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Pathophys > Derm patho > Flashcards

Derm patho Flashcards

1
Q

What are the functions of the skin?

A

Barrier against microorganisms, ultraviolet radiation, loss of body fluids, and the stress of mechanical forces
Regulates body temperature
Involved in the production of vitamin D
Touch and pressure receptors provide important protective functions and pleasurable sensations

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2
Q

What is the deepest layer of the skin and what is its function?

A

Stratum basale: Location of mitosis for keratinocytes, melanocytes, merkel cells

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3
Q

What is the 2nd layer of the skin and what is its function?

A

Stratum spinosum: new keratinocytes (desmosomes)

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4
Q

What is the 3rd layer of the skin and what is its function?

A

Stratum granulosum: granular layer with keratohyaline granules

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5
Q

What is the 4th layer of the skin and what is its function?

A

Stratum lucidum: Keratinocytes

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6
Q

What is the 5th layer of the skin and what is its function?

A

stratum corneum: contains anucleate cells with keratin

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7
Q

What is the stratum basale AKA?

A

stratum germinativum

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8
Q

What do squamous epithelial cells produce?

A

Produce keratin protein and cytokines

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9
Q

what are melanocytes derived from

A

neural crest cells in the ectoderm

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10
Q

what are melanosomes?

A

synthesize melanin

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11
Q

what is melanin derived from

A

Tyrosine(AA from phenoalanin) to DOPA (by tyrosinase)

DOPA to melanin

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12
Q

what is PKU

A

disorder where you cant metabolise phenoalanine=cant produce melanin= pale/albino

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13
Q

what is different in melanin between AA and whites?

A

Number of melanocytes is the same in all races
Melanin degraded more rapidly in whites
Whites: melanosomes concentrated in basal layer
AA: melanosomes present throughout all layers
AA: Melanocytes are larger with more dendritic processes

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14
Q

Where do Langerhan dendritic cells come from and where are they located

A

bone marrow derived

migrate to epidermis and lymph nodes (uncommonly to dermis)

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15
Q

what is the role of Langerhan cells

A

regulate contact hypersensitivity and self recognition(graft vs host rejection) by expresion of MHC1, MHC2, and FC igG and IgE receptors

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16
Q

how do steriods affect Langerhans cells

A

slow down their function

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17
Q

what are merkel cells associated with

A

terminal neuronal axon

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18
Q

what body locations are merkel cells typically found

A

specialized regions such as lips, oral cavities, palmar skin

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19
Q

where is the greatest amount of eccrine glands located

A

distributed over the body with greatest number on face, chest, and back

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20
Q

what do eccrine glands release and what is their funciton

A

salt water, regulates body temp

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21
Q

what do apocrine glands release

A

salt water and other chemicals

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22
Q

where do hair follicles originate from

A

originate in the primitive epidermis but grow downward to the matrix located in the deep dermis

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23
Q

what is the dermis composed of

A

Collagen, elastin reticulum, gel-like ground substance

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24
Q

what structures are present in the dermis

A

Hair follicles, sebaceous glands, sweat glands, blood vessels, lymphatic vessels, nerves

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25
Q

what cells are present in the dermis

A

Fibroblasts, mast cells, macrophages

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26
Q

what is the papillary dermis

A

Loose CT layer dirctly beneath the epidermis

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27
Q

what is the reticular dermis

A

lower dermal layer composed of dense dermal collagen (continuous with subcutaneous collegen)

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28
Q

what is the function of collagen layers seperating adipose layers

A

helps with heat regulation

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29
Q

what are the 4 structural units of the nail

A

The matrix from which the nail grows
The hyponychium (nail bed)
Nail plate

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30
Q

how much does the nail grow in a day

A

1mm or less

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31
Q

what are Cutaneous lymphocyte associated antigens(CLA)

A

Expressed on the memory T cells to Mediates cutaneous inflammatory and infectious diseases

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32
Q

what skin layer is know as the horny layer

A

stratum corneum

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33
Q

what are the changes to skin associated with aging

A

Atrophy of sebaceous, eccrine, and apocrine glands
Changes in hair color
Fewer hair follicles and growth of thinner hair

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34
Q

what are macule characteristics

A

Flat
Distinguished by coloration
Patch: flat irregular shaped macule >1cm diameter

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35
Q

what are papule characteristics

A

Elevated
Domed shape or flat topped
1 cm or less across (Nodule is greater than 5mm

