The Skin Flashcards
hypodermis
- bottom most layer
- made of fat and loose CT
dermis
- middle layer
- tough CT
- hair follicles
- sweat glands
- sensory nerve endings
epidermis
- top most layer
- dead keratinocytes at surface that flake off
- living keratinocytes just below with dendritic cells
- melanocytes and dividing keratinocytes just above dermis
macule
- primary skin lesion
- flat, circumcised area with change in skin color
- less than 1 cm
- i.e. freckle
patch
- primary skin lesion
- larger macule
- flat, nonpalpable irregular shaped macule
- i.e. vitiligo
papule
- primary skin lesion
- elevated, firm circumcised area
- less than 1 cm
- i.e. wart, insect bite
nodule
- primary skin lesion
- larger papule
- elevated, firm circumscribed lesion
- deeper in dermis in dermis than papule
- 1-2 cm
- i.e. lipoma
plaque
- primary skin lesion
- elevated, firm and rough lesion with flat top surface
- greater than 1 cm
- i.e. psoriasis
vesicle
- 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
bulla
- primary skin lesion
- larger vesicle
- more than 1 cm in diameter
- i.e. blister
pustule
- primary skin lesion
- elevated, superficial lesion
- similar to vesicle but filled with purulent fluid
cyst
- 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
telangiectasia
- 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
tumor
- primary skin lesion
- elevated solid lesion
- may be clearly demarcated
- deeper in dermis
- more than 2 cm in diameter
- i.e. neoplasms, neurofibroma
scale
- secondary skin lesion
- heaped up, keratinized cells, flakey skin
- irregular shape
- dry or oily
- variation in size
lichenification
- secondary skin lesion
- rough, thickened epidermis secondary to persistent rubbing, itching, or skin irritation
- often involves flexor surface of extremities
- i.e. chronic dermatitis
excoriation
- secondary skin lesion
- loss of epidermis
- linear, hollowed out crusted area
- i.e. abrasions or scratches, scabies
fissures
- 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
erosion
- secondary skin lesion
- loss of epidermis
- depressed, moist, glistening
- follows rupture of vesicle or bulla or chemical burn
ulcer
- secondary skin lesion
- loss of epidermis or dermis
- concave
- varies in size
- i.e. pressure ulcer
psoriasis risk factors
- genetics- PSORS1 mutation and IL-23 related genes
- smoking
- obesity
- drugs- beta blockers, lithium, antimalarials
- infection
- alcohol
pre-psoriasis pathogenesis
- autoimmune inflammatory disease
- macrophages, dendritic cells, T cells and cytokines -> pathologic changes
- differentiation of T cells stimulated by IL-23
psoriasis pathogenesis
- 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)
people with psoriasis are at in increased risk of:
- obesity
- insulin resistance
- metabolic syndrome
- atherosclerosis
- CVD
- depression/ stress
is SJS or TEN worse
TEN
SJS/ TEN
- severe mucocutaneous reaction
- usually triggered by drugs
- extensive necrosis and detachment of epidermis
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
acne vulgaris
- most common cutaneous disorder of adolescents and young adults
- disease of pilosebaceous follicles
what is the precursor lesion of acne
microcomedos
whitehead
- accumulation of sebum and keratinous material
- closed comedo
blackhead
- follicular surface is opened with continuous distension
- open comedo
- color due to densely packed keratinocytes, oxidized lipids and melanin
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
rosacea
- acneform lesion
- common chronic inflammatory skin disorder
- variety of clinical manifestations localized to central face
subtypes of rosacea
- erythematotelangiectatic
- papulopustular
- phymatous
- ocular
risk factors for rosacea
- genetic predisposition
- abnormalities in immunity - innate and adaptive
melanocyte nevus
- benign proliferation of nevus cells
- cluster as nests within lower epidermis or dermis
- congenital or acquired
junctional nevi
nests that are at the dermal- epidermal junction
compound nevi
nests that are at the dermal-epidermal junction and in the dermis
intradermal nevi
nests in the dermis
predisposing factors for melanocyte nevi
- heredity
- germline polymorphisms- IRF4 and TERT
- degree of sun exposure as a child
- phenotypic characteristics like skin
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
eclipse nevus
- compound nevus on scalp of children
- tan center and brown
- benign
congenital melanocyte nevi
- benign proliferation of melanocytes that arise during embryogenesis
- cell proliferation via MAPK
complications of congenital melanocyte nevi
- melanoma after puberty
- many melanomas arising with large CMN have earlier onset and deeper origin
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
melanoma
- most serious form of skin cancer
- aggressive, may spread in unpredictable manner to involve an organ in body
melanocyte biology
- developmnet regulated by MITF
- MSH stimulates the melanocortin 1 receptor (MC1R)
- induction of MC1R activates expression of MiTF -> melanin pigments
UV exposure and melanoma
- keratinocyte DNA damage -> p53 mediated induction and POMC expression
- secretion of MSH and stimulation of MC1R
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
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
warning signs of melanoma
- A- asymmetry
- B- border
- C- color
- D- diameter
- E- evolving
basal cell carcinoma (BCC)
- common skin cancer in basal layer of epidermis
- “epithelioma”
- low metastatic potential
risk factors for BCC
- sun exposure, especially in childhood
- intermittent intense increments of sun exposure increases risk
- tanning beds
- ionizing radiation
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
cutaneous squamous cell carcinoma (cSCC)
- arises from malignant proliferation of epidermal keratinocytes
- second most common type of skin cancer
risk factors for cSCC
- UVB exposure -> p53 mutation
- UVA exposure increases risk for cSCC and BCC
- ionizing radiation
- immunosuppression
cSCC pathophysiology
- malignant transformation of epidermal keratinocytes
- UV induced mutations in p53
- mutation of RAS pathway
impetigo
- contagious superficial bacterial infection
- most common in kids 2-5
- due to s. aureus, beta-hemolytic streptococci
risk factors for impetigo
- crowding
- poor hygiene
- underlying scabies
classifications of skin lesions in impetigo
- non-bullous (most common)
- bullous
- ecthyma
non- bullous impetigo
- lesions begin as papules, progress to vesicles
- surrounded by erythema
- rapidly form crust with golden appearance
bullous impetigo
- strains of s. aureus produce exfoliative toxin A
- loss fo cell adhesion into epidermis
ecthyma
- ulcerative form
- extends into dermis
- consists of punched out ulcers covered with yellow crust
acanthosis nigricans
- velvety, hyperpigmented plaques on neck and axillae
- associated with obesity and diabetes
pathophysiology of acanthosis nigricans
mutations in IGFR1, FGFR, EGFR
vitiligo
- acquired pigmentary disorder
- most frequent cause of depigmentation worldwide
- dev white macules due to loss of functioning melanocytes
- autoimmune response against melanocytes
koebner phenomenon
- repeated mechanical trauma and other types of physical trauma causes discoloration of skin
- associated with vitiligo
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