Mss 09: Adnexal Structures And Associated Disorders

Front 1

How many hair follicles does the average human have?

Back 1

5 million

Front 2

When is hair density the greatest? What happens to it throughout the lifetime?

Back 2

Greatest hair density at birth, decreases throughout life

Front 3

What are the three types of Pilosebaceous units?

Back 3

- LANUGO (fetal) - shed in utero or during first weeks of life
- VELLUS (fine) - may change to terminal hairs after puberty d/t androgens
- TERMINAL (coarse, often darker) - found on scalp, eyelashes, eyebrows, and later in beard, armpits, and pubic area)

Front 4

What conditions may lead to abnormal presences of hair types?

Back 4

- Anorexia - presence of lanugo (fetal hair)
- Hirsutism - presence of more terminal hairs (in females in male pattern of distribution - androgen excess or polycystic ovarian syndrome)

Front 5

What are the components of the Pilosebaceous unit?

Back 5

Hair follicle and associated sebaceous gland

Front 6

What are the components of the hair follicle?

Back 6

- HAIR BULB (inferior segment)
- ISTHMUS (middle segment) - extends from point of insertion of arrector pili muscle to sebaceous gland
- INFUNDIBULUM (upper segment) - portion from skin surface to sebaceous gland

Front 7

What does the hair shaft grow from?

Back 7

Mitotically active undifferentiated cells of matrix portion of hair bulb

Front 8

Where are sebaceous glands in the greatest density?

Back 8

- Face and scalp (but everywhere, also a lot on chest and back)
- Associated w/ hair follicles (exception: vermilion lips, orogenital mucosa, areolae, and eyelids)

Front 9

What is the purpose of Sebaceous Glands?

Back 9

- Produce sebum (oil) via HOLOCRINE secretion

Front 10

What are the contents of sebum?

Back 10

- Triglycerides
- Free FA
- Squalene
- Wax
- Sterol esters
- Free sterols

Front 11

What does Holocrine secretion refer to?

Back 11

- Secretion of sebum from sebaceous glands
- Sebocytes disintegrate and release sebum as they migrate toward duct
- Flow is continuous but variable

Front 12

When are sebaceous glands active?

Back 12

- Birth d/t maternal hormones
- Decreases during infancy
- Increased during puberty d/t stimulation by androgens (especially DHT)
- Remains constant after puberty until menopause and 6th/7th decade in men

Front 13

What hormone during puberty stimulates sebum production? Implications?

Back 13

DHT (5-alpha-dihydro-testosterone) --> acne

Front 14

What microorganisms are present in hair follicles?

Back 14

- Malassezia species
- Staphylococcus epidermidis
- Propionibacterium species
- Demodex folliculorum, hair follicle mite

Front 15

What are the phases of the hair cycle?

Back 15

1. Growth phase (ANAGEN)
2. Transition phase (CATAGEN)
3. Resting phase (TELOGEN)

Front 16

What happens during the first phase of the hair cycle?

Back 16

Growth Phase (ANAGEN)
- Majority of hair on scalp is in anagen (85% of scalp)
- Duration corresponds to hair length (2-6 years)

Front 17

What happens during the second phase of the hair cycle, after the growth phase (anagen)?

Back 17

Transition Phase (CATAGEN)
- Regression
- 2-3 weeks
- <1% of follicles on scalp

Front 18

What happens during the third phase of the hair cycle, after the transition phase (catagen)?

Back 18

Resting phase (TELOGEN)
- Hair shed during this phase (about 100-200 hairs)
- 3 months
- 10-15% of hair on scalp

Front 19

What are the disorders of hair?

Back 19

- Telogen Effluvium
- Alopecia Areata
- Anagen Effluvium

Front 20

What causes Telogen Effluvium?

Back 20

Greater proportion of hair follicles enter telogen phase simultaneously d/t stressor (pregnancy, fever, surgery, illness, malnutrition)

Front 21

What are the clinical characteristics of Telogen Effluvium?

Back 21

- Increased amount of hair being shed approx. 3 months after event
- Hair loss slowly abates, and hair returns to more normal distribution
- In neonate, greater amount of hair follicles are in telogen phase causing hair loss a few months after birth

Front 22

What causes Alopecia Areata?

Back 22

- Autoimmune

Front 23

What are the clinical characteristics of Alopecia Areata?

Back 23

- Smooth patches of complete alopecia (hair loss)
- Nail pits (indentations in nail plate), rough texture, or brittle nature
- Unpredictable course
- Can progress to alopecia totalis (entire scalp) or alopecia universalis (entire body)
- Spontaneous regrowth can occur

Front 24

How do you treat Alopecia Areata?

