Adnexal structures Flashcards
What are the three types of pilosebaceous units?
- lanugo (fetal)
- vellus (fine)
- terminal (coarse, often darker).
What is a pilosebaceous unit?
- hair follicle
- hair bulb (inferior segment)
- isthmus (middle segment) point of insertion of the arrector pili muscle to the sebaceous gland
- infundibulum (upper segment) skin surface to the sebaceous gland
- associated sebaceous gland
**Mitotically active undifferentiated cells in the matrix of the hair bulb
What are sebaceous glands? Where are they most dense?
Produce sebum “oil” (triglycerides, free FAs, squalene, wax/sterol esters, and free sterols)
Greatest density on face and scalp (but located everywhere!)
How do sebaceous glands release secretions? When are they most active?
Holocrine secretion; “explosive” secretion that also releases part of the cells cytoplasm
**Active at birth but decreased during infancy. Sebum again stimulated by androgen production (5 alpha dihydrotestosterone) in puberty
What are the steps of the hair cycle?
- Growth phase (anagen) **majority of hair on scalp in anagen, duration dictates hair length
- Transition phase (catagen)
- Resting phase (telogen); hair shed
Describe telogen effluvium
- stressor results in greater proportion of hair follicles entering telogen phase (e.g. pregnancy, broken bone, severe psychosocial stress)
- results in increased amount of hair being shed (observe club hairs) **thinning, NO discrete patches of alopecia
- occurs ~3 months after event and slowly returns to normal
- Secondary changes (scaling, erythema) not common
Describe alopecia areata
- autoimmune condition
- smooth patches of complete alopecia develop (variable in size, tends to be focal)
- nail pits (indentations in the nail plate) may be seen
- secondary changes (crusting, erythema) not common
- topical corticosteroids are mainstay of treatment
(Often asymptomatic)
Contrast eccrine and apocrine sweat glands
Eccrine
- “sweaty”
- everywhere but a lot in palms and soles
- secretions directly to skin surface
- innervated by sympathetic fibers via acetylcholine
Apocrine
- “sweaty and smelly”
- axillae, anogenital, periumbilical, areolae, vermilion border of lips
- secretions into hair follicle
Describe Anagen effluvium
- Hair loss that is the result of medications (e.g. chemotherapy)
- 2-3 weeks after drug administration
- Hair regrows after the medication is stopped
How can you differentiate eccrine and apocrine glands in histology?
Eccrine
- coiled secretory portion in the lower dermis/subcutaneous tissue **opens directly onto the skin surface
- ductal epithelium composed of 2 or more layers of cuboidal cells
Apocrine
- larger than eccrine glands
- secretory portion (single layer of columnar epithelial cells surrounded by myoepithelial cells) in the deep dermis/subcutaneous fat
- duct (double layer of cuboidal cells, as well as myoepithelial cells) opens into the upper portion of the hair follicle
Define hyperhidrosis and anhidrosis
hyperhidrosis; overactivity of sweat glands
anhidrosis/hypohydrosis; when sweat glands are absent/reduced (e.g. ectodermal dysplasia)
Describe acne vulgaris
Primary lesions= papules, pustules, nodules, cysts
- peaks in adolescence (though persistence into adulthood is not uncommon)
- closed/open comedo formation (sebum accumulates and follicle enlarges)
- Propionibacterium acnes (bacteria deep in follicle)
What are comedones?
the characteristic lesions in non-inflammatory acne
- closed (small skin-colored papules; whiteheads)
- open (dilated follicular opening; blackheads)
Describe inflammatory acne
Still presents with comedones, but the type of inflammatory lesions vary dependent on the type of inflammatory response;
- pustules (from neutrophil predominant response)
- inflammatory papules, nodules and cysts (from a mixed inflammatory response; lymphocytes, giant cells, and neutrophils)
**more commonly causes scarring than non-inflammatory
What are the treatments for acne?
- Drying:
- Topical retinoids (tretinoin, adapalene, and tazarotene) target the comedone
- Systemic retinoids (Isotretinoin and acitretin)
- Anti-inflammatory (also target P. acnes):
- benzoyl peroxide (BPO) breaks down FAs
- topical antibiotics (clindamycin)
- Systemic:
- oral antibiotics (First line tetracyclines… also use erythromycin, bactrim, and penicillins)
- oral contraceptives
- isotretinoin “Accutane”
How does puberty make acne worse?
Androgens (testosterone/DHT) stimulate sebum production and hyperproliferation of follicular kertainocytes
Describe Propionibacterium acnes
“P. acnes”
- Gram-positive anaerobic rod
- Dependent on glycerol (hydrolysis of sebum triglycerides)
- Produces porphyrins and lypases
- Produces proinflammatory mediators -> neutrophil recruitment and Th1 responses
What is the MOA of systemic antibiotics for acne? What are some side effects?
**Tetracyclines (tetracycline, doxycycline, minocycline)
- Inhibit P. acnes
- Antiinflammatory (decrease proinflammatory mediators)
SE:
- doxycycline= pill esophagitis, photosensitivity
- minocycline= drug hypersensitivity syndrome, drug induced lubus, hepatits
What is the MOA of oral contraceptives for acne? What are some side effects?
- Block production of androgens (adrenal and ovarian)
- Increase sex hormone binding globulin= decreased free testosterone
**Good for inflammatory papules/pustules, peri-menstrual flare
SE: N/V, abnormal menses, weight gain, breast tenderness, thrombophlebitis, hypertension
What is isotretinoin? When is it indicated?
A systemic retinoid, indcated with:
- severe nodulocystic acne
- scarring
- severe acne recalcitrant to systemic antibiotic therapy and topicals
**Want cumulative dose 120-150 mg/kg (1mg/kg/day BID x 5 months)
Describe tinea versicolor
Primary lesions= macules, patches
Secondary lesions= color (hyper/hypo), scale
- Malassezia globosa/furfur (commensal yeast)
- Oval to round scaly patches with fine overlying scale
- Hyperpigmented or hypopigmented
