light brown macules (flat lesions) that appear after sun exposure

A

freckle (ephelis)

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25
Q

what results from increased amounts of melanin pigment within basal keratinocytes

A

freckle (ephelis)

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26
Q

T/F: when freckles arise, melanocytes increase

A

FALSE! number of melanocytes remain the same

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27
Q

are freckles capable of fading and darkening depending on the season?

A

YES

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28
Q

what results from benign localize hyperplasia of melanocytes

A

lentigo

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29
Q

when does lentigo appear

A

all ages - but most common in infants and children

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30
Q

what does lentigo involve

A

skin and mucous membranes

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31
Q

what does lentigo appear as

A

small (5-10 mm), oval tan brown macules

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32
Q

T/F: lentigo darkens when exposed to sunlight

A

FALSE

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33
Q

what is solar lentigo

A

lentigo appear in older people due to sun damage

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34
Q

what is a flat lesion that is hyper or hypo pigmented

A

macule

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35
Q

what are benign neoplasms by acquiring activating mutations in components of BRAF or less often RAS signaling pathways

A

melanocytic nevus (moles)

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36
Q

what are tan to brown, uniformly pigmented, small (< 6mm) relatively flat macules or elevated papules (small round topped elevated lesion) with well-defined, rounded borders

A

melanocytic nevus (moles)

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37
Q

are nevus cells rounded cells

A

yes

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38
Q

origin of nevus cells

A

neural crest

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39
Q

small bump = ___
large bump = ___

A

papule; nodule

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40
Q

what is a direct precursor of melanoma

A

dysplastic nevus (but a vast majoring never progress to melanoma)

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41
Q

when ___ increased in number they are a marker of an increased risk for melanoma

A

dysplastic nevus

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42
Q

how does dysplastic nevus appear

A

macules or target like lesions (dark raise center and irregular flat periphery)

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43
Q

what are slightly raised plaques (raised lesions with flat surface)

A

macules

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44
Q

does dysplastic nevus occur in sun exposed or protected body surfaces

A

occurs in BOTH!

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45
Q

what is the most deadly of skin cancers?

A

melanoma

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46
Q

what mutation causes skin cancer

A

BRAF mutations due to exposure to UV radiation in sunlight

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47
Q

can melanoma be inherited?

A

YES! 10-15% inherited as AD trait w/ variable penetrance

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48
Q

what is the ABCDE of melanoma?

A
  1. ASYMMETRIC lesions
  2. BORDERS are irregular and often notched
  3. COLOR is variable and not uniform
  4. DIAMETER is larger than nevi and increasing
  5. EVOLVING/evolution - lesions are constantly enlarging either superficially or in nodular fashion
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49
Q

what is the size of melanoma lesions

A

> 6 mm

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50
Q

when (age) does seborrheic keratosis frequently occur

A

common but most frequently occurs in middle-aged or older individuals

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51
Q

where is seborrheic keratosis numerous

A

trunk

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52
Q

small SK on the face in people of color are called what

A

dermatosis papulose nigra (seen in 35% of African-American adults)

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53
Q

seborrheic keratosis may appear suddenly in large numbers as part of what

A

paraneoplastic syndrome (Leser-Trelat sign) a sign of potential internal cancer

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54
Q

what are round, elevated, coin-like waxy plaque that varies in diameter from mm to several cm “pasted on” look

A

seborrheic keratosis

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55
Q

what is uniformly tan to dark brownl velvety to granular surface

A

seborrheic keratosiss

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56
Q

what is a thickened, hyperpigmented skin with velvet-like texture

A

acanthosis nigricans

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57
Q

where does acanthhosis nigricans most commonly appear

A

flexural areas (axillae, skin folds of neck, groin-area where upper thighs meet the lowest part of abdomen, and anogenital areas)

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58
Q

what are the 2 types of acanthosis nigricans

A
  1. 80% - benign conditions (gradually during childhood and puberty)
  2. 20% - associated with cancers (most commonly GI adenocarcinomas)
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59
Q

what malignant cancer would acanthosis nigricans be associated with

A

GI adenocarcinoma (in middle-aged or older individuals)

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60
Q

what is an important cutaneous sign of several underlying benign and malignant conditions

A

acanthosis nigricans

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61
Q

what are benign disease acanthosis nigricans associated with

A

insulin resistance, DM, PCOS, thyroid disorder, adrenal gland disorders, and medications

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62
Q

what are fibroepithelial polyps also called

A

skin tag and acrochordon

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63
Q

where are skin tags present? age?

