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From Flashcardlet > Dermatology Patho > Flashcards

Dermatology Patho Flashcards

1
Q

What is the primary function of the skin?

A

To protect the body from microorganisms, UV radiation, loss of body fluids and the stress of mechanical forces. Regulates body temp and produces vitamin D. Also has touch and pressure receptors.

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2
Q

Epidermis layers

A 
Stratum basale
Stratum germinativum
Stratum Spinosum
Stratum Granulosum
Stratum Lucidum
Stratum Corneum
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3
Q

Keratinocytes

A

basal cells, squamous cells. They are formed by upward migration of cornified basal cells. Produce keratin and cytokines.

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4
Q

Melanocytes

A

derived from neural crest cells in the stratum basalis. Melanin is synthesized in melanosomes by the conversion of Tyrosine to DOPA to melanin.

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5
Q

Langerhans cells

A

process antigens in the epidermis and migrate to regional lymph nodes (like macrophages).
They play a role in hypersensitivty, allograft rejection and GVH.
Express MHC-1 and MHC-2, FcIgG and IgE receptors on their surface.

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6
Q

Dendrocytes

A

Process antigens in the dermis and act like mast cells.

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7
Q

Merkel cells

A

associated with terminal neuronal axons. Seen in specialized regions like the lips, oral cavity and palmer skin.

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8
Q

Eccrine Glands

A

distributed all over the body with the greatest number on the face, chest and back. They release salt water as a mechanism of body temp regulation.

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9
Q

Apocrine glands

A

Located in the axilla, scalp, face, abdomen and genital area. They release fluid and bacteria break it down producing odor.

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10
Q

Hair Follicles

A

harbor protected niches capable of regenerting superficial epithelial skin structures. They arise from the matrix located deep in the dermis.

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11
Q

Hair Follicles

A

harbor protected niches capable of regenerting superficial epithelial skin structures. They arise from the matrix located deep in the dermis

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12
Q

Epidermis layers

A 
Stratum basale
Stratum germinativum
Stratum Spinosum
Stratum Granulosum
Stratum Lucidum
Stratum Corneum
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13
Q

Keratinocytes

A

basal cells, squamous cells. They are formed by upward migration of cornified basal cells. Produce keratin and cytokines.

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14
Q

Melanocytes

A

derived from neural crest cells in the stratum basalis. Melanin is synthesized in melanosomes by the conversion of Tyrosine to DOPA to melanin.

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15
Q

Langerhans cells

A

process antigens in the epidermis and migrate to regional lymph nodes (like macrophages).
They play a role in hypersensitivty, allograft rejection and GVH.
Express MHC-1 and MHC-2, FcIgG and IgE receptors on their surface.

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16
Q

Dendrocytes

A

Process antigens in the dermis and act like mast cells.

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17
Q

Merkel cells

A

associated with terminal neuronal axons. Seen in specialized regions like the lips, oral cavity and palmer skin.

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18
Q

Eccrine Glands

A

distributed all over the body with the greatest number on the face, chest and back. They release salt water as a mechanism of body temp regulation.

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19
Q

Apocrine glands

A

Located in the axilla, scalp, face, abdomen and genital area. They release fluid and bacteria break it down producing odor.

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20
Q

Hair Follicles

A

harbor protected niches capable of regenerting superficial epithelial skin structures. They arise from the matrix located deep in the dermis

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21
Q

Piloerection

A

contraction of the erector pili muscles in the mid-dermis that straightens the follicle following SNS activation.

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22
Q

Components of the Dermis

A

Collagen, elastin reticulum, gel-like ground substance, hair follicles, sebaceous glands, sweat glands, blood vessels, lymphatic vessels, nerves, fibroblasts, mast cells and macrophages.

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23
Q

Components of the subcutaneous layer

A

Adipocytes, dermal-subcutaneous collagen continues into Subcutaneous to anchor the adipocytes to the dermal layer.

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24
Q

What do patients with multiple layers of fat have between each layer or fat?

A

Layers of collagen split up layers of fat, possibly to help in thermal regulation and energy stores.

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25
Q

Structural units of the nails

A

The proximal nail fold, the matrix from which the nail grows, the hyponchium (nail bed) and the nail plate.

