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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
is SJS or TEN worse
TEN
26
SJS/ TEN
- severe mucocutaneous reaction - usually triggered by drugs - extensive necrosis and detachment of epidermis
27
pathogenesis of SJS/ TEN
- 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
28
acne vulgaris
- most common cutaneous disorder of adolescents and young adults - disease of pilosebaceous follicles
29
what is the precursor lesion of acne
microcomedos
30
whitehead
- accumulation of sebum and keratinous material | - closed comedo
31
blackhead
- follicular surface is opened with continuous distension - open comedo - color due to densely packed keratinocytes, oxidized lipids and melanin
32
pathogenesis of acne vulgaris
- 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
rosacea
- acneform lesion - common chronic inflammatory skin disorder - variety of clinical manifestations localized to central face
34
subtypes of rosacea
- erythematotelangiectatic - papulopustular - phymatous - ocular
35
risk factors for rosacea
- genetic predisposition | - abnormalities in immunity - innate and adaptive
36
melanocyte nevus
- benign proliferation of nevus cells - cluster as nests within lower epidermis or dermis - congenital or acquired
37
junctional nevi
nests that are at the dermal- epidermal junction
38
compound nevi
nests that are at the dermal-epidermal junction and in the dermis
39
intradermal nevi
nests in the dermis
40
predisposing factors for melanocyte nevi
- heredity - germline polymorphisms- IRF4 and TERT - degree of sun exposure as a child - phenotypic characteristics like skin
41
atypical acquired nevi
- 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
eclipse nevus
- compound nevus on scalp of children - tan center and brown - benign
43
congenital melanocyte nevi
- benign proliferation of melanocytes that arise during embryogenesis - cell proliferation via MAPK
44
complications of congenital melanocyte nevi
- melanoma after puberty | - many melanomas arising with large CMN have earlier onset and deeper origin
45
melanocyte nevus pathogenesis
- 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
melanoma
- most serious form of skin cancer | - aggressive, may spread in unpredictable manner to involve an organ in body
47
melanocyte biology
- developmnet regulated by MITF - MSH stimulates the melanocortin 1 receptor (MC1R) - induction of MC1R activates expression of MiTF -> melanin pigments
48
UV exposure and melanoma
- keratinocyte DNA damage -> p53 mediated induction and POMC expression - secretion of MSH and stimulation of MC1R
49
Mitogen activated protein kinase (MAPK)
- activated in almost all melanomas - in nonmalignant cells promotes cellular growth and survival - dev BRAF mutations, associated with poor prognosis
50
treatment option for melanomas
- BRAF inhibitors - causes tumor regression and overall survival in pts with BRAF mutations - tumors can dev resistance to therapy by bypassing BRAF
51
warning signs of melanoma
- A- asymmetry - B- border - C- color - D- diameter - E- evolving
52
basal cell carcinoma (BCC)
- common skin cancer in basal layer of epidermis - "epithelioma" - low metastatic potential
53
risk factors for BCC
- sun exposure, especially in childhood - intermittent intense increments of sun exposure increases risk - tanning beds - ionizing radiation
54
BCC pathogenesis
- 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
cutaneous squamous cell carcinoma (cSCC)
- arises from malignant proliferation of epidermal keratinocytes - second most common type of skin cancer
56
risk factors for cSCC
- UVB exposure -> p53 mutation - UVA exposure increases risk for cSCC and BCC - ionizing radiation - immunosuppression
57
cSCC pathophysiology
- malignant transformation of epidermal keratinocytes - UV induced mutations in p53 - mutation of RAS pathway
58
impetigo
- contagious superficial bacterial infection - most common in kids 2-5 - due to s. aureus, beta-hemolytic streptococci
59
risk factors for impetigo
- crowding - poor hygiene - underlying scabies
60
classifications of skin lesions in impetigo
- non-bullous (most common) - bullous - ecthyma
61
non- bullous impetigo
- lesions begin as papules, progress to vesicles - surrounded by erythema - rapidly form crust with golden appearance
62
bullous impetigo
- strains of s. aureus produce exfoliative toxin A | - loss fo cell adhesion into epidermis
63
ecthyma
- ulcerative form - extends into dermis - consists of punched out ulcers covered with yellow crust
64
acanthosis nigricans
- velvety, hyperpigmented plaques on neck and axillae | - associated with obesity and diabetes
65
pathophysiology of acanthosis nigricans
mutations in IGFR1, FGFR, EGFR
66
vitiligo
- acquired pigmentary disorder - most frequent cause of depigmentation worldwide - dev white macules due to loss of functioning melanocytes - autoimmune response against melanocytes
67
koebner phenomenon
- repeated mechanical trauma and other types of physical trauma causes discoloration of skin - associated with vitiligo
68
vitiligo pathogenesis
- 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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