Adnexal Structures Flashcards

1
Q

3 types of pilosebaceous units?

A

lanugo (fetal), vellus (fine), terminal (coarse, often darker)

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

pilosebaceous unit consists of?

A

a hair follicle and its associated sebaceous gland

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

The hair follicle consists of?

A

3 longitudinal segments: the hair bulb (inferior segment), the isthmus (middle segment) which extends from the point of insertion of the arrector pili muscle to the sebaceous gland), and the infundibulum (upper segment) refers to the portion from the skin surface to the sebaceous gland.

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

Sebaceous glands found where?

A

in greatest density on the face and scalp, but are found everywhere except palms and soles. The chest and back also have a high density of sebaceous glands. With the exception of a few distinct locations (vermilion lips, orogenital mucosae, areolae, and eyelids), sebaceous glands are always associated with hair follicles.

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

Sebaceous glands produce what?

A

sebum. composed of triglycerides, free fatty acids, squalene, wax and sterol esters, and free sterols. Secretion is holocrine (sebocytes disintegrate and release their sebum as they migrate toward the duct.) Flow of sebum is continuous, but variable among individuals.

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

factors affecting sebum production?

A

Androgen production at puberty, especially 5α-dihydrotestosterone (DHT), stimulates the sebaceous gland and increases sebum production. major contributor to the development of acne. Sebum production remains constant after puberty until menopause in women or until the 6th or 7th decade in men

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

microorganisms that can be present in hair?

A

Malassezia spp., Staphylococcus epidermidis, and Propionibacterium spp., Demodex folliculorum, the hair follicle mite. inhabit the hair follicles in sebaceous-rich sites.

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

hair follicle cycle?

A

3 stages. majority in the growth phase with the rest in the resting phase. length of the growth phase varies by site, longest duration on the scalp where hair grows the longest. Hairs shed after they have transitioned to the resting phase at which point the cycle begins again. 100-200 hairs shed each day. Each follicle cycles independently, fairly uniform density of hair

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

3 phases of hair cycle?

A

anagen (growth, 2-6 yrs), catagen (regression, 2-3 weeks), telogen (resting, 3 mo)

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

what is telogen effluvium?

A

occurs when a greater proportion of hair follicles enter telogen phase simultaneously as the result of a stressor (pregnancy, fever, surgery, illness, malnutrition)

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

clinical manifestation of telogen effluvium?

A

increase in hairs being shed approximately 3 months (duration of the telogen phase) after the event. Hair loss slowly abates, and hairs return to a more normal distribution of phases.

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

telogen effluvium in neonates?

A

In neonates, a greater proportion of hair follicles are present in telogen phase resulting in shedding or hair loss a few months after birth. This has been referred to as telogen effluvium of the newborn

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

what is alopecia areata?

A

autoimmune condition characterized by the sudden development of round, smooth patches of hair loss (alopecia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

possible outcomes of alopecial areata?

A

Progression to large areas of hair loss can occur to the point of complete hair loss on the scalp (alopecia totalis) or the entire body (alopecia universalis). Spontaneous regrowth of hair can also be seen. nail changes including pitting.

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

how can you differentiate alopecia areata from tinea capitis?

A

lack of erythema, scaling, or pustules

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

treatment for alopecia areata?

A

Treatment includes topical corticosteroids and intralesional corticosteroids most commonly. Chronic use of systemic immunosuppressants not commonly employed d/t associated risks.

17
Q

what is Anagen effluvium? course?

A

hair loss that is the result of medications, such as chemotherapy. This typically develops 2-3 weeks after drug administration. Hair regrows after the medication is stopped.

18
Q

what are the major sweat glands in humans?

A

eccrine and apocrine glands. They vary in type and density, depending on anatomic location.

19
Q

eccrine sweat glands activity/innervation?

A

active from birth. Innervation is provided by postganglionic sympathetic fibers which are controlled by the hypothalamic sweat center. In contrast to other sympathetic fibers, acetylcholine (not norepinephrine) is the principal neurotransmitter.

20
Q

the eccrine secretory unit is composed of?

A

coiled secretory portion in the lower dermis and subcutaneous tissue. This drains into a long thin duct with an apical portion (acrosyringium) that opens directly onto the skin surface.

