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Unit 3 D&D > DD 03-03-14 09-10am Dermal Structures and Diseases - High > Flashcards

DD 03-03-14 09-10am Dermal Structures and Diseases - High Flashcards

1
Q

Dermis - structure/position

A

= a tough but elastic support structure that lies beneath the epidermis & above the subcutaneous tissue
= contains blood vessels, nerves, & cutaneous appendages (hairs, sweat glands/ducts, etc.) that are important to the structure & function of skin as an organ
= ranges in thickness from ~1-4 mm, depending upon body location (much thicker than the epidermis, which is paper thin generally)

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2
Q

Dermis - functions

A
  • provides nutritional support for the avascular epidermis

= provides strength, resiliency & plasticity of skin

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3
Q

Dermal zones (2)

A
  1. Papillary dermis
    - located immediately beneath the epidermis
  2. Reticular dermis
    - located deeper in the tissue
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4
Q

Dermal matrix

A

= term often used to describe the admixture of collagen fibers, elastic fibers & ground substance all of which are synthesized by dermal fibroblasts

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5
Q

Adnexal structures

A
  • aka skin appendages
    = term used by dermatopathologists to refer to the hair follicles, sebaceous glands (oil glands), & sweat glands found in skin that are vital to protection and homeostasis
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6
Q

Basic structure of skin

A
  • Epidermis = on top, protective

- Dermis = immediately beneath epidermisbut above the fat.

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7
Q

Dermoepidermal junction

A

Interlocking dermoepidermal junction

  • Epidermal rete (downward projections of epidermis) interdigitate w/ upward projections of dermal papillae
  • -> interlocking pattern affords both strength of adherence & increased surface area btwn epidermis & dermis (important as dermis is sole source of nutrients for epidermis)
  • -> On hands & feet, interlocking pattern so pronounced that it contributed to epidermal ridges, known better as “fingerprints.”
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8
Q

Dermal papillae

A

= taken in total comprise the papillary dermis, while the deeper layer of the dermis is referred to as the reticular dermis

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9
Q

Composition of the dermis

A 
Composed predominantly of;
-  collagen fibers
- elastic fibers 
- ground substance
All these materials are synthesized by a highly productive, but sparsely populated fibroblasts in the derims
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10
Q

Collagen

A

= one of the basic building-blocks of the dermis
= provides essentially all skin’s tensile strength
- Collagen I, III, IV, VII are the main types of collagen important to the skin
= form large eosinophilic (pink) bundles, easily recognized under the light microscope

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11
Q

Collagen I

A
  • comprises >85 wt.% of adult dermis

- also a major component of bone

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12
Q

Collagen III

A
  • comprises large part of fetal dermis but is not a major portion of adult dermis
  • thought that this difference in expression explains why adult skin forms scars & fetal skin is much more resistant to scar formation
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13
Q

Collagen IV

A
  • in high concentration in “basement membrane zone,” in the dermoepidermal junction
  • also more prominent around vessels, explaining vascular fragility in some forms of Ehlers-Danlos syndrome
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14
Q

Collagen VII

A
  • found in anchoring fibrils which are used by the body to attach the epidermis to the dermis
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15
Q

Structure & Synthesis of Collagen – PROCOLLAGEN

A
  • synthesized intracellularly w/in fibroblasts
  • consists of 3 separate chains of proteins arranged in an α-helical structure
  • –> Under electron microscope, yields characteristic pattern of striations w/ 68 nm intervals
  • Chains generally consist of repeated strings of glycine &2 other proteins, forming Gly-X-Y structure (with X & Y usually proline & hydroxyproline)
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16
Q

Structure & Synthesis of Collagen – COLLAGEN ASSEMBLY

A
  • synthesized collagen proteins are secreted, then assembled into collagen fibrils EXTRA-CELLULARLY
  • Several cofactors are required to facilitate this extracellular assembly of collagen fibrils, the most famous of which is vitamin C (ascorbic acid)
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17
Q

Vitamin C & Collagen Synthesis

A
  • W/out vitamin C, collagen fibers will not attain their final desired strength
    Results in:
  • minor wounds failing to heal
  • abnormal hair growth
  • blood vessels fragility due to inadequate support from surrounding collagen
  • teeth falling out also for lack of surrounding collagen support

Condition used to be common in sailors who went w/out fresh fruits or vegetables on long ocean journeys
= scurvy
= a classic example of an acquired abnormality in collagen production