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36
Q

what are Plaque characteristics

A

Elevated
Flat topped
Usually greater than 1cm across

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37
Q

what are vesicle characteristics

A

1 cm or less across
Bulla is greater than 1cm (Blister)
Blister is common term for Vesicle and Bulla

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38
Q

what are wheal characteristics

A 
Itchy
Transient
Elevated lesion
Variable blanching
Erythema due to dermal edema
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39
Q

what are scale characteristics

A

Dry
Horny
Plate like
Imperfect cornification

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40
Q

what are charcacteristics of lichenification

A

Thickened rough skin

Prominent skin markings (due to repeated rubbing)

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41
Q

what is onycholysis

A

separation of nail plate from nail bed

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42
Q

what is excoriation

A

Traumatic lesion breaking the epidermis

Raw linear area (deep scratch)

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43
Q

what is hyperkeratosis

A

Thickening of stratum corneum

Qualitative abnormality of the keratin

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44
Q

what is parakeratosis? Where is it normal?

A

Keratinization with retained nuclei of the stratum corneum

Normal on mucous membranes

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45
Q

what causes retained nuclei

A

improper maturation

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46
Q

how can radiation affect the epidermis

A

can cause hyperkeratosis

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47
Q

what is hypergranulosis

A

Hyperplasia of stratum granulosum

Usually due to rubbing

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48
Q

what is acanthosis

A

Diffuse epidermal hyperplasia

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49
Q

what is papillomatosis

A

Surface elevation caused by hyperplasia and enlargement of contiguous dermal papilla

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50
Q

what causes cafe au lait macule

A

increased melanogenesis

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51
Q

what is cafe au lait associated with

A

neurofibromatosis

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52
Q

what is beckers nevus

A

solitary lesions that break up into smaller macules at the periphery

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53
Q

what is dermal melanocytosis and how does it appear

A

condition where melanocytes are found in the dermis and actively synthesize melanin. A blue color is given off from shorter wavelengths(Tyndall effect)

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54
Q

what conditions have dermal melanocytosis

A

mongolian spots, nevus of ota and ito

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55
Q

how are nevus of ota/ito similar

A

congenital: apparent within 1st year of life
apperaance: mottled
asians and AA

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56
Q

how are nevus of ota/ito different

A

divisons

Ito: Posterior supraclavicular and lateral brachiocutaneous nerves

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57
Q

what is acantholysis and what is an example of it

A

Loss of intercellular cohesion between keratinocytes

Pemphigus vulgaris-chronic blistering skin condition

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58
Q

what is spongiosis

A

Intracellular edema of the epidermis

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59
Q

what is hydropic swelling(or ballooning)? When does it occur?

A

Intracellular edema of keratinocytes

Seen in viral infections

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60
Q

what is exocytosis

A

Infiltration of epidermis by inflammatory cells

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61
Q

what is erosion

A

incomplete loss of the epidermis

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62
Q

what is ulceration

A

Complete loss of the epidermis revealing dermis(bleeding)

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63
Q

what is vacuolization

A

Formation of vaculoes within or adjacent to cells

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64
Q

what is lentiginous

A

linear pattern of melanocyte proliferation within epidermal basal layer

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65
Q

what are nested melanocytes

A

the melanocytes are clumped together (not in linear pattern like lentiginous)

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66
Q

What is vitiligo and what causes it?

A

Depigmentation from Autoimmune,Genetic,Oxidative stress(surgery)

67
Q

What is the diff bt segmented and non-segmented vitiligo?

A

Non-Segmented
Most common, at any age, symmetry
Segmented
Aggressive, dorsal root presentation

68
Q

what are freckles caused from?

A

Increase amount of melanin within basal keratinocytes

Melanocytes may be slightly enlarged but normal density

69
Q

how are lentigo diff from freckles

A

Benign localized hyperplasia of epidermal melanocytes (freckles don’t increase #)
Do not darken with sunlight

70
Q

T/F lentigo involves skin and mucous membranes

71
Q

what is melisma, where is it located, and what causes it

A

Dark, irregular, well demarcated, hyperpigmented macules to patches
Location: upper cheek, nose, lips, upper lip, and forehead.(mask of preg)
Stimulation of melanocytes or pigment-producing cells by estrogen and progesterone to produce more melanin pigments when exposed to sun

72
Q

what is the melanocyte nevus size ranking

73
Q

are nevi more commonly acquired or congenital

A

Can be both, acquired more common

74
Q

how are nevus cells(type of melanocyte) diff from epidermal melanocytes

A

Nevus cells cluster as nests within the lower epidermis and/or dermis
Nevus cells do not have dendritic processes
Epidermal melanocytes are evenly dispersed

75
Q

what are the earliest types of nevi and what is characteristic of them

A

Junctional
Located along the dermoepidermal junction in nests
Nuclei uniform
Little or no mitotic activity

76
Q

what do junctional nevi progress to

A

Compound-growth from dermoepidermal junction to underlying dermis

77
Q

what do compound nevi progress to?

