Adnexal structures Flashcards

1
Q

What are the three types of pilosebaceous units?

A
  1. lanugo (fetal)
  2. vellus (fine)
  3. terminal (coarse, often darker).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a pilosebaceous unit?

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are sebaceous glands? Where are they most dense?

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the steps of the hair cycle?

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe telogen effluvium

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe alopecia areata

A
  • 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Contrast eccrine and apocrine sweat glands

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe Anagen effluvium

A
  • 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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can you differentiate eccrine and apocrine glands in histology?

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define hyperhidrosis and anhidrosis

A

hyperhidrosis; overactivity of sweat glands

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe acne vulgaris

A

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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are comedones?

A

the characteristic lesions in non-inflammatory acne

  • closed (small skin-colored papules; whiteheads)
  • open (dilated follicular opening; blackheads)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe inflammatory acne

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the treatments for acne?

A
  • 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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does puberty make acne worse?

A

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

17
Q

Describe Propionibacterium acnes

A

“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
18
Q

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

A

**Tetracyclines (tetracycline, doxycycline, minocycline)

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

SE:

  • doxycycline= pill esophagitis, photosensitivity
  • minocycline= drug hypersensitivity syndrome, drug induced lubus, hepatits
19
Q

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

A
  • 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

20
Q

What is isotretinoin? When is it indicated?

A

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)

21
Q

Describe tinea versicolor

A

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