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Patho 2 > The Skin > Flashcards

The Skin Flashcards

1
Q

hypodermis

A
  • bottom most layer

- made of fat and loose CT

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2
Q

dermis

A
  • middle layer
  • tough CT
  • hair follicles
  • sweat glands
  • sensory nerve endings
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3
Q

epidermis

A
  • top most layer
  • dead keratinocytes at surface that flake off
  • living keratinocytes just below with dendritic cells
  • melanocytes and dividing keratinocytes just above dermis
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4
Q

macule

A
  • primary skin lesion
  • flat, circumcised area with change in skin color
  • less than 1 cm
  • i.e. freckle
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5
Q

patch

A
  • primary skin lesion
  • larger macule
  • flat, nonpalpable irregular shaped macule
  • i.e. vitiligo
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6
Q

papule

A
  • primary skin lesion
  • elevated, firm circumcised area
  • less than 1 cm
  • i.e. wart, insect bite
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7
Q

nodule

A
  • primary skin lesion
  • larger papule
  • elevated, firm circumscribed lesion
  • deeper in dermis in dermis than papule
  • 1-2 cm
  • i.e. lipoma
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8
Q

plaque

A
  • primary skin lesion
  • elevated, firm and rough lesion with flat top surface
  • greater than 1 cm
  • i.e. psoriasis
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9
Q

vesicle

A
  • primary skin lesion
  • elevated, circumscribed, superficial
  • doesnt extend into dermis
  • filled with serous fluid
  • less than 1 cm
  • i.e. chicken pox, herpes zoster, herpes simplex
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10
Q

bulla

A
  • primary skin lesion
  • larger vesicle
  • more than 1 cm in diameter
  • i.e. blister
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11
Q

pustule

A
  • primary skin lesion
  • elevated, superficial lesion
  • similar to vesicle but filled with purulent fluid
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12
Q

cyst

A
  • primary skin lesion
  • elevated, circumscribed, encapusulated lesion
  • in dermis or subcutaneous layer
  • filed with liquid or semi-solid material
  • i.e. sebaceous cyst, cystic acne
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13
Q

telangiectasia

A
  • primary skin lesion
  • fine irregular red lines produced by capillary dilation
  • can be associated with acne roscacea, venous HTN, systemic sclerosis, dev abnorm
  • i.e. rosacea
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14
Q

tumor

A
  • primary skin lesion
  • elevated solid lesion
  • may be clearly demarcated
  • deeper in dermis
  • more than 2 cm in diameter
  • i.e. neoplasms, neurofibroma
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15
Q

scale

A
  • secondary skin lesion
  • heaped up, keratinized cells, flakey skin
  • irregular shape
  • dry or oily
  • variation in size
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16
Q

lichenification

A
  • secondary skin lesion
  • rough, thickened epidermis secondary to persistent rubbing, itching, or skin irritation
  • often involves flexor surface of extremities
  • i.e. chronic dermatitis
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17
Q

excoriation

A
  • secondary skin lesion
  • loss of epidermis
  • linear, hollowed out crusted area
  • i.e. abrasions or scratches, scabies
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18
Q

fissures

A
  • secondary skin lesion
  • linear crack or break from the epidermis to dermis
  • may be moist or dry
  • i.e. athletes foot, cracks at corner of mouth
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19
Q

erosion

A
  • secondary skin lesion
  • loss of epidermis
  • depressed, moist, glistening
  • follows rupture of vesicle or bulla or chemical burn
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20
Q

ulcer

A
  • secondary skin lesion
  • loss of epidermis or dermis
  • concave
  • varies in size
  • i.e. pressure ulcer
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21
Q

psoriasis risk factors

A
  • genetics- PSORS1 mutation and IL-23 related genes
  • smoking
  • obesity
  • drugs- beta blockers, lithium, antimalarials
  • infection
  • alcohol
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22
Q

pre-psoriasis pathogenesis

A
  • autoimmune inflammatory disease
  • macrophages, dendritic cells, T cells and cytokines -> pathologic changes
  • differentiation of T cells stimulated by IL-23
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23
Q

psoriasis pathogenesis

A
  • activated dendritic cells produce TNF alpha
  • TNF alpha amplifies inflammation and induces adhesion molecules
  • cross talk between innate immunity (dendritic cells) and adaptive immunity (t cells)
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24
Q

people with psoriasis are at in increased risk of:

A
  • obesity
  • insulin resistance
  • metabolic syndrome
  • atherosclerosis
  • CVD
  • depression/ stress
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25
Q

is SJS or TEN worse

A

TEN

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26
Q

SJS/ TEN

A
  • severe mucocutaneous reaction
  • usually triggered by drugs
  • extensive necrosis and detachment of epidermis
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27
Q

pathogenesis of SJS/ TEN

A
  • meds up regulate death- receptor mediated apoptotic pathway
  • drug specific CD8 cells release perforin and granzyme
  • drugs also trigger activation of CD8, NK cells, and NKT cells to secrete granulysin
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28
Q

acne vulgaris

A
  • most common cutaneous disorder of adolescents and young adults
  • disease of pilosebaceous follicles
29
Q

what is the precursor lesion of acne

A

microcomedos

30
Q

whitehead

A
  • accumulation of sebum and keratinous material

- closed comedo

31
Q

blackhead

A
  • follicular surface is opened with continuous distension
  • open comedo
  • color due to densely packed keratinocytes, oxidized lipids and melanin
32
Q

pathogenesis of acne vulgaris

A
  • follicular hyperkeratinization causes partial obstruction of follicle with sebum and keratin
  • increased sebum production
  • propionibacterium acnes within follicle
  • inflammation d/t proliferation of p. acnes
33
Q