A

middle-aged or older individuals -> neck, trunk, and face

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64
Q

what are soft, flesh-colored bad like tumros often attached to surrounding skin by slender stalk

A

fibroepithelial polyp (Skin tag)

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65
Q

what can undergo ischemia due to torsion which may cause pain and precipitate their removal

A

fibroepithelial polyp (skin tag)

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66
Q

are adnexal (appendage) tumors benign or malignant

A

BOTH (either benign or malignant)

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67
Q

what is adnexal tumors associated with

A

germline mutations of tumor suppressor genes

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68
Q

what may be numerous and disfiguring OR relativelly trivial but warn predisposition of an internal malignancy

A

Adnexal (appendange) tumors

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69
Q

what is this an example of:

relationship between multiple trichilemmomas (benign tumor arising from hair follicle) and Cowden syndrome, a disorder caused by germline mutation gene PTEN that is associated with an increased risk of endometrial cancer, breast cancer, and other malignancies

A

adnexal (appendage) tumors

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70
Q

what are benign tumor of sweat gland

A

cylindroma (turban tumor)

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71
Q

where does cylindroma usually occur

A

forehead and scalp where coalescene of nocules with time may produce hat like growth

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72
Q

is cylindroma AD or AR? when does it appear?

A

AD - appears early in life

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73
Q

what is associated with inactivation of tumor suppresor gene CYLD

A

cylindroma (CYLD is the cylindromatosis gene)

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74
Q

what is a benign tumor of sebaceous glands

A

sebaceous adenoma

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75
Q

what can be associated w/ internal malignancy in Muir-Torre syndrome

A

sebaceous adenoma

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76
Q

what is defined as the occurrence of at least one sebaceous-gland tumor, or keratoacanthoma, in conjunction with internal malignant diseases, often in the GI tract

A

sebaceous adenoma

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77
Q

what are benign tumors of hair follicle, common on face and neck

A

pilomatricoma

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78
Q

how does pilomatricoma usually appear

A

solitary nodule, occasionally multiple nodules occur

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79
Q

where does actinic keratosis occur? what does it exhibit

A

sun damaged skin and exhibit hyperkeratosis

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80
Q

is actinic keratosis greater in light or dark skin individuals

A

light skinned

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81
Q

what may show progressively worsening dysplatic changes that culminate in squamous cell carcinoma

A

actinic keratosis

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82
Q

what is the dimension of actinic keratosis

A

<1 cm

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83
Q

what is a tan-brown, red, or skin-colored and have a rough sandpaper-like consistency

A

actinic keratosis

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84
Q

does actinic keratosis remain stable or regress?

A

it can remain stable BUT can regress to enough lesions to transform to a malignant lesion (squamous cell carcinoma)

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85
Q

is local eradication necessary in actinic keratosis? if so, how

A

yes - gentle curettage, freezing, topical application of chemotherapeutic agents (imiquimod)

86
Q

what is the second most common tumor arising in sun exposed sites in older people

A

squamous cell carcinoma

87
Q

squamous cell carcinoma more common in men or women? exception?

A

men BUT in lower leg lesions more common in women

88
Q

what percent of squamous cell carcinoma metastasize to regional lymph nodes

A

<5%

89
Q

what is the most common cause in DNA damage resulting in squamous cell carcinoma? second cause?

A
  1. exposure to UV light
  2. chronic immunosuppression
90
Q

what are other risk factors to DNA leading to squamous cell carcinoma

A

(1. exposure to UV light
2. chronic immunosuppression)
3. tobacco
4. betel nut chewing
5. industrial carcinogens
6. ionizing radiations
7. chronic ulcers
8. old burn scars

91
Q

what is the most common muted gene that leads to SCC?

A

TP53

92
Q

what is the general muted gene that leads to SCC?

A

NOTCHI

93
Q

Distinctive, locally aggressive cutaneous tumor
associated with mutations in PTCHI PTCH2, SMO
and SUFU genes

A

basal cell carcinoma

94
Q

what is the most common locally invasive cancer in humans

A

basal cell carcinoma

95
Q

is BCC slow growing or fast? are they common or rarely metastazie

A

slow growing; rarely metastasize

96
Q

what occurs on sun exposed skin; incidence increases in setting of immunosuppression, has pearly papules

A

basal cell carcinoma

97
Q

what is present on the papules of BCC?