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18
Q

Ehler-Danlos Syndrome (EDS)

A

= a group of related congenital disorders of collagen synthesis
= is a classic example of disordered collagen production due to genetic defects.
- at least 10 subtypes, but all of subtypes share varying degrees of the 4 major clinical features including:
— skin hyperextensibility
— joint hypermobility
— tissue fragility
— poor wound healing

  • hyperextensible skin in EDS NOT due to disorder in elastic fibers, but due to abnormally formed collagen
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19
Q

Elastic Fibers

A

= provide skin with resiliency (ability of skin to be distorted but then return to original shape)
= much smaller than collagen fibers

= difficult to ID w/ standard staining techniques
= BUT argyrophilic (silver-loving) & can use special silver stains (Verhoff-Van Gieson stain) that will not stain collagen fibers

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20
Q

Solar elastosis

A

= most common acquired disorder of elastic fibers

  • Over a lifetime, a person accumulates significant sunlight exposure –> degeneration of elastic fibers
  • -> These collagen bundles become dystrophic & tend to “clump” and aggregate
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21
Q

Solar elastosis & microscopy

A

The abnormal, sun-damaged collagen bundles which aggregate are easy to appreciate on routine microscopy
= basophilic (blue) staining material w/in superficial portions of dermis

IMPORTANT CLUE UNDER THE MICROSCOPE that informs you instantaneously that the tissue:

  • is from a middle-aged or older person
  • was taken from a sun-exposed skin site
  • –> helpful in study of sun-induced neoplasms
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22
Q

Pseudoxanthoma elasticum (PXE) - pverview

A

Classic example of inherited elastic disorder
Caused by mutation in gene encoding part of the “multidrug resistance complex”
- this complex is responsible for pumping compounds out of cells
- when mutated in cancerous cell, may result in resistance to certain forms of chemo
- not well-understood how this MDR defect leads to disease

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23
Q

Pseudoxanthoma elasticum (PXE) - pathogenesis

A

Gene mutation in “multidrug resistance complex”
Elastic fibers of dermis become enlarged, tangled, & calcified
—> characteristic purple-blue color upon routine histological examination

Clinically, skin of flexural areas of body maintains “plucked chicken” appearance
= clue to Dx

Elastic fibers of blood vessels are also damaged
—> HTN, bleeding disorders (esp. in eye)

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24
Q

Ground Substance defn.

A

= general term for a gelatinous material intercalated between & amongst collagen bundles, elastic fibers, and appendageal structures of the dermis
= “pie filling” made of long chains of sugar molecules (glycosaminoglycans)

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25
Q

Ground Substance - components

A

Consists principally of 2 glycosaminoglycans:

  • hyaluronic acid
  • dermatan sulphate

Also, fibronectins
= serve as “glue”

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26
Q

Glycosaminoglycans

A

= complex molecules made up of proteins & sugars

- capable of absorbing >10,000x their weight in water

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27
Q

Ground substance - action

A

Glycosaminoglycans + Fibronectins = gel-like mass functions like a sponge
= under pressure it can expel bound water
= then it can take it up again
—> helps to facilitate nourishment of overlying epidermis by easily allowing a water-based environment for diffusion

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28
Q

Ground substance - destruction / renewal

A
  • In contrast to collagen fibers, which are renewed mostly when necessary (injury), ground substance is constantly being destroyed and then renewed
  • destroyed by enzymes like hyaluronidase
  • renewed via production from fibroblasts
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29
Q

Restylane

A

= an excellent example of ground substance
= cosmetic filler product
= simply pure hyaluronic acid produced via recombinant (yeast + plasmid) technology

Cosmetic dermatologists place this material under skin to augment the tissue & remove lines/wrinkles

Well-suited for this for two reasons:

  1. It is a natural substance that is already present in skin & it does not engender immune response
  2. It absorbs a tremendous amount of water & amplifies the augmentation

Just like endogenously produced hyaluronic acid, Restylane is broken down by tissue hyaluronidases and it is not a permanent augmentation.

