Dermis and adnexal structures Flashcards

1
Q

What is the dermis?

What kind of strenght does it provides?

A

• Structural & physiologic support network • Contains:

blood vessels
– nerves
appendageal structures (hair, glands, etc.)

  • Provides major *tensile strength* of the skin
  • Thickness varies with location

– on average 1 - 4 mm in depth

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2
Q

What are the two layers of the dermis?

A

1) Papillary dermis – upperlayer

– *thin collagen bundles

– interlockswith epidermal rete

Functions:

  • increases strength
  • increases surface area

2) Reticular dermis

– deepe rlayer

– thick collagen bundles

– visible elastic fibers

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3
Q

What are the three building block of the dermis?

Which one forms the tensile strenght?

Which one facilitates diffusion of substances?

A

Three “Building Blocks” of the Dermis

  1. Collagen – forms the tensile strength
  2. Elastic fibers–allow for resilience

3. Ground substance–facilitates diffusion

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4
Q

Basic of collagen in the skin:

What pattern with what AA does it usually have?

Which collagen is the most common?

Which collagen forms a large part of the fetal epidermis?

Which one is part of the basement membrane?

Anchorin fibrils is the role of collagen ___.

A

α-helical structure,

-Gly-X-Y pattern • X = proline, Y = hydroxyproline
• >25 types synthesized by the body

• A few are of particular relevance:

Collagen I = >85 wt.% of adult dermis

Collagen III = large part of fetal dermis
Collagen IV = “basement membrane zone” –

Collagen VII = **anchoring fibrils*

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5
Q

Collagen production:

Procollagen is synthesized where?

Cross-linking of procollagen depends upon_______.

A
  • PROcollagen is synthesized within fibroblasts
  • Excreted extracellularly
  • Cleaved enzymatically into TROPOcollagen
  • Tropocollagen aggregates, becomes cross-linked
  • Cross-linking dependent upon vitamin C (co-factor).
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6
Q

What is scurvy?

Due to deficiency in________.

How long does it take to show up after deficiency?

A

Scurvy is an acquired disease, not congenital.

–> Vitamin C is a required co-factor in collagen synthesis.

-Deficiency results in decreased mature collagen

Signs and symptoms 1-3 mos. after deprivation

Key Findings:

keratotic plugging of hairs

perifollicular hemorrhage

“corkscrew” hairs
hemorrhagic gingivitis

Also weakness, delayed healing.

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7
Q

Ehler-Danlos Syndrome

Congenital

What are 4 findings characteristics of this syndrome?

A

A family of disorders based upon erroneous collagen synthesis

• Mutations at various stages of collagen production yield findings such as

hyperextensible skin

hyperextensible joints

fragile blood vessels

poor wound healing

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8
Q

Ehler-Danlos Syndrome

Which one is caused by a defect in collagen V and is characterized by hypermobility, joint laxity, absent frenula, molluscoid tumors, hernias?

Which one is caused by defective collagen III and is characterized by arterial, uterine, intestinal rupture, atrophic scars, limited lifespan?

Which one is due to a defect in collagen I and is characterized by congenital hip dislocation severe hypermobility, skin fragility, atrophic scarring?

A

Classification schema

Classical

Vascular

Arthrochalasia

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9
Q

Ehler-Danlos Syndrome

Absence of what also characterizes EDS?

A

Absence of the **inferior labial and lingual frenula in Ehlers-Danlos syndrome.

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10
Q

Elastic fibers

A

**Minor constituent of dermis, provides resiliency

  • Thin fibers (1-3 um)
  • Intertwined among collagen bundles

• Special stains are required to visualize (VVG=Verhoff Van giesof)

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11
Q

Solar Elastosis –
An Acquired Disorder of Elastic Fibers

A

Sun-damaged elastic fibers

Basophilic (blue) material within superficial dermis

**HISTOLOGICCLUE UNDER MICROSCOPE**

Indicates tissue is from older person in a sun-exposed site

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12
Q

Pseudoxanthoma Elasticum

Results in _______.

Arterial rupture seen particularly in the ____.

A

Caused by a mutation in MDR gene

• Net result - calcified, brittle elastic fibers

Disease is associated with:

– “plucked chicken” skin
systemic hypertenision
– angioid streaks in the retina

– arterial rupture (particularly in the eye)

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13
Q

Ground Substance

What are the two main glycosaminoglycans?

A

“Pie filing” of the dermis

Protein-sugar moieties

– absorb 10,000x their weight in water:

hyaluronic acid

dermatan sulphate
• “Glued” together with fibronectins

• Gelatinous mass that functions as a sponge

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14
Q

Blood Vessels of the Dermis

Do the epidermis contains vasculature?

A

Epidermis contains NO vasculature!

  • Depends entirely on the dermis for nutritional support via diffusion.
  • Skin vessels considered as two plexi

superficial plexus
deep plexus

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15
Q

What are some disorders of capillary loops?

–>Dilated, tortuous capillaries are noted in diseases with increased epidermal turnover.

A

Inflammation of Capillaries and Venules Causes Vasculitis:

Immune complexes from:

– drug hypersensitivity
– infection
– neoplastic disorders

– collagen vascular disease

***Deposit in small blood vessel walls

Type III Gel & Coombs reaction

Palpable purpura” - combination of inflammation and hemorrhage

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16
Q

Nervous tissue

What are the two important types of nerve fibers to be aware of?

Which ones are heavily myelinated and conduct rapidly?

Which of the Type A fibers is the largest and is used for propioception and large motor units?

Which type A fiber carries touch?

Which type A fiber forms the spindle organs in the muscle stretch receptors?

Which type is unmyelinated and slow-conducting?