21
Q

2 cell types within single cell layer in secretory coils?

A

1) large clear cells responsible for the gland’s secretion of electrolytes and water
2) dark cells, of unknown function, thought to produce sialomucin.
Myoepithelial cells surrounding these cells are thought to enhance delivery of sweat to the skin surface

22
Q

Continuous secretion of sweat provides what 3 major functions for the body?

A

1) thermoregulation via evaporative heat loss
2) maintenance of electrolyte balance
3) maintenance of a moist stratum corneum to facilitate tactile skills and pliability of the palms and soles.

23
Q

where are apocrine sweat glands found?

A

localized to specific anatomic sites (axillae, anogenital region, periumbilical region, areolae, nipples, vermilion border of the lip)

24
Q

Modified apocrine glands are found where?

A

external auditory canals (ceruminous glands) and eyelid margins (glands of Moll). These glands secrete oily, viscous, odorless fluid that is rich in precursors of odoriferous substances. bacteria degradation (on skin) results in BO

25
Q

what causes increased secretion?

A

response to local or systemic catecholamines and cholinergic agonists, but mechanisms involved in physiologic secretion are poorly understood. Enlargement of the glands occurs with puberty likely due to androgenic stimulation.

26
Q

apocrine gland anatomy?

A

larger than eccrine glands. consist of a secretory portion and a duct that opens into the upper portion of the hair follicle. secretory unit is composed of a single layer of columnar epithelial cells surrounded by myoepithelial cells. duct is composed of a double layer of cuboidal cells, as well as myoepithelial cells

27
Q

acne vulgaris develops why, initially?

A

result of an increase in sebum production (under hormonal influences) in combination with increased production and impaired shedding of the corneocytes lining the upper portion of the hair follicle leading to plugging of the hair follicles (comedo formation). plugged follicles may rupture, inflammatory response to extruded keratin and sebum

28
Q

what bacteria plays a role in acne pathogenesis?

A

Propionibacterium acnes, a Gram- positive non-motile rod, found deep within the follicle, also plays an important role. P. acnes releases enzymes that promote follicular rupture and stimulates release of proinflammatory mediators leading to neutrophil recruitment and Th1 responses.

29
Q

what is the non-inflammatory acne?

A

Comedones are characteristic lesions in non-inflammatory acne, and may be closed (whiteheads) or open (blackheads). Comedones are typically small skin-colored papules (closed), which may have a dilated follicular opening (open).

30
Q

what is inflammatory acne?

A

Inflammatory acne presents with comedones, but type of inflammatory lesions vary dependent on the type of inflammatory response: pustules develope as the result of a neutrophil predominant response; inflammatory papules, nodules and cysts develope from a mixed inflammatory response (lymphocytes, giant cells, and neutrophils)

31
Q

treatment of acne?

A

topical retinoids. topical anti-inflammatory agents. systemic agents like abx, contraceptives, isotretinoin

32
Q

what do topical retinoids target? how?

A

target comedone. mech: normalization of follicular keratinization, expulsion of existing keratinaceous follicular plugs and prevention of formation of new lesions

33
Q

what are topical anti-inflammatory agents? work how?

A

benzoyl peroxide (BPO) and topical antibiotics (clindamycin, erythromycin). These agents have both anti-bacterial activity against P. acnes as well as anti-inflammatory properties. often used together

34
Q

what are systemic agents used to treat acne?

A

oral antibiotics, oral contraceptives, and isotretinoin. Oral antibiotics most commonly include doxycycline and minocycline,

35
Q

pathogenesis of rosacea?

A

multifactorial, but is related to vascular hyperreactivity. Patient present with a history of easy blushing, and over time develop a reddened complexion.

36
Q

additional rosacea features? how different from acne vulgaris?

A

papules and pustules, telangiectasia, and phymatous change in which overgrowth of sebaceous glands can be seen resulting in the skin appearing swollen or bumpy. The lack of comedones helps to differentiate this from acne vulgaris.

37
Q

rosacea treatment?

A

overlaps with that for acne, but topical metronidazole and sodium sulfacetamide are more commonly used. more easily irritated, and their tolerance of topical therapy (like retinoids, BP) may be limited. Systemic agents include antibiotics such as doxycycline, minocycline, and erythromycin.