Back 24

Topical corticosteroids (autoimmune disease)

Front 25

How can you distinguish Alopecia Areata from Tinea Capitis?

Back 25

Alopecia Areata does not have erythema, scaling, or pustules

Front 26

What is the cause of Anagen Effluvium?

Back 26

Medications, such as chemotherapy (2-3 weeks after administration)

Front 27

What happens in Anagen Effluvium?

Back 27

- Hair loss d/t meds (chemo) - 2-3 weeks after administration
- Hair regrows after medication is stopped

Front 28

What are the major sweat glands in humans?

Back 28

- Eccrine glands
- Apocrine glands

Front 29

Where are eccrine glands found? Characteristics? How are they stimulated?

Back 29

- Everywhere, but especially palms and soles
- Sweat only (no smell)
- Innervated by sympathetic fibers via ACh (not NE)
- Active from birth

Front 30

What are the components of the eccrine secretory unit?

Back 30

- Coiled secretory portion in lower dermis and subcutaneous tissue
- Drains into long thin duct w/ apical portion (Acrosyringium) open directly onto skin surface
- Secretory coils contain 2 cell types interspersed w/in single cell layer (large clear cells that secrete electrolytes and water and dark cells of unknown function that may produce sialomucin)
- Myoepithelial cells enhance delivery of sweat to skin
- Ductal epithelium made of 2+ layers of cuboidal cells

Front 31

What are the characteristics of the sweat from an eccrine sweat gland?

Back 31

- Depends on emotional and environmental stimuli
- Near isotonic primary sweat released from secretory coil w/ partial reabsorption of NaCl by duct cells
--> HYPOTONIC Fluid to skin surface

Front 32

Continuous secretion of sweat from Eccrine Glands provides what functions?

Back 32

1) Thermoregulation via evaporative heat loss
2) Maintenance of electrolyte balance
3) Maintenance of moist stratum corneum to facilitate tactile skills and pliability of palms and soles

Front 33

Where are apocrine glands found? Characteristics? How are they stimulated?

Back 33

- Axillae, anogenital area, periumbilical, areolae, vermilion border of lips
- Modified versions in external auditory canals (ceruminous glands) and eyelid margins (glands of Moll)
- Sweaty and smelly

Front 34

Secretion of sweat from Apocrine Glands provides what functions?

Back 34

Function is unclear

Front 35

What causes the apocrine gland sweat to be smelly?

Back 35

- Secrete oily, viscous, odorless fluid that is rich in precursors of odoriferous substances
- Bacteria on skin degrade substances resulting in body odor

Front 36

When does apocrine gland secretion increase?

Back 36

In response to local or systemic catecholamines and cholinergic agonists

Front 37

What are the components of the apocrine secretory unit?

Back 37

- Secretory portion, present in deep dermis and subcutaneous fat
- Duct that opens into upper portion of hair follicle
- Secretory unit composed of a single layer of columnar epithelial cells surrounded by myoepithelial cells
- Duct composed of double layer of cuboidal cells and myoepithelial cells

Front 38

How does the duct opening differ for Eccrine and Apocrine glands?

Back 38

- Eccrine: directly onto skin surface
- Apocrine: upper portion of hair follicle

Front 39

What are the disorders of sweat glands?

Back 39

- Hyperhidrosis
- Anhidrosis / Hypohidrosis (occurs when sweat glands are absent / reduced, eg., ectodermal dysplasia)

Front 40

What are the disorders of the Pilosebaceous Unit?

Back 40

- Acne Vulgaris
- Acne Rosacea
- Tinea Versicolor

Front 41

What is the cause of Acne Vulgaris?

Back 41

- Initially, d/t increased sebum production (d/t hormones) in combination w/ increased production and impaired shedding of corneocytes lining upper hair follicle --> plugging / comedo formation
- Plugged follicle may rupture --> inflammatory response to keratin and sebum
- Propionibacterium acnes (G+, non-motile rod) releases enzymes promoting follicular rupture and stimulates release of pro-inflam. mediators --> neutrophil recruitment and Th1 response

Front 42

What kind of inflammatory response is mediated by P. acnes?

Back 42

- Releases enzymes that promote follicular rupture
- Stimulates release of pro-inflammatory mediators
- Recruits neutrophils
- Th1 response

Front 43

What are comedones?

