Adnexal structures

Question 1

What are the three types of pilosebaceous units?

Answer 1

1. lanugo (fetal)
2. vellus (fine)
3. terminal (coarse, often darker).

Question 2

What is a pilosebaceous unit?

Answer 2

• 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

Question 3

What are sebaceous glands? Where are they most dense?

Answer 3

Produce sebum “oil” (triglycerides, free FAs, squalene, wax/sterol esters, and free sterols)

Greatest density on face and scalp (but located everywhere!)

Question 4

How do sebaceous glands release secretions? When are they most active?

Answer 4

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

Question 5

What are the steps of the hair cycle?

Answer 5

1. Growth phase (anagen) **majority of hair on scalp in anagen, duration dictates hair length
2. Transition phase (catagen)
3. Resting phase (telogen); hair shed

Question 6

Describe telogen effluvium

Answer 6

• 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

Question 7

Describe alopecia areata

Answer 7

• 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)

Question 8

Contrast eccrine and apocrine sweat glands

Answer 8

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

Question 9

Describe Anagen effluvium

Answer 9

• Hair loss that is the result of medications (e.g. chemotherapy)
• 2-3 weeks after drug administration
• Hair regrows after the medication is stopped

Question 10

How can you differentiate eccrine and apocrine glands in histology?

Answer 10

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

Question 11

Define hyperhidrosis and anhidrosis

Answer 11

hyperhidrosis; overactivity of sweat glands

anhidrosis/hypohydrosis; when sweat glands are absent/reduced (e.g. ectodermal dysplasia)

Question 12

Describe acne vulgaris

Answer 12

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)

Question 13

What are comedones?

Answer 13

the characteristic lesions in non-inflammatory acne

• closed (small skin-colored papules; whiteheads)
• open (dilated follicular opening; blackheads)

Question 14

Describe inflammatory acne

Answer 14

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

Question 15

What are the treatments for acne?

Answer 15

• 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”

Question 16

How does puberty make acne worse?

Answer 16

Androgens (testosterone/DHT) stimulate sebum production and hyperproliferation of follicular kertainocytes

Question 17

Describe Propionibacterium acnes

Answer 17

“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

Question 18

What is the MOA of systemic antibiotics for acne? What are some side effects?

Answer 18

**Tetracyclines (tetracycline, doxycycline, minocycline)

• Inhibit P. acnes
• Antiinflammatory (decrease proinflammatory mediators)

SE:

• doxycycline= pill esophagitis, photosensitivity
• minocycline= drug hypersensitivity syndrome, drug induced lubus, hepatits

Question 19

What is the MOA of oral contraceptives for acne? What are some side effects?

Answer 19

• 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

Question 20

What is isotretinoin? When is it indicated?

Answer 20

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)

Question 21

Describe tinea versicolor

Answer 21

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