rosacea

A
  • acneform lesion
  • common chronic inflammatory skin disorder
  • variety of clinical manifestations localized to central face
34
Q

subtypes of rosacea

A
  • erythematotelangiectatic
  • papulopustular
  • phymatous
  • ocular
35
Q

risk factors for rosacea

A
  • genetic predisposition

- abnormalities in immunity - innate and adaptive

36
Q

melanocyte nevus

A
  • benign proliferation of nevus cells
  • cluster as nests within lower epidermis or dermis
  • congenital or acquired
37
Q

junctional nevi

A

nests that are at the dermal- epidermal junction

38
Q

compound nevi

A

nests that are at the dermal-epidermal junction and in the dermis

39
Q

intradermal nevi

A

nests in the dermis

40
Q

predisposing factors for melanocyte nevi

A
  • heredity
  • germline polymorphisms- IRF4 and TERT
  • degree of sun exposure as a child
  • phenotypic characteristics like skin
41
Q

atypical acquired nevi

A
  • share to a lesser degree some clinical features of melanoma
  • greater density on the areas of body that receive sporadic sun exposure
  • can form eclipse nevus
42
Q

eclipse nevus

A
  • compound nevus on scalp of children
  • tan center and brown
  • benign
43
Q

congenital melanocyte nevi

A
  • benign proliferation of melanocytes that arise during embryogenesis
  • cell proliferation via MAPK
44
Q

complications of congenital melanocyte nevi

A
  • melanoma after puberty

- many melanomas arising with large CMN have earlier onset and deeper origin

45
Q

melanocyte nevus pathogenesis

A
  • commonly form during early childhood d/t sun
  • traumatic stimuli -> scattering of nevus cells over large area of blistering
  • formation of multiple melanocytic nevi in injured area
  • FGF released by keratinocytes
46
Q

melanoma

A
  • most serious form of skin cancer

- aggressive, may spread in unpredictable manner to involve an organ in body

47
Q

melanocyte biology

A
  • developmnet regulated by MITF
  • MSH stimulates the melanocortin 1 receptor (MC1R)
  • induction of MC1R activates expression of MiTF -> melanin pigments
48
Q

UV exposure and melanoma

A
  • keratinocyte DNA damage -> p53 mediated induction and POMC expression
  • secretion of MSH and stimulation of MC1R
49
Q

Mitogen activated protein kinase (MAPK)

A
  • activated in almost all melanomas
  • in nonmalignant cells promotes cellular growth and survival
  • dev BRAF mutations, associated with poor prognosis
50
Q

treatment option for melanomas

A
  • BRAF inhibitors
  • causes tumor regression and overall survival in pts with BRAF mutations
  • tumors can dev resistance to therapy by bypassing BRAF
51
Q

warning signs of melanoma

A
  • A- asymmetry
  • B- border
  • C- color
  • D- diameter
  • E- evolving
52
Q

basal cell carcinoma (BCC)

A
  • common skin cancer in basal layer of epidermis
  • “epithelioma”
  • low metastatic potential
53
Q

risk factors for BCC

A
  • sun exposure, especially in childhood
  • intermittent intense increments of sun exposure increases risk
  • tanning beds
  • ionizing radiation
54
Q

BCC pathogenesis

A
  • UV induced inflammation -> erythema and prostaglandin synthesis through induction of COX2
  • hedgehog protein- directs embryonic development through sonic hedgehog signaling pathway
  • inactivating PTCH1 gene causes over expression of SHH signaling
55
Q

cutaneous squamous cell carcinoma (cSCC)

A
  • arises from malignant proliferation of epidermal keratinocytes
  • second most common type of skin cancer
56
Q

risk factors for cSCC

A
  • UVB exposure -> p53 mutation
  • UVA exposure increases risk for cSCC and BCC
  • ionizing radiation
  • immunosuppression
57
Q

cSCC pathophysiology

A
  • malignant transformation of epidermal keratinocytes
  • UV induced mutations in p53
  • mutation of RAS pathway
58
Q

impetigo

A
  • contagious superficial bacterial infection
  • most common in kids 2-5
  • due to s. aureus, beta-hemolytic streptococci
59
Q

risk factors for impetigo

A
  • crowding
  • poor hygiene
  • underlying scabies
60
Q

classifications of skin lesions in impetigo

A
  • non-bullous (most common)
  • bullous
  • ecthyma
61
Q

non- bullous impetigo

A
  • lesions begin as papules, progress to vesicles
  • surrounded by erythema
  • rapidly form crust with golden appearance
62
Q

bullous impetigo

A
  • strains of s. aureus produce exfoliative toxin A

- loss fo cell adhesion into epidermis

63
Q

ecthyma

A
  • ulcerative form
  • extends into dermis
  • consists of punched out ulcers covered with yellow crust
64
Q

acanthosis nigricans

A
  • velvety, hyperpigmented plaques on neck and axillae

- associated with obesity and diabetes

65
Q

pathophysiology of acanthosis nigricans

A

mutations in IGFR1, FGFR, EGFR

66
Q

vitiligo

A
  • acquired pigmentary disorder
  • most frequent cause of depigmentation worldwide
  • dev white macules due to loss of functioning melanocytes
  • autoimmune response against melanocytes
67
Q

koebner phenomenon

A
  • repeated mechanical trauma and other types of physical trauma causes discoloration of skin
  • associated with vitiligo
68
Q

vitiligo pathogenesis

A
  • depigmentation is result of hyperactive response of immune system against melanocytes
  • defects in T cells
  • increased autoreactive C8 and CD4
  • generation of antimelanocyte autoantibodies

Patho 2 (15 decks)

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