Which fiber conveys sensation of diffuse, dull, and is non-localizing and also used fot temperature and itching sensation??

A

Type A- heavily myelinated,–> conduct rapidly
– Type A fibers subdivided into four groups by fiber size

Type A-α (largest) - proprioception and large motor units

  • Type A-β - carries touch
  • Type A-γ - **spindle organs in the muscle stretch receptors
  • Type A-δ (smallest) - fast-localizing initial component of pain.

Type C fibers -unmyelinated,slow-conducting

– convey sensation of diffuse, dull, non-localizing
– **temperature and itching sensations

17
Q

What is ITCH?

Where in the skin are Meissner’s corpuscles found?

What do Meissner’s corpuscles do?

Which corpuscles have “onion-like” structures located in the dermis and are involved in pressure and vibration?

Where are pacinian corpuscles highest in density?

A

Meissner’s Corpuscles – “pine- cone” like structures located near DEJ, involved in fine touch, highest density on pulps of digits.

Pacinian Corpuscles“onion” like structures located in the dermis, involved in pressure and vibration, highest density on genitals

18
Q
A
19
Q

Adnexal structures of the classical dermis:

A
20
Q

Basics of hair

Which type of hair is fine, thin, apigmented?

Wich type of hair is dark, thick, coarse?

Hair follicle is divided into infundibulum, isthmus, and ______.

A

Types of hair

– Terminal hair

  • dark
  • thick
  • coarse

– Vellus hair

  • fine
  • thin
  • apigmented
  • Hair follicle anatomy – Divided into thirds

Infundibulum (upper third), isthmus (middle third), matrical region (lower third)

21
Q

Embryonic origin of hair

upper bulge–> _____

Middle bulge–> _____

Lowe bulge–> ______

A

Follicular unit is derived from the PEG (“primitive ectodermal germ”)

Classic example of embryologic “induction

–>Mesenchyme “induces” the overlying neuroectoderm

Downward bud with 3 “bulges”

upper = apocrine gland (+/-)
middle = *sebaceous gland
lower = attachment arector pilori

22
Q

What are the cycles of the normal scalp?

Anagen—>_________

Telogen–>_________

Catagen—>_______

A

Contains > 100,000 hairs
• Hairs randomly engaged in 1 of 3 cycles

anagen (growth) – 85%
telogen (rest) – 10-15%
– catagen (involution: transition phase between anagen and telogen) – 1-5%

• Cycles follow a “basic rule of threes”

– anagen – 3 years
– telogen – 3 months
– catagen – 3 weeks (or less)

23
Q

Androgenic alopecia

A

Treatment of hair loss

Finasteride makes hair follicles become deeper in dermis/fat.

24
Q

Sebaceous glands

Are an example of holocrine glands in that the method of secretion involved entire sebocytes (sebaceous gland cells) being secreted and in the process breaking-down to extrude the contents.

A

What causes acne?

Disease of pilosebaceous unit

– abnormal follicular maturation

comedone formation (black/white heads)

– plugged follicular environment allows overgrowth of P. acnes

– P. acnes liberates FFAs and/or ruptures follicle

– later events yield dermal inflammation

25
Q

Eccrine glands

Sweating is vital to_____.

numerous on the____, _____, _____.

What is merocrine secretion?

Develop of PEG?

A

-Odorless, watery sweat

  • VITAL to thermoregulation
  • Numerous upon forehead, upper cutaneous lip, palms/soles

***Merocrine secretion (Merocrine glands secrete WITHOUT either the apocrine blebbing, or holocrine shedding).

Sympathetic innervation but utilizes acetylcholine

NOT derived from the PEG (develop from en eccrine germ).

26
Q

Are there acquired disorders of sweating?

  1. Heat shock (“classic”)
  2. Antiperspirants
A

How do antiperspirants work?

Active agent – AlClOH3, selectively soluble

Perspiration raises pH - insoluble AlClOH3 precipitates to block sweat duct

Washing with soap raises pH - AlClOH3 becomes soluble again, duct is unblocked

27
Q

What is miliaria (“prickly heat”)?

–>the **Blocked sweat ducts**

–>Babies, febrile, etc.

Manifestations depend upon site of blockage

– miliaria crystalina

– miliaria rubra
– miliaria profunda

Miliaria is an acquired disorder of eccrine function.

A

Anhidrotic Ectodermal Dysplasia (Congenital disease of eccrine glands)

1875 - Described by Darwin
• Mutation in EDA gene
• Aberrant eccrine development

  • Severely decreased sweating
  • Poor temperature regulation

• Other ectodermal problems
– sparse hair, abnormal teeth, etc

28
Q

Apocrine glands

Moll’s glands are found in the ______.

A

Outgrowths of the upper bulge of PEG

• Located in axillary and anogenital area

  • Small and nonfunctional until puberty
  • Specialized variants of apocrine glands:

Moll’s glands of the eyelids,
cerumen glands of the external auditory canal

lactation glands of the breasts

29
Q

Aprocrine glands

A

Decapitation secretion (a process where the apical portion of the secretory cell cytoplasm pinches-off and enters the lumen).

Structure otherwise similar to eccrine glands

Apocrine sweat “stickier” (sialomucin)

Odorless (initially)

Odor develops upon contact with normal skin flora

30
Q

Apoeccrine glands

Located mainly in the______-

A
  • Hybrid sweat glands
  • Located mainly in axilla
  • Likely play a role in axillary hyperhidrosis
  • Apoeccrine glands secrete nearly ten times as much sweat as eccrine glands
31
Q

Treatment of hyperhidrosis?

A

Secretion is dependent upon acetycholine release

Botulinum toxin blocks secretion by preventing acetylcholine release

–>Expensive & painful