Back 43

Characteristic lesions in non-inflammatory acne
- Closed = whiteheads
- Open = blackheads
- Small skin-colored papules (closed), which may have dilated follicular opening (open)

Front 44

What happens to the papules in Acne Vulgaris during an inflammatory response?

Back 44

- Leads to Pustules d/t neutrophil response
- Leads to Inflammatory Papules, Nodules, and Cysts d/t mixed inflammatory response (lymphocytes, giant cells, and neutrophils)

Front 45

What kind of acne leads to scarring?

Back 45

Inflammatory acne more commonly leads to scarring

Front 46

What can happen after acne goes away?

Back 46

Leave post-inflammatory hyperpigmentation (persistent discoloration at sites of previous lesions) - can persist for months - not permanent

Front 47

What are some methods of treatment of Acne Vulgaris?

Back 47

- Topical retinoids (tretinoin, adapalene, tazarotene) - target comodone
- Systemic retinoids (isotretinoin and acitretin)
- Benzoyl Peroxide (BPO)
- Topical antibiotics (clindamycin, erythromycin)
- Systemic antibiotics (doxycycline, minocycline)
- Oral contraceptives

Front 48

What is the big picture mechanism of Retinoids?

Back 48

- Comedolytic
- Normalize follicular keratinization
- Expel existing keratinaceous follicular plugs
- Prevent formation of new lesions

Front 49

What is the molecular mechanism of Retinoids?

Back 49

- Derivative of vitamin A
- Enters cell cytoplasm and converted to Retinaldehyde, and then Retinoic Acid
- Binds nuclear receptors called retinoid receptors (2 types)
- Retinoid A receptors (RAR) and Retinoid X receptors (RXR)
- Once RAR and RXR both bound, they heterodimerize
- Heterodimer binds hormone response elements of DNA and acts as transcription factor to promote transcription of target gene

Front 50

What are the actions of Benzoyl Peroxide (BPO) and topical antibiotics (Clindamycin, Erythromycin)?

Back 50

- Anti-bacterial activity against P. acnes as well as anti-inflammatory properties
- Use together to limit development of resistance to topical antibiotics

Front 51

What is the mechanism of action of the systemic antibiotics? Which ones are used for Acne Vulgaris?

Back 51

- Inhibit P. acnes
- Anti-inflammatory (decrease mediators)
- Doxycycline and Minocycline

Front 52

What are the side effects of the oral antibiotics used for Acne Vulgaris?

Back 52

- Doxycycline - pill esophagitis, photosensitivity
- Minocycline - drug hypersensitivity syndrome, drug-induced lupus, hepatitis

Front 53

What is the mechanism of oral contraceptives for Acne Vulgaris?

Back 53

- Blocks production of androgens (Adrenal and Ovarian)
- Works on inflammatory papules / pustules and peri-menstrual flares

Front 54

What are the side effects of Oral Contraceptives?

Back 54

- Nausea / vomiting
- Abnormal menses
- Weight gain
- Breast tenderness
- Thrombophlebitis
- Hypertension

Front 55

When is Isotretinoin (systemic retinoid) indicated?

Back 55

- Severe nodulocystic acne
- Scarring
- Severe acne recalcitrant to systemic antibiotic therapy and topicals (ie. 3-4 month trial of minocycline)

Front 56

What is the dosing of Isotretinoin?

Back 56

- Cumulative dose 120-150 mg/kg
- 1 mg/kg/day divided BID x 5 months

Front 57

What is the cause of Tinea Versicolor?

Back 57

Malassezia species (globosa and furfur)

Front 58

What are the symptoms of Tinea Versicolor?

Back 58

- Oval to round scaly patches w/ fine overlying scale
- Hyperpigmented (brown) or hypopigmented (lighter in color)

Front 59

What is the pathogenesis of Acne Rosacea related to?

Back 59

Multi-factorial, but related to vascular hyperreactivity

Front 60

What is wrong in a patient who has a history of easy blushing?

Back 60

- Acne Rosacea
- Vascular hyperreactivity
- Persistent erythema
- Papules and pustules
- Telangiectasia
- Phymatous change in which overgrowth of sebaceous glands can be seen resulting in skin appearing swollen or bumpy

Front 61

How can you distinguish Acne Vulgaris and Acne Rosacea?

Back 61

Lack of comedones in Rosacea

Front 62

How do you treat Acne Rosacea?

Back 62

- Topical Metronidazole
- Sodium Sulfacetamide
- Easily irritated, so tolerance for topical therapy may be limited
- Systemically: doxycycline, minocycline, and erythromycin