A

telangiectasia (new BV forming)

98
Q

nevoid basal cell carcinoma syndrome is also called what

A

gorlin syndrome

99
Q

is gorlin syndrom AD or AR? this is a mutation of what gene

A

AD - mutation of tumor suppressor gene PTCH

100
Q

what is gorlin syndrome characterized by

A
  1. Development of multiple BCCAs, often before age 20
  2. Accompanied by various other tumors, especially medulloblastoma and ovarian fibroma
  3. Odontogenic keratocysts
  4. Palmar and plantar pits
101
Q

what is a benign dermal tumor of UNCERTAIN lineage often seen on legs of young and middle-aged women, asymptomatic or tender

A

benign fibrous histiocytomas (dermatofibroma)

102
Q

are dermatofibroma capable of increasing or decreasing in size over time

A

yes

103
Q

cause of dematofibroma

A

unknown -> few cases show ALK gene mutation

104
Q

what is a first, tan to brown papule usually <1 cm in diameter; actively growing lesions may reach several cm

A

dermatofibroma

105
Q

what is a well-differentiated primary fibrosarcoma of the skin

A

dermatofibrosarcoma protuberance

106
Q

is dermatofibrosarcoma protuberance slow or fast? local or systemically aggresive? common or rarely metastazie?

A

slow growing
locally agressive
rarely metastasize

107
Q

what results with the translocation involving the gene encoding collagen I A I and platelet derived growth factor beta

A

dermatofibrosarcoma protuberance

108
Q

what appears as a protuberant nodule, within a form plaque which may ulcerate; most often on the trunk

A

dermatofibrosarcoma protuberance

109
Q

Lymphoma of skin-homing CD4+ T-helper cells that presents in the skin

A

mycosis fungoides (cutaneous T-cell lymphoma)

110
Q

does mycosis fungoides remain localize in skin?

A

yes it remains localized for many years but may eventually evolve into systemic lymphoma

111
Q

when does mycosis fungoides occure (age)?

A

> in people older than 40 but may occur at any age in truncal areas

112
Q

Scaly red-brown patches; raised scaling plaques that may
be confused with psoriasis

A

mycosis fungoides

113
Q

what is the seeding of blood with malignant T cells resulting in erythema and scaling of entire body

A

Sezary syndrome (related to mycosis fungoides)

114
Q

Disorder associated with excessive keratin buildup (hyperkeratosis) that result in fish-like scaliness

A

ichthyosis

115
Q

when does ichthyosis appear

A

at or around the time of birth

116
Q

is ichthyosis acquired or inherited?

A

BOTH!

acquired is associated with lymphoid or visceral malignancies
inherited (occurs later in life)

117
Q

Common; usually caused by localized degranulation of mast cells and is uniformly associated with dermal microvasculature hyperpermeability

A

urticaria (hives)

118
Q

what produces pruritic edematous plaques called wheals; small pruritic papules to large erythematous plaques

A

urticaria (hives)

119
Q

when does urticaria (hives) common (age)? where?

A

> between ages 20 and 40; all ages are susceptible; > in areas exposed to pressure (trunk, distal extremities, and ears)

120
Q

when do hives develop and fade? how long?

A

Individual lesions develop and fade within hours (usually, 24
hours); episodes may last for days or persist for months

121
Q

how to treat uticaria (hives)

A

Treatment: antihistamines; oral corticosteroids

122
Q

Uncommon; self-limiting hypersensitivity reaction to
certain infections and drugs

A

erythema multiforme

123
Q

what age does erythema multiforme occur

A

any age

124
Q

what is erythema multiformed associated with

A
  1. infections (YOUNG PEOPLE)
  2. exposure to certain drugs (OLDER PEOPLE)
  3. cancers
  4. collagen vascular disease

ICCE

125
Q

erythema multiforme is characterized by what injury? what cells?

A

Characterized by keratinocyte injury mediated by skin-homing CD 8+ cytotoxic T lymphocytes

126
Q

what are the diverse array of lesions present in erythema multiforme

A

macules, papules, vesicles, bullae, and characteristic targetoid lesions

127
Q

erythema multiforme often show ___ on extremities

A

symmetric distribution

128
Q

what is a febrile form of erythema multiforme associated with extensive involvement of the skin; lesions also involve the lips, oral mucosa, conjunctiva, urethra, and genital and perianal areas

A

Stevens-Johnson Syndrome

129
Q

what is characterized by diffuse necrosis and sloughing of cutaneous and mucosal epithelial surface (in relation to erythema multiformed)

A

toxic epidermal necrolysis (TEN)