A

Intradermal- they have no epidermal nests

78
Q

What does activation of RAS gene do

A

Increases proliferation of melanocytes

79
Q

what is the role of BRAF

A

encodes serine/threonine kinase

Positive mediator of RAS signals=increases proliferation of melanocytes

80
Q

what is the effect of a mutated BRAF

A

Mutation causes it to be always activated= increases proliferation of melanocytes

81
Q

what does the CDKN2A(p16) gene do

A

turns off CDK4= dec melanocyte proliferation

82
Q

what are characteristics of dysplastic nevus

A

Larger than acquired nevi (> 5mm)
Flat macules, slightly raised plaques or target like lesions with darker raised center (pebbly surface)
Irregular flat periphery
Variability in pigmentation (Variegation)
Irregular borders
Usually compound

83
Q

what is cytologic atypia

A

irregular cells- irregularly shaped, dark staining nuclei

84
Q

what is the effect of a mutated CDKN2A(p16)

A

normally it is a cyclin dependent kinase inhibitor to inhibit CDK4 kinase= stop proliferation.
Mutation= proliferation

85
Q

what are the sites of origin:

A

skin, oral, anogenital mucosal surfaces, esophagus, meninges, eye

86
Q

when does malignant melanoma typically become resistant to therapy?

A

once it metastasizes

87
Q

what are the deadly skin Ca

A

malignant melanoma

Rarely Merkel cell tumor

88
Q

does malignant melanoma grow vertical or horizontal?

89
Q

what is lentigo maligna

A

indolent melanoma on face of elderly

90
Q

what are acral lentiginious

A

malignant melanoma with radial growth unrelated to sun exposure (trunk, anogenital, sinus)

91
Q

what gender has a worst prognosis for malignant melanoma

92
Q

why do malig melanoma on extremities have a better prognosis than the trunk

A

people see them faster

93
Q

what are prognostic factors of malig melanoma

A

Tumor depth (Breslow thickness)
Number of mitoses
Evidence of tumor regression (presumably due to host immune response)
Presence and number of tumor infiltrating lymphocytes

94
Q

what depth of malig melanoma has a “good” prognosis

A

<1.7mm (clarks level 1 or 2)

95
Q

what is the role of the p14ARF gene

A

inhibits MDM2=inc p53

96
Q

what is the role of the MDM2 gene

A

inhibits p53= inc survival of melanoma cells

97
Q

what are benign epidermal tumors derived from

A

keratinizing stratified squamous epithelium of the epidermis, hair follicles, and ductular epithelium of cutaneous glands

98
Q

what is a fibroepithelial polyp

99
Q

what is seborrheic keratosis

A

Round, flat, coin-like, waxy plaques
Vary in diameter from mms to cms
Uniformly tan to dark brown
Velvety to granular surface

100
Q

how do you differentiate seborrheic keratosis from malig melanoma

A

hand lens will reveal Small, round, porelike ostia impacted with keratin

101
Q

what is the path report of sevborrheic keratosis

A

Keratin filled horn cysts, some communicate with surface (pseudo-horn cysts)

102
Q

what is dermatosis papulosa nigra

A

multiple small SK lesions on face due to keratin deposition in epidermis

103
Q

what is the pathogenesis of SK

A

Mutation in FGFR3 gene
Fibroblast growth factor receptor-3
Drives the growth of the tumor

104
Q

what is paraneoplastic syndrome

A

disease or symptom that is the consequence of the presence of cancer in the body, but is not due to the local presence of cancer
ie explosively large numbers of SK can result from inc ADH from a tumor or stimulation of transforming growth factor alpha(GI carcinoma)

105
Q

what is the Leser-Trelat sign

A

explosive onset of multiple seborrheic keratoses

106
Q

what are characteristics of benign acanthosis nigricans

A

80% of cases
Develops gradually
Occurs in childhood or during puberty
Various presentations
Autosomal dominant with variable penetrance
In association with obesity or endocrine abnormalities (pituitary or pineal tumors, and diabetes)
Part of several rare congenital syndromes