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30
Q

Blood vessels in skin (cutaneous vascular system)

A

Epidermis has no blood supply
- derives its nourishment via diffusion of materials through ground substance of dermis
Important also for:
- Wound healing
- Control of homeostasis
- Modulation of inflammation/leukocyte trafficking

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31
Q

Blood vessels of the dermis

A

Divided into superficial & deep vascular plexi

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32
Q

Wound healing & Cutaneous Blood System

A

<–- the endothelium (single-cell lining on innermost surface of vessels) elaborates important cytokines including endothelial growth factor

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33
Q

Control of homeostasis & Cutaneous Blood System

A

<– via structure called Sucquet-Hoyer canal
= smooth muscle derived valve-like structure
- blood may be directed toward skin during overheating, or away from skin in hypothermia

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34
Q

Modulation of inflammation/leukocyte trafficking & Cutaneous Blood System

A

may exit vasculature to fight infection in skin & soft tissue

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35
Q

Capillary structures of the skin

A
  • Contained in uppermost portion of papillary dermis (suprapapillary plate)
  • involved in Auspitz sign & Verruca
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36
Q

Auspitz sign

A
  • when thickened scales of psoriasis are forcefully removed, pinpoint bleeding is noted at area of removal
  • In truth, sudden removal of epidermal scale leads trauma to capillaries of uppermost papillary dermis
  • –> pin-point bleeding observed
  • Please note the scale of psoriasis is entirely w/in the epidermis, and Auspitz sign does not violate the rule that there are no blood vessels in the epidermis!
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37
Q

Verruca

A

= aka warts
= benign, virally induced neoplasms (growth) that require increased blood supply to support virally-proliferating cells
- These proliferating vessels may be IDed as brownish, thrombosed capillary structures in the center of the verruca
- Presence of central thombosed capillary loops is a reassuring sign that the lesion is in fact a wart

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38
Q

Leukocytoclastic vasculitis - overview

A

= common disease involving post-capillary venules

Some type of insult –> immune complexes form & deposit in vessel walls, causing inflammation (Type III immunopathology)

  • Most common cause is Strep infection, but may be medicine allergies, cryoglobulin production from hepatitis C, or a myriad of other conditions
39
Q

Inflammation in leukocytoclastic vasculitis

A

Neutrophils attach to vessel wall & degranulate
—> damage & extravasation of RBCs into dermis

Leukocytoclasia = this process of fibrinoid deposition in vessel walls, w/ infiltrating neutrophils & neutrophil debris

40
Q

Clinical manifestation of leukocytoclastic vasculitis

A

“Palpable purpura”
- palpable b/c of the inflammation
- purpuric (& non-blanchable) due to extravasation of RBCs into dermis
(if vessels were simply dilated, but still intact, pressure applied to skin would redness go away)

41
Q

Disruption to dermal vascular plexi —>

A

—> necrosis and sloughing of the epidermis
B/c epidermis is completely dependent upon dermis for nutrition & support
<— may be caused by any process which corrupts the dermal vascular plexi, whether vasculitis (inflammation), vasculopathy (mechanical occlusion) or otherwise, if prolonged and/or severe

42
Q

Nervous tissue of the dermis

A 
= function similar to nervous tissue in other areas of the body, specifically to inform & protect
Most important structure:
- Meissner's corpuscles
- Free nerve endings
- Pacinian corpuscles
43
Q

Free nerve endings

A
  • pass through upper dermis to terminate at dermoepidermal junction
  • thought to be involved in sensation both of pain & of itch (pruritus)
44
Q

Pruritus - sensation’s travels to the brain

A
  • originates in free nerve endings near dermoepidermal junction
    –> conducted centripetally by afferent nerves entering spinal cord via dorsal roots
    (small, unmyelinated C fibers w/ slow conduction)

After entering spinal cord, primary neurons synapse w/ secondary neurons

  • –> axons cross to opposite side of body
  • –> travel cephalad

Sensations arrive at cerebral cortex

  • –> body can ID location, nature, intensity, etc.
  • –> secondary activation of pre-motor areas of brain
  • –> probably synaptic connections to motor area of cortex (which prepare for scratching)
45
Q

Pruritis & Pain

A
  • For a long time it was thought that itch represents a weak pain
  • Debated whether same nerves conduct itch & pain
  • Now recognized that itch & pain are different & independent sensory modalities, even if local anesthesia or cutting of sensitive nerves may abolish both
46
Q

Observations that led to belief that receptors / transmission apparatus for itch & pain differ:

A
  • itch elicits scratching, while pain yields withdrawal
  • morphine relieves pain but can produce pruritus
  • heating of skin to 41°C relieves itch but not pain
  • removal of epidermis & upper dermis abolishes pruritus, but not pain
47
Q

Pacinian corpuscles

A

= resemble an onion in cross-section (see pic in notes)

  • involved in pressure & vibratory sensation
  • most concentrated in genital area
48
Q