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26
Q

A subset of lymphocytes in the skin express which specific antigen?

A

CLA - cutaneous lymphocyte associated antigen.

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27
Q

CLA function

A

mediate cutaneous inflammatory and infectious diseases. Innate is the response without the presence of T cells and the adaptive is the response with the presence of T cells on subsequent exposures to the same pathogen. An altered response will lead to an over-response to the pathogen (ie. allergy)

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28
Q

Layers of the skin

A

Stratum corneum & Stratum Lucidum (horny layer), Stratum granulosum, stratum spinosum, stratum basale, dermal-epidermal junction, papillary dermis, reticular dermis, subcutaneous.

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29
Q

Hyperkeratosis

A

thickening of the stratum that is a qualitative abnormality of keratin. Common at areas of radiation exposure because of the cell damage (formerly radiation was used to remove plantar warts but they later cause hyperkeratosis.

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30
Q

Parakeratosis

A

keratinization with retained nuclei of the stratum corneum. This is normal on mucous membranes (mouth and vagina) but on other skin surfaces it indicates that the cells are not maturing properly so they don’t lose their nucleus as they move up with maturation.

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31
Q

Hypergranulosis

A

hyperplasia of the stratum granulosum usually due to rubbing.

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32
Q

Acanthosis

A

diffuse epidermal hyperplasia that is the result of chronic irritation and inflammation. This can only be diagnosed with histology. NOT raised.

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33
Q

Papillomatosis

A

surface elevation (slightly raised) caused by hyperplasia and enlargement of contiguous dermal papilla (right beneath the epidermis)

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34
Q

acantholysis (pemphigus vulgaris)

A

loss of intercellular cohesion between keratinocytes (no desmasomes holding things together allowing fluid and cells to enter the space and form a papule.

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35
Q

Spongiosis

A

intracellular edema of the epidermis.

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36
Q

hydropic swelling (ballooning)

A

intracellular edema of keratinocytes seen in viral infections.

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37
Q

exocytosis

A

infiltration of the epidermis by inflammatory cell from the dermis.

38
Q

erosion

A

incomplete loss of the epidermis

39
Q

ulceration

A

complete loss of the epidermis resulting in the dermis being exposed and therefore bleeding

40
Q

vacuolization

A

formation of vaculoes within or adjacent to cells that occurs with aging (age spots)

41
Q

Lentiginous

A

linear pattern of melanocyte proliferation within the basal layer.

42
Q

Vitiligo

A

depigmentation of the skin caused by autoimmune, genetic and oxidative stress. Non-segmented type is the most common and is seen at any age without symmetry of the lesion itself. Segmented is less common and shows up in a dermatomal (dorsal root presentation) pattern.

43
Q

Freckle (Ephelis)

A

small to several mm macules that are tan-red to light brown. They appear after sun exposure and lighten/darken with the seasons due to the increased amount of melanin active during sun exposure. Melanocytes are enlarged but of normal density (no nesting)

44
Q

Lentigo

A

benign localized hyperplasia of the epidermal melanocytes in a linear pattern in the basal layer. Pathogenesis is unknown, and can involve both skin and mucus membranes. They are small (5-10mm) macules or patches that are tan-brown. These don’t darken or lighten based on sun exposure, the are permanent.

45
Q

Cafe au lait

A

flat pigmentd (macule) lesion that is present at birth or shortly after caused by increased melanogenesis. Size varies from a few mm to >15cm. These enlarge as the person grows and are commonly called ‘birth marks’. Associated with neurofibromatosis, esp. if there are >6.

46
Q

Neurofibromatosis

A

associated with multiple cafe au lait spots at birth. Melanocytes are derived from neural crest cells.

47
Q

Beckers Nevus

A

solitary lesions that break up into smaller macules at the periphery. Lacks nevus cells, may develop hair. Irregular and sharply demarcated lesion that is associated with other genetic disorders but melanomas are not reported.

48
Q

Dermal Melanocytosis (Mongolian Spots, Nevus of Oto and Ito)

A

Melanocytes in the dermis actively synthesize melanin resulting in blue color (d/t scattering of shorter wave lengths by dermal melanin)

49
Q

Mongolian spots

A

common in Asians and African Americans. May fade, watch closely.