107
Q

what are characteristics of malignant acanthosis nigricans

A

Arise in middle aged or older individuals

Occurs in association with underlying cancers(GI adenocarcinomas)

108
Q

what is the morphology of acanthosis nigricans

A

Numerous repeated peaks and valleys in epidermis
Variable hyperplasia
Slight basal cell layer hyperpigmentation (no melanocyte hyperplasia)

109
Q

what is the pathogenesis of acanthosis nigricans

A

Familial form associated with FGFR3
May be an isolated finding or seen together with skeletal deformities
Achondroplasia (mutation in FGFR3)
Thanatophoric dysplasia(mutation in FGFR3)

110
Q

what is a fibroepithelial polyp

111
Q

what is the morphology of fibroepithelial polyps

A

Fibrovascular cores
Covered by benign squamous epithelium
Can undergo ischemic necrosis due to torsion

112
Q

what disorders are fibroepithelial polyps associated with

A

Diabetes
Obesity
Intestinal polyposis

113
Q

what lesions become more numerous or prominant during preg

A

fibroepithelial polyps, melanocyte nevi, hemangiomas due to hormones

114
Q

what is a epidermal cyst and what is does it form

A

Invagination & cystic expansion of epidermis or hair follicle
Cyst filed with keratin and lipid debris from sebaceous secretions forming a wen

115
Q

what are characteristics of a epidermal (inclusion) cyst

A 
Dermal or subcutaneous
Well circumscribed
Firm
Often moveable nodules
Can undergo traumatic rupture and be expressed
116
Q

what is the wall and center like in epidermal inclusion cyst and how does this differ from pilar or trichilemmmal cysts

A

Epidermal inclusion cyst
Wall: Resembles normal epidermis
Center: Filled with laminated strands of keratin

Pilar or trichilemmal cysts
Wall: Resembles folliclular epithelium without granular cell layer
Center: Filled with homogenous mixture of keratin and lipid

117
Q

what is the wall like for Dermoid cyst

A

Similar to epidermal inclusion with multiple appendages budding outward

118
Q

what is steatocystoma simplex

A

Resembling sebaceous gland duct from which numerous compressed sebaceous lobules originate

119
Q

what is steatocystoma multiplex

A

different than steatocystoma simplex. caused by a missense mutation in keratin

120
Q

what are adnexal appendage tumors

A

BENIGN but confused with basal cell carcinoma

121
Q

what is the inheritance pattern of adnexal appendage tumors

A

some have mendelian pattern of inheritance causing a predisposition for internal malignancy

122
Q

what type of structures do adnexal appendage tumors involve

A

HAIR FOLLICLES
SEBACEOUS GLANDS
SWEAT GLANDS

123
Q

what are characteristics of adnexal tumors

A 
Appendage tumors
Flesh colored
Solitary or multiple
Papules and nodules
Some have predisposition for specific body surfaces
124
Q

what is a eccrine poroma

A

adnexal tumor on palms and soles

125
Q

what is cylindroma

A

adnexal tumor of the forehead and scalp

126
Q

what is the pathogenesis of cylindroma

A

dominantly inherited causing inactivation mutation in TSG CYLD
Islands of cells resembling normal epidermal or adnexal basal cell layer
Fit together like jigsaw puzzle

127
Q

what is trichoepithelioma and what is the pathogenesis

A

adnexal follicular tumor

Proliferation of basaloid cells that forms primitive structures resembling hair follicles

128
Q

what are syringomas

A

adnexal tumor of eccrine glands forming Multiple small tan papules in lower eyelids

129
Q

what are sebaceous adenomas associated with

A

Associated with internal malignancy in Muir Torre syndrome (a subset of hereditary nonpolyposis carcinoma syndrome)

130
Q

what are characteristics of actinic keratosis and what causes it

A 
Dysplastic changes prior to carcinoma
Sun damaged skin
Other causes
Ionizing radiation
Industrial hydrocarbons
Arsenicals
Exhibit heperkeratosis
Lightly pigmented individuals.
131
Q

what is the hallmark sign of actinic keratosis

A

Parakeratosis-corneum cells retain nuclei

132
Q

what are the lesions like in actinic keratois and where are they located

A 
Lesions
Most are <1m
Tan-brown, red or skin colored
Rough sandpaper like
Cutaneous horn
Locations:  sun exposed sites
133
Q

what is actinic chilitis

A

keratosis on the lips

134
Q

what is the pathogenesis of actinic keratosis

A

cytologic atypia in lower most layers of epdermis. May be associated with hyperplasia of basal cells