Meissner’s corpuscles

A

= resemble pine-cone (see pic in notes)

  • involved in fine touch & tactile discrimination
  • in highest concentration on distal aspects of digits, esp. pulps of the fingers
49
Q

Insensitivity to pain

A
  • rarely congenital; usually w/ co-exisiting anhidrosis (inability to sweat)

Caused by mutations in neurotrophic tyrosine receptor kinase 1 (NTRK1) gene
–> encodes for nerve growth factor receptor (NGFR)

  • Such children suffer from enormous number of injuries to skin & integument, including corneal erosions in >70%
  • cannot feel common danger signs which normally lead to protective responses
  • must be examined several times a day for cuts, scrapes, sand stuck in the eye, materials in the skin & other perils common to small children
50
Q

Areas & Types of hair

A
  • Nearly entire body surface is covered by hair
  • Areas specifically NOT covered w/ hair include palms, soles, glans penis, and labia minora

Two different types of hair:

  • Terminal Hairs
  • Vellus Hairs
51
Q

Terminal Hairs

A
  • large, thick, coarse, pigmented
  • on scalp, a man’s beard area & possibly chest / back, pubic area
  • begin deep in dermis at/near dermal-subcutaneous junction
52
Q

Vellus Hairs

A
  • small, fine, apigmented
  • located diffusely on body
  • represented the types of hairs often on the ear, the lateral face of women, and the body in general
53
Q

Anatomy of the average hair follicle

A

Arrector pili muscle
Sebaceous gland

Common to divide hair follicle into thirds
1. Infundibulum = upper third
2. Isthmus = middle third (from sebaceous duct to insertion of arrector pili)
3. Matrical area = lower third
(see pic in notes)

54
Q

Arrector pili muscle

A

= small, smooth-muscle

- when activated by autonomic nervous system, brings hair into more erect position (“goose bumps”)

55
Q

Sebaceous glands

A
  • secrete oily substance called sebum onto hair & indirectly onto skin surface
  • more prominent in oily” areas of body (face, neck, chest, upper back)
56
Q

Basic embryology of dermal structures

A

Follicular unit is derived from primitive ectodermal germ (PEG), whose development is an excellent examnple of embryonic induction

57
Q

Development of PEG via embryologic induction

A

Induction
= means underlying mesenchyme (which will become dermal papillae of hair) induces formation of PEG in overlying fetal skin

Several bulges of PEG are significant:

  • Lower bulge – attachment for arrector pili
  • Middle bulge – sebaceous gland
  • Upper bulge – apocrine gland (axillae, groin, or other areas with apocrine glands)
58
Q

Androgenic alopecia overview

A
  • aka androgenetic alopecia, or pattern baldness
    = common “illness” which illustrates some of the important properties of hair growth

Scalp hairs are terminal hairs (thick, pigmented, deep in dermis/subcutis)
In androgenic alopecia, hairs become miniaturized, finer & lie higher in the dermis
—> Ultimately, resemble vellus hairs

59
Q

Normal adult scalp - growth/rest phases of hair

A

Scalp of adult contains >100,000 hairs

  • ~85% are in anagen (growth phase)
  • ~10-15% in telogen (resting phase)
  • remainder (1-5%) in catagen (transition phase btwn anagen & telogen)
60
Q

Androgenic alopecia - men vs. women patterns

A

MEN: –> classic fronto-temporal or postero-occipital balding

WOMEN: –> thinning of hair on crown area

Nearly 50% of both sexes are affected to some degree, though not as widely discussed in women

61
Q

Androgenic alopecia - process & treatment

A

= not understood completely, but known that conversion of testosterone to 5-dihydrotestosterone is important in promoting this change

  • Finasteride (5-α-reductase inhibitor) blocks this conversion & is used in treatment of male pattern baldness
  • Both men & women also treated w/ minoxidil, a drug known to promote anagen phase of hair growth

Neither treatment is entirely satisfactory

62
Q

Sebaceous glands - overview

A

= oil-secreting glands located predominantly in oily” areas of the body including scalp, face, neck, upper chest, and upper back
= the classic example of a holocrine gland
- persons vary widely with respect to basal level of sebum (oil) production
- sebum secretion is dependent on sex hormone
- these glands do not appear to be innervated by the autonomic nervous system, but exact mechanism governing sebum production is poorly understood

63
Q

Holocrine gland

A

= method of secretion involved entire sebocytes (sebaceous gland cells) being secreted & in the process breaking-down to extrude the contents

