Adnaxial Structures Flashcards
What is the divisions of the hair follicle?
Infindibulum - Opening to connection to sebaceous gland
Isthmus - Sebaceous gland down to erector pillae muscle
Inferior segment - Remainder, includes hair bulb and matrix
Classes of pilosebaceous unit
Laguno (fetal)
Vellus (fine)
Terminal (coarse)
Conditions which may be heralded by abnormal presence of hair types:
Anorexia - Lanugo
Hirsutism - Terminal (Females with male pattern hair, indicating androgen excess/polycystic ovarian syndrome PCOS)
Sebaceous glands (Where, what how when)
Where - Greatest density on face and scalp but everywhere
What - Produce sebum: TriGly, Free FA, Squalene, Wax/Sterol esters, Free sterols
How - Holocrine secretion
When - Active at birth, but decreaes during infancy. Sebum production stimulated by androgen production (5-alpha dihydrotestosterone) in puberty
Hair cycle
Growth phase (Anagen) - Majority of hair on scalp is in anagen, duration corresponds to hair length, deepest hair bulbs (in dermis) Transition phase (Catagen) - Hair migrates up towards epidermis, degeneration of roots Resting phase (Telogen) - Hair shed during this phase, rest in phase for 3-5 months
Telogen effulvium
Stressor results (i.e. childbirth, febrile illness in children) in greater proportion of hair follicles entering telogen phase Results in increase amount of hair being shed Occurs approx. 3 mos after event, slowly returns to normal Patient doesn't look bald, but can detect difference in hair thickness
Alopecia Areta
Autoimmune condition
Smooth patches of complete alopecia develop
Nail pits (indentations in the nail plate) can also be assoc.
Tx: Topical cortical steroids
Sweat gland types, location, communication to surface
Eccrine (Sweaty) - Palms and soles, Innervated by sympathetic fibers via ACh
Directly communicate to surface
Apocrine (Sweaty and smelly) - Axillae, Anogenital, Periumbilical
Part of hair follicle unit
Disorders of sweat glands
Hyperhidrosis
Ani/hypohidrosis - Occur when sweat glands are absent/reduced, e.g. ectodermal dysplasia
Acne development factors
Sebaceous cells: Sebum, Fatty Acids
Follicular keratinocytes: Hyperproliferation, keratohaline granules increase, disturbed desquamation
P. acnes: Immune reaction
Androgens increase sebum production and hyperproliferation
Propionibacterium acnes - Type and activity
Anaerobic Gram + Rod
Dependent on glycerol, hydrolyzes sebum triglycerides
Produces - Porphyrins, proinflammatory mediators, lipases
Inflammatory action
Acne treatment (Topical)
Retinoids - Counter follicular keratinocyte hyperproliferation, some action against P. acnes immune reactions
Benzoyl peroxide - Anti-P. acnes, also reduce fatty acids
Antibiotics - Anti-P. acnes, anti-inflammatory
Systemic treatment for Acne
Antibioitcs
Oral Contraceptives
Isotretinoin
Often used for patients which have trunk involvement
Antibiotic specifics
Tetracyclines: Tet, Dox, Mino
Mechanism - Inhibition of P. acnes, anti-inflammatory (decreases proinflammatory mediators)
Side effects - Dox - Pill esophagitis, photosensitivty
Mino - Drug hypersensitivity syndrome, drug induced lupus, hepatitis
Erythromycin
Bactrim
Penicillins
Oral contraceptive specifics
Mechanism: Block production of androgens (adrenal and ovarian)
Types of acne: Inflammatory papules/pustules, peri-menstrual flare
Side effects: Nausea, vomiting, abnormal menses, weight gain, breast tenderness, thrombophlebitis, HTN
