Exam IV Skin Flashcards
The three layers of the skin
The Epidermis provides a waterproof barrier and creates the skin tone
The Dermis contains tough connective tissue, hair follicles, and sweat glands
The Hypodermis is made of fat and connective tissue
Primary Skin Lesions: Macule and Patch
Macule:
A flat circumscribed area that is a change in color of skin; less than 1 cm in diameter
Examples” Freckles, flat moles (nevi), petechiae, measles, scarlet fever
Patch:
Bigger Macule
Example: Vitiligo
Primary Skin Lesions: Papule and Nodule
Papule:
An elevated, firm, circumscribed area less than 1 cm in diameter
Examples” Wart, elevated moles, lichen planus, fibroma, insect bite
Nodule:
A bigger version of a papule
Example: lipomas
Primary Skin Lesions: Plaque and Wheal
Plaque:
Elevated, firm. and rough lesion with flat top surface greater than 1 cm in diameter
Example: Psoriasis, seborrheic and actinic keratoses
Wheal:
Elevated, irregular-shaped area of cutaneous edema; solid, transient; variable diameter
Examples: Insect bites, urticaria, allergic reaction
Primary Skin Lesions: Vesicle and Bulla
Vesicle:
Elevated, circumscribed, superficial; does not extend into dermis; filled with serous fluid; less than 1 cm in diameter
Examples: Varicella (chicken pox), herpes zoster (shingles), herpes simplex
Bulla:
A bigger Vesicle
Examples: Blister, pemphigus vulgaris
Primary Skin Lesions: Pustule and Cyst
Pustule:
Elevated, superficial lesion; similar to a vesicle, but filled with purulent fluid
Example: Impetigo, acne
Cyst:
Elevated, circumscribed, encapsulated lesion; in dermis or subcutaneous layer; filled with fluid or semisolid material
Example: Sebaceous Cyst, cystic acne
Primary Skin Lesions: Telangiectasia and Tumor
Telangiectasia :
Fine (0.5-1 mm), irregular, red lines produced by capillary dilation; can be associated with acne rosacea (face), venous HTN (spider veins in legs), systemic sclerosis, or developmental abnormalities (port wine birthmarks)
Example: Telangiectasia in rosecea
Tumor:
Elevated, solid lesion; may be clearly demarcated; deeper in dermis; more than 2 cm in diameter
Example: Neoplasms, benign tumor, lipoma, neurofibroma, hemangioma
Scale
Heaped-up. keratinized cells; flaky skin; irregular-shape; thick or thin; dry or oily; variations in size.
Ex. Think flaking skin
Lichenification
Rough THickened epidermis secondary to persistant rubbing, itching, or skin irritation; often involves flexor surface extremity.
Ex - Chronic dermatitis
Excoriation
Loss of epidermis; linear, hollowed out crusted area
Ex - Abrasion/scratch/scabies
Fissure
Linear crack or break
ex - athletes foot, anal fissure
Erosion
Loss of a part of the epidermis
ex - think remains after a ruptured blister
Ulcer
Loss of epidermis and dermis; concave; varies in size.
ex - larger version of eroision / pressure ulcer
Steven-Johnson Syndrome/Toxic Epidermal Necrolysis
Severe mucocutaneous reactions to certain drugs (oral, ocular, genital) –> keratinocyte necrosis
- apoptotic pathway
- drug-specific CD8+ cytotoxic T cells release perforin, granzyme B and granulysin to kill keratinocytes
Psoriasis
Autoimmune inflammatory, a hyperproliferative state of epidermal cells
Most common clinical presentation: erythematous plaques with silver scale
Pre-psoriasis skin:
- dendritic cells, T cells
- Differentiation of T cells is stimulated by IL-23
Psoriasis skin:
- activated dendritic cells mainly produce TNFα
- The clinical success of TNF-blocking agents is therefore not surprising
Acne Vulgaris
- disease of pilosebaceous follicles
- Follicular hyperkeratinization
- Increased sebum production
- Cutibacterium (formerly known P. acnes) within the follicle
- Inflammation
- microcomedo (a precursor) might lead to closed comedos by accumulation of sebum and keratinous material
- Androgens stimulates the growth and secretory function of sebaceous glands
- all women with the combination of acne and oligomenorrhea should be evaluated for PCOS
Rosacea
- chronic inflammatory skin condition
Four main clinical manifestations:
- Erythematotelangiectatic
- Papulopustular
- Phymatous
- Ocular
Pathogenesis:
- Immune dysfunction
- Ultraviolet radiation
- Vascular hyperreactivity
Melanocytic Nevus
benign proliferations of a type of melanocyte known as a “nevus cell” that cluster as nests
- types:
congenital (CMN)
acquired types:
common (not mentioned in the lecture)
atypical - terminology of acquired nevi:
junctional
intradermal
compound
Congenital Melanocytic Nevi
Pathogenesis:
- Cellular proliferation by mitogen-activated protein kinase (MAPK)
Clinical Features:
- Present at birth or within the first few months of life
Atypical Acquired Nevi
- nevi with an architectural disorder such as eclipse nevus
- Benign acquired melanocytic nevi that share, to a lesser extent, some of the clinical features of melanoma
Melanoma
- The mitogen activated protein kinase (MAPK) pathway is activated in almost all melanomas (much more than in CMN).
Clinical Features:
BRAF inhibitors -> tumor regression and prolonged overall survival
- UV causes p53 mutation & POMC increased expression -> secretion of MSH -> stimulation of MC1R -> expression of MITF
- growth phases of melanoma melanocytic nevus pathogenesis): benign nevus -> atypical nevus -> radial/horizontal growth phase (curable by excision) -> vertical growth phase (have metastatic potential) -> melanoma
Basal Cell Carcinoma (BCC)
- cancer in Basel layer of epidermis
- called epithelioma
Pathogenesis:
- UV-induced inflammation
- PTCH1 gene
- UVB: intense & intermittent (sunburn/childhood exposure) –> BCC & melanoma
Cutaneous Squamous Cell Carcinoma (cSCC)
- malignant proliferation of keratinocytes
Pathophysiology:
- UV-induced mutations in the p53 gene
- Mutation of RAS pathway
UVB exposure: cumulative/occupational –> cSCC
Impetigo
- contagious S. aureus infection
Clinical Features:
- Non-bullous impetigo:
- Lesions begin as papules -> vesicles surrounded by erythema -> thick crusts with a golden appearance