64
Q

Sebaceous gland disorders - timing

A

As sex hormones are requisite to sebum secretion, disorders associated w/ the sebaceous glands (like acne) are not prevalent until after adrenarche (puberty)

65
Q

Medication to decrease sebum production

A

Isotretinoin (Accutane)
= one of the only meds to significantly decrease sebum production
= rather toxic
= decreases sebum production by up to 90%, often permanently
= mechanism largely unknown

66
Q

Acne

A

= ubiquitious disorder of the pilosebaceous unit
- multifactorial (no single cause)

Plugging of ostia of pilosebaceous unit by hyperkeratotic debris
–> accumulation of oil w/in
Propionibacterium acnes (normal commensal bacteria) then begins to multiply
–> converts sebum to pro-inflammatory fatty acids
Pilosebaceous unit ruptures
—> characteristic inflammatory “zit”

67
Q

Pilosebaceous unit

A

the combined hair follicle and oil glands

68
Q

Blocked pores

A

Blocked pores themselves constitute comedones, that are further classified to be:

  • open - “black heads”
  • closed - “white heads”
69
Q

Eccrine glands - overview

A

= aka “general sweat glands”

  • Primary function is thermoregulation
  • –> accomplished through cooling effects of evaporation of this sweat on skin surface
  • classic example of merocrine secretion
70
Q

Location of eccrine glands

A
  • located throughout the body b/c so important in temperature regulation
  • most numerous on forehead, upper cutaneous lip, and palms/soles
71
Q

Merocrine glands

A

secrete WITHOUT either the apocrine blebbing, or holocrine shedding

72
Q

Embryologic development of Eccrine glands

A

Develop from an eccrine germ

- DISTINCTLY different from primitive ectodermal germ of the follicular unit

73
Q

Three main components to the eccrine gland

A
  • Coiled secretory portion deep in the dermis
  • Intradermal duct (coiled & straight duct)
  • Intraepidermal portion (called the acrosyringium)
    (see pic in notes)
74
Q

Eccrine sweat - composition

A
  • water
  • sodium
  • potassium lactate
  • urea
  • ammonia
  • serine
  • ornithine
  • citrulline
  • aspartic acid
  • heavy metals
  • organic compounds
  • proteolytic enzymes
75
Q

Regulation / Initiation of Sweating

A

CRITICAL TO RECOGNIZE that

  • even though sweating is mediated by sympathetic portion of autonomic nervous system
  • it is triggered via acetylcholine secretion

Acetylcholine
= chemical otherwise associated w/ the parasympathetic nervous system

76
Q

Results of Sympathetic vs. ACh control of sweating

A

Control by sympathetic nervous system:
- explains sweating under stress

Mediation via acetylcholine (NT often associated w/ parasympathetic responses)
- explains why certain drugs that increase acetylcholine levels result in increased sweating despite parasympathetic response systemically

Furthermore, this is why atropine poisoning (a drug which has anticholinergic activity) results in a warm, flushed, but anhidrotic (non-sweating) patient.

77
Q

Anticholinergics / “Parasympathetic” drugs & Sweating

A

Drugs that increase ACh despite their parasympathetic action

  • Neostigmine
  • Physostigmine
  • Organophosphate-based pesticides
  • –> increase sweating despite parasympathetic systemic response

Atropine poisening
= anticholinergic activity
–> results in warm, flushed, but ANHIDROTIC (non-sweating) patient

78
Q

Apocrine Glands - embryological development

A

= outgrowths of upper bulge of primitive ectodermal germ (fetal structure yielding the follicular unit)

79
Q

Location & timing of apocrine glands

A
  • only in axillary & anogenital area
  • present at birth, but remain small & nonfunctional until after puberty
  • At puberty, hormonal stimulation causes apocrine glands to become functional
  • Glands respond mainly to sympathetic adrenergic stimuli initiated by emotional stress
80
Q

Specialized variants of apocrine glands

A
  • Moll’s glands on the eyelids
  • Cerumen (ear wax) glands of external auditory canal
  • Lactation glands of the breasts
81
Q

Apocrine gland structure

A
  • coiled portion deep in the dermis
  • straight duct traversing dermis & emptying into hair follicle

Coiled gland
= one layer of secretory cells around a lumen that is ~10x the diameter of its eccrine counterpart
= surrounded by contractile myoepithelial cells

Straight duct
= runs from coiled gland to hair follicle

82
Q

