Structure and function of eccrine, apocrine and sebaceous glands Flashcards

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1
Q

Where are Eccrine glands found in greatest density?

What is their morphology?

Cell types?

Present at birth? Innervation?

Associated with hair follicle?

Function/ role?

A

Palms and soles

Long, thin duct with narrow lumen and secretory coil

Large clear secretory cells, dark cells and myoepithelial cells

Yes present at birth, innervated by sympathetic nervous system/ ACH

No relationship to pilosebaceous unit

Role in Thermoregulation/ hyperhidrosis/ hypohydrosis

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2
Q

Where are Apocrine glands found in greatest density?

What is their morphology?

Cell types?

Present at birth? Innervation?

Associated with hair follicle?

Function/ role?

A

Axilla, anogenital, periumbilical, nipples and areola

Short thick duct which opens into follicular canal/ secretory coil with wide lumen

Epithelial cells and myoepithelial cells

Maybe B adrenergic receptor agonist innervation

Present at birth/ associated with terminal hair follicle

Unclear roll

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3
Q

Where are Apoeccrine glands found in greatest density?

What is their morphology?

Cell types?

Present at birth? Innervation?

Associated with hair follicle?

Function/ role?

A

Axilla

Similar duct to eccrine gland

Similar to Eccrine and apocrine morphologically

Innervated with sympathetic fibers/ acetylcholine

No relationship to pilosebaceous follicle

Unclear / possible roles in thermoregulation

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4
Q

Increased (pathologic) activity of eccrine glands is AKA

Proteolytic activity by resident and transient skin flora (microbiota) can lead to odor-producing substances (e.g. ammonia, short-chain fatty acids); this is referred to

A

hyperhidrosis

Eccrine Bromhidrosis

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5
Q

Ductal plugs within the stratum corneum leads to ____

Intraepidermal and dermal duct occlusion induces ____

A

superficial milaria (milaria crystallina)

Miliary rubra or profunda (dermal)

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6
Q

Apocrine sweat glands are bigger/ smaller than ecrrine

A

Larger

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7
Q

Apocrine glands secretions include

A

TGs, cholesterol, fatty acids, squalene, pheremones

stinky shit = bromhidrosis

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8
Q

A sebaceous follicle contains 4 parts:

A

Keratinized follicular infundibulum

Hair

Sebaceous gland

Sebaceous duct

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9
Q

Cells within sebaceous glands contain androgen receptors that bind ___

A

DHT

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10
Q

The first pathogenic steps of Acne Vulgaris is ___

A

Abnormal keratinization → increased proliferation and retention of corneocytes in the infundibulum resulting in microcomedo

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11
Q

Free fatty acids in Sebum acts as a chemotactic for ____

A

Neutrophils

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12
Q

EGFR inhibitors cause what effect to keratinocytes

A

disturbs normal differentiation/ morphogenesis of hair follicles → inducing hyperkeratosis/ follicular plugging, growth of microoganisms and dilated infundibula

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13
Q

memorize this

A
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14
Q

Are thre functional eccrineglands at birth>

A

Yes

They have no developmental relationship with the pilosebaceous follicle

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15
Q

How are eccrine glands implicated in toxic erythema of chemotherapy and neutrophilic eccrine hidradenitis?

A

It is thought that the chemotherapy is excreted into the eccrine ducts

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16
Q

What are apocrine glands on the eyelids called?

A

Glands of Moll

17
Q

Apocrine glands are thought to be stimulated by?

Versus Eccrine glands which are stimulated by?

A

Apocrine → catecholamines through humoral mechanisms

Eccrine glands are stimulated through postganglionic sympathetic fibers with acetylcholine receptors

18
Q

Apocrine glands are part of the ______ layer (embryological)

A

primary epithelial germ layer

19
Q

Which hormone is the main one in production of sebum/ glands that stimulate production of sebum?

sebum decreases in which decade for men and women

A

5 alpha dihydrotestosterone (DHT)

women after menopause

men in 6-7th decade

20
Q

how does EGFR normally work within keratinocytes/ hair follicles?

A

EGFR is strongly expressed in keratinocytes and in cells of eccrine and apocrine glands. Inhibition of the EGFR disturbs the normal differentiation and morphogenesis of hair follicles, inducing excessive follicular hyperkeratosis, follicular plugging, and growth of microorganisms in the dilated infundibula