135
Q

what is imipuimod

A

med that activates immune system by stimulating Toll-like receptors. used for actinic keratosis or SCC

136
Q

what are the most common tumors from sun exposure

A

1st=basal cell carcinoma

2nd= squamous cell carcinoma

137
Q

does SCC metastasize to nodes

A

Yes but <5%

138
Q

what is the morphology of SCC in situ (Bowen’s disease)

A

no invasion through dermatoepidermal junction
Sharply defined, red, scaling plaques
Involves all levels of epidermis

139
Q

what is the morphology of advanced SCC

A

Invasive and nodular: variable degrees of differentiation
Variable keratin
May ulcerate

140
Q

what is the pathogenesis of SCC

A

UV light damages DNA p53. P53 is normally upregulated by kinases(ATM and ATR) but not if mutated p53.UV also dec immune surveillance

141
Q

besides UV, what else increases SCC risk

A

immunosuppression (chemo, organ transplants), HPV 5 and 8, steriods

142
Q

besides UV what else inc BCC risk

A

immunosuppression,

143
Q

what is xeroderma pigmentosum

A

inherited defects in DNA repair(both PTCH and p53. Cannot be exposed to sun at all

144
Q

what are blue palisading nests

A

cells line up and squish together. only seen in BCC

145
Q

what are characteristics of BCC lesions

A

Pearly papules
Prominent dilated subepidermal blood vessels(telangiectasias)
May contain melanin

146
Q

what are characteristics of advanced BCC lesions

A

ulcerate, local invasion of bone or facial sinuses

147
Q

what is the morphology of BCC

A

Tumor cells resemble normal basal cell layer of epidermis
Arise from epidermis or follicular(deeper) epithelium
2 patterns(multifocal growths and nodular lesions)

148
Q

what is characteristic of multifocal BCC growths

A

Originate from epidermis

Extend over several square cms

149
Q

what is characteristic of nodular BCC lesions

A

grow downward into dermis

150
Q

what is the pathogenesis of Nevoid BCC(gorlin syndrome)

A

Autosomal dominant: Chr9, PTCH gene mutation
2nd normal allele becomes inactivated by UV light.
PTCH gene encodes a receptor for Sonic Hedgehog gene(normally prevents BCC)
Absence of PTCH causes activation of SMO which leads to basal cell carcinoma

151
Q

what is the genetic component of Non NBCCS

A

Genetic component
30% have PTCH mutation
40-60% have p53 mutation
Xeroderma pigmentosa: defects in PTCH and p53

152
Q

what is merkel cell carcinoma

A

VERY MALIGNANT AND LETHAL, LOOK LIKE SMALL CELL CA. OF LUNG

153
Q

what are acute dermatoses

A

urticaria, eczema, erythema multiforme

154
Q

what are chronic dermatoses

A

psoriasis, seborrheic dermatitis, lichen planus, lupus erthymatosus

155
Q

what causes urticaria

A

Localized Mast Cell degranulation from IgE=Hist release=Dilation of vessels and Increase vascular permeability

156
Q

what is the diff bt angioedema and urticaria

A

Angioedema is closely related to urticaria but characterized by deeper edema of both the dermis and subcutaneus fat.

157
Q

what is ASA effect on urticaria

A

ASA blocks COX path so inc leukotriene path=inc hist release= inc urticaria

158
Q

what is hereditary angioneurotic edema

A

inherited deficiency of C1 inhibitor(normally dec complement activation preventing Hist release) causes a complement mediated urticaria (in a majority of cases there is no cause)

159
Q

why does IgE have more SE than IgG

A 
IgG= activate macrophage and neutrophiles
IgE= activeate mast cells=hist release= more SE than IgG
160
Q

what may cause persistent urticaria

A

collagen vascular disorder, hodgkin lymphoma

161
Q

what are characteristics of eczema

A

red, papulovesicular, oozing, and crusted lesions.

If persistent develop into raised, scaling plaques due to acanthosis and hyperkeratosis

162
Q

what cells in the epidermis have a central role in contact dermatitis

A

langerhan cells

163
Q

what is the pathway of eczema causing chronic lesions

A

A: initial dermal edema and perivascular infiltration by inflammatory cells. Is followed within 24-48 hours by
B: epidermal spongiosis and microvesicle formation
C: Abnormal scale along with acanthrosis
D: Hyperkeratosis
E: Chronic lesion

Pathophys (15 decks)

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