50
Q

Nevus of Oto and Ito

A

congenital spots within a year of birth, mottled appearance, more frequent in Asians an African Americans. Oto is from the trigeminal divisions 1 and 2. Ito is from the posterior supraclavicular and lateral brachiocutaneous nerve.

51
Q

Melasma

A

dark, irregular, well demarcated hyperpigmented macules to patches on the upper cheek, nose, lip, upper lips, and forehead. They develop over time and generally go away after delivery. Caused by stimulation of the melanocytes to start producing by estrogen and progesterone hormones when exposed to sun. Pregnancy and OCPs.

52
Q

Trophic hormones

A

stimulate cells to grow and produce more of its product (ie. estrogen and progesterone in pregnancy and with OCP use)

53
Q

Melanocyte nevus

A

tan to brown, uniformly pigmented, solid regions that are relatively flat with well defined borders. May be congenital or acquired.

54
Q

Nevus cell

A

type of melanocyte. They cluster in nests in the lower epidermis and or dermis. They do not have dendritic processes and are not evenly dispersed like melanocytes in the epidermis.

55
Q

Stages of a Nevus

A

Junctional nevus (located at the dermoepidermal junction, nuclei are uniform, there is little/no mitotic activity, they are nested together), Grow into the underlying dermis and become Compound, older lesions no longer have nests when they are Intradermal and therefore they lose their pigmentation.

56
Q

Genetic mutation in Nevus

A

Mutation in BRAF or NRAS. Once the levels of p16 rise, they stop proliferation and the growth halts. This is why there are growth and rest cycles with a nevus.

57
Q

Compound nevus appearance

A

raised, dome shaped, symmetrical with uniform pigmentation, intradermal nevus cell nests with cords of nevus cells in the dermis.

58
Q

1978 dysplastic nevi

A

may progress to melanoma although most never transform, but by age 60 the risk is 50%. There are extensive changes in RAS.

59
Q

dysplastic nevus

A

larger than acquired nevi (>5mm), flat macules, slightly raised papules or target like lesions with darker raised center (pebbly surface), irregular borders, compound, and in both sun exposed and protected areas. Appears with nuclear atypia and odd arrangements that are not true nest.

60
Q

Genetic mutation in a dysplastic nevus

A

mutation in CDKN2A (p16) making it ineffective or CDK4 making it resistant so cell proliferation continues without inhibition.

61
Q

Malignant Melanoma

A

evolves from localized skin lesions to aggressive tumors that metastasize and are resistant to therapy.

62
Q

Characteristics of Malignant Melanoma

A

Asymptomatic (no itching or pain), size greater than 10mm at time of dx, change in color, size and/or shape, variations in color (esp. patriotic, indicating that it’s deeper in the dermis), borders are irregular and notched, ABCDEs.

63
Q

Progression of malignant melanoma

A

Radial growth - horizontal spread within the epidermis and superficial dermis.
Vertical growth - invades downward

64
Q

Types within radial growth

A

Lentigo maligna - indolent on the face and commonly in the elderly
Superficial spreading - most common, on sun exposed areas
Acral/mucosal lentiginous - unrelated to sun exposure

65
Q

Prognostic factors for melanoma

A

Tumor depth (breslow’s, <1.7mm=good), number of mitoses (higher = worse prognosis), evidence of tumor regression, presence and number of tumor infiltrating lymphocytes, gender (males = worse), location (extremity = better, trunk = worse)

66
Q

Melanoma histology

A

deeply pigmented melanosomes and melanocytes

67
Q

Melanoma’s genetics

A

CDKN2a is mutated in 40% of familial melanoma which codes for p15/INK4b, p16/INK4a, and p14/ARF (inhibits MDM2 to inhibit p53 normally). All of these suppress proliferation, therefore without it there will be excess proliferation.
In fair skinned individuals there is also a MCIR, ASIP and TYR mutation.

68
Q

Seborrheic Keratosis

A

round, flat, coin-like, waxy plaque that is uniformly tan to dark brown with a velvety to granular survace. With a hand lens small, round, porelike ostia impacted with Keratin will be seen. Mutation in the FGFR3 gene drives the growth of the tumor.