130
Q

what is chronic inflammatory dermatosis that appears to have an autoimmune basis

A

psoriasis

131
Q

are environmental and genetic factors at play in psoriasis

A

yes

132
Q

what areas of skin are psoriasis affected

A
  1. knees
  2. elbows
  3. scalp
  4. lumbosacral areas
  5. intergluteal clefts
  6. glans penis
133
Q

Well-demarcated, pink to salmon-colored plaques covered by loosely adherent silver-colored scales

A

psoriasis

134
Q

what is a local trauma that can induce psoriatic lesions in susceptible individuals

A

Koebner phenomenon

135
Q

what is a chronic inflammatory dermatosis that is more common than psoriasis

A

chronic inflammatory dermatosis

136
Q

what involves regions with high density of sebaceous glands but is NOT a sebaceous gland disease

A

seborrheic dematitis

137
Q

what causes seborrheic dermatitis

A

UNKOWN - increased sebum production is a contributory factor

138
Q

what has macules and papules on an erythematous yellow, often greasy base, associated with scaling and crusting

A

seborrheic dematitis

139
Q

what is the most common clinical expression of seborrheic dermatitis

A

dandruff

140
Q

whata disorder of skin and mucous membrane

A

lichen planus

141
Q

what are the 6Ps associated with lichen planus

A
  1. pruritis
  2. purple
  3. polygonal
  4. planar
  5. papules
  6. plaques
142
Q

what are itchy, purple, flat-topped, papules that may coalesce to form plaques; symmetrically distributed and multiple lesions

A

lichen planus

143
Q

are lichen planus self-limiting? when do they resolve

A

yes and may resolve 1-2 years after onset

144
Q

how long do ORAL lichen planus lesions persist

A

YEARS

145
Q

pathogenesis of lichen planus

A

unknown

146
Q

what can be seen in relation to lichen planus

A

Wickhams striae (radiating white lines)

147
Q

what age is lichen planus present

A

> in middle aged and on extremities

148
Q

what are inflammatory blistering disorders

A
  1. pemphigus
  2. bullous pemphigoid
149
Q

what are noninflammatory blistering disorders

A

epidermolysis bullosa

150
Q

what is desmosome made of

A

desmoglein 1 or 3

151
Q

what is a blistering disorder caused by autoantibodies (IgG) that result in dissolution of intracellular attachments (desmoglein of DESMOSOMES) within the epidermis and mucosal epi?

A

pemphigus

152
Q

when does pemphigus occur? m or f?

A

4-6th decade of life, equal in both M and F

153
Q

what is the most common variant of pemphigus that involves skin and mucosa

A

pemphigus vulgaris

154
Q

T/F: oral ulcers may persist for years before pemphigus skin lesion appear

A

TRUE

155
Q

primary lesions of pemphigus

A

vesicles or bullae that rupture easily, leaving shallow erosions

156
Q

what skin disease has a chicken wire looking cells in microscope

A

pemphigus vulgaris

157
Q

what is caused by autoantibodies that bind to the proteins (HEMIDESMOSOMES) that are required for adherence of basal keratinocytes to the basement membrane

A

bullous pemphigoid

158
Q

in bullous pemphigoid, antibody deposition occurs in continuous linear pattern where?

A

dermoepidermal junction

159
Q

what are tense bullae filled with clear fluid involving erythematous or normal appear skin, 2 cm in diamer, and do not rupture easily

A

bullous pemphigod

160
Q

does bulloud pemphigoid heat with scarring?

A

NO! heals without scarring

161
Q

how does bullous pemphigoid appear in microscopy

A

linear band of antibodies that DO NOT have chicken wire appearance

162
Q

what are groups of disorders caused by inherited defects in structural proteins that lend mechanical stability to the skin

A

epidermolysis bullosa

163
Q

what is a common clinical feature of epidermolysis bullosa

A

ability to form blisters at site of pressure, rubbing, or trauma at or soon after birth

164
Q

age of ppl with acne vulgaris? more common in m or f?