69
Q

Dermatosis papulosa nigra

A

multiple small seborrheic keratosis lesions on the face.

70
Q

Leser-Trelat sign

A

patient who previously had no lesions comes in with many lesions suddenly - look for another cause besides seborrheic keratosis, perhaps paraneoplastic syndrome.

71
Q

Acanthosis nigricans

A

hyperpigmented and thickened skin with velvet like texture. Located in flexural areas (esp. axillae, skinfolds of neck and groin). 2 types: benign develops slowly and often in childhood or puberty, malignant develops suddenly in middle aged or older adults in association with underlying cancers (esp. GI adenocarcinomas)

72
Q

what is GI adenocarcinoma associated with?

A

Acanthosis nigricans

73
Q

Acanthosis nigricans histology

A

numerous peaks and valleys in epidermis, variable hyperplasia, slight basal cell layer hyperpigmentation.

74
Q

Achondroplasia

A

Skeletal deformity due to mutation in FGFR3 that is associated with acanthosis nigricans

75
Q

Thanatophoric dysplasia

A

Skeletal deformity due to mutation in FGFR3 that is associated with acanthosis nigricans.

76
Q

Fibroepithelial polyp

A

skin tag, acrochordon, squamous papilloma. Common, located on neck, trunk and face. Soft, flesh colored, bag like tumor that is attached by a slender stalk. Has fibrovascular core covered by benign squamous epithelium that can undergo ischemic necrosis d/t torsion.

77
Q

What disorders are associated with fibroepithelial polyps?

A

Diabetes, obesity, intestinal polyposis (familial polyposis), pregnancy (hormonal driven)

78
Q

Epidermal inclusion cyst (Wen)

A

invagination and expansion of epidermis or hair follicle that is filled with keratin and lipid debris from sebaceous secretions. Dermal or subcutaneous, well circumscribed, firm, often movable and can undergo traumatic rupture.

79
Q

Epidermal inlcusion cyst morphology

A

the wall resembles normal epidermis and the center is filled with laminated strands of keratin.

80
Q

Pilar or trichilemmal cyst morphology

A

wall resembles follicular epithelium without granular cell layer and the center is filled with a homogenous mix of keratin and lipid.

81
Q

Dermoid cyst morphology

A

wall is simliar to epidermal inclusion cyst with multiple appendages budding outward.

82
Q

Steatocystoma simplex morphology

A

Resembling sebaceous gland duct from which numerous compressed sebaceous lobules originate. Is a missense mutation in keratin.

83
Q

Benign adnexal tumors

A

can involve hair follicles, sebaceous glands and sweat glands (both eccrine and apocrine). They are flesh colored, solitary or multiple, papules or nodules and may have a predisposition for a specific body surface.

84
Q

Eccrine poroma

A

benign adnexal tumor on the palms and soles

85
Q

Cylindroma

A

benign adnexal tumor on the forehead and scalp with hat like growth (turban tumor) that is dominantly inherited (inactivation mutations in TSG CYLD).

86
Q

Trichoepithelioma

A

benign adnexal tumor of the follicle with proliferation of the basaloid cells that form primitive structures resembling follicles.

87
Q

Syringomas

A

benign adnexal tumor of the eccrine gland that forms multiple small tan papules in the lower eyelids.

88
Q

Sebaceous adenomas

A

benign adnexal tumor associated with internal malignancy in Muir Torre syndrome (a subset of hereditary nonpolyposis carcinoma syndrome). Can convert to adenocarcinoma.

89
Q

Actinic keratosis

A

precursor to SCC that has dysplastic changes prior to carcinoma on sun damaged skin from ionizing radiation, industrial hydrocarbons, and arsenicals. Exhibit hyperkeratosis of the corneum layer and seen more in lightly pigmented individuals. Most are <1cm, tan-brown, red or skin colored that are rough/sand paper like and possibly a cutaneous horn. On sun exposed sites.

90
Q

Actinic cheilitis

A

keratosis on the lips

91
Q

cytologic aytpia in lower-most layers of epidermis

A

assocaited with hyperplasia of the basal cells

92
Q

parakeratosis

A

corneum cells retain nucleus

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