A

univeral in middle to late teenage years
m=f

165
Q

what can cause acne vulgaris

A
  1. induced or exacerbated by drugs
  2. occupational exposures
  3. conditions that favor occlusion of sebaceous glands
166
Q

what is inflammatory acne

A

erythematous papule, nodules and pustules

167
Q

what is noninflammatory acne

A

comdones: small papules with or without black central plug (oxidation of melanin pigmentation)

168
Q

what age of ppl w rosacea? men or women

A

middle aged or beyond
greater in f

169
Q

4 stages of rosacea

A
  1. flushing episodes (pre-rosacea)
  2. persistent erythema and telangiectasia
  3. pustules and papules
  4. rhinophyma
170
Q

what is permanent thickening of nasal skin by confluent papules and prominent follicles

A

rhinophyma

171
Q

development of ___ is associated with hypertrophy of sebaceous glands and follicular plugging by keratotic debris

A

rhinophyma

172
Q

what is an inflammatory rxn in subcutaneous adipose tissue

A

panniculities

173
Q

panniculitis primary affects what regions of adipose

A
  1. lobules of fat
  2. CT that separates fat into lobules
174
Q

where does panniculitis mostly occur

A

lower legs

175
Q

what is oorly defined, exquisitely tender, erythematous plaques and nodules that may be more palpated than seen; biopsy needed for diagnosis

A

erythema nodosum

176
Q

what is erythema nodosum MOSTLY associated with

A

strep

177
Q

can fever and malaise accompany erythema nodosum

A

yes

178
Q

T/F: over the course of weeks, erythema nodosum lesions usually flatten and leave no clinical scars and no lesions develop

A

TRUE

179
Q

what is OUTWARD panniculitis

A

erythemanodosum

180
Q

is erythema induratum common?

A

no - uncommon, but greater in adolescents and menopausal women

180
Q

what is INWARD panniculitis

A

erythema induratum

181
Q

what causes erythema induratum

A

unknown but regarded as primary vasculitis of deep vessels supplying fat lobules of subcutis

182
Q

erythema induratum can lead to what

A

fat necrosis and inflammation

183
Q

is erythema induratum an erythematous, slightly tender nodule that usually ulcerates

A

YES

184
Q

what are verrucae also called

A

warts

185
Q

what are squamopoliferative lesions caused by HPV

A

verrucae (warts)

186
Q

age range of ppl with warts

A

children and adolescents

187
Q

where are warts present

A

> on hands; dorsal surface and periungal areas

188
Q

what is multiple, grey-white to tan, flat to convex, 0.1- to 1 cm papules with a rough pebbly surface

A

verrucae (Warts)

189
Q

how does warts transmission occur

A

involves direct contact between individuals or autoinoculation

190
Q

are warts self limiting

A

yes - regressing spontaneously within 6 months to 2 years

191
Q

what is a common, self limiting viral disease of skin caused by poxvirus

A

molluscum contagiosum

192
Q

what age is mollusum contagiousm present

A

children and young adults

193
Q

how is molluscum contagiosum spread

A

direct contact

194
Q

where are molluscum contagiousum lesions present

A

skin and mucous membranes of trunk and anogenital reas

195
Q

what are firm, often pruritic lesions, pink to skin-colored umbilicate papules, generally ranging in diameter from 0.2 to 0.4

A

molluscum contagiosum

196
Q

what is a common superficial bacterial infection of skin

A

impetigo

197
Q

what is highly contagious; frequently seen in otherwise healthy children and adults in poor health

A

impetigo

198
Q

where is impetigo present on body

A

exposed skin, particularly face and hands

199
Q

what bacteria causes impetigo

A

S. aureus

200
Q

Erythematous macules with multiple small pustules; as pustules break, shallow erosions form, covered with drying serum giving the appearance of honey colored crust

A

impetigo

201
Q

what happens if impetigo crust is not removed

A

new lesions form on the periphery of crust

202
Q

how is impetigo treated

A

topical or systemic antibiotics

203
Q

where is superficial fungal infection confined to

A

stratum corneum

204
Q

what primarily causes superficial fungal infections

A

dematophytes (grow in soil and on animals)

205
Q

what are the diverse lesions of superficial fungal infection

A
  1. tinea capities
  2. tinea barbae
  3. tinea corporis
  4. tinea pedis
206
Q

___: > children, rare in infants and adults; > scalp; asymptomatic, patchy skin lesions associated with mild erythema, crust formation, scaling, and frequent hair loss

A

Tinea capitis

207
Q

___: Infection of beard; adult men; uncommon

A

Tinea barbae

208
Q

___: > all ages; common skin infection; predisposing factors: excessive heat and humidity and exposure to infected animals

A

Tinea corporis

209
Q

___: affects 30%-40% of population at some point of life; diffuse erythema and scaling; nail infection (onychomycosis) produces discolored, thick, and deformed nails

A

Tinea pedis

23 General Pathology (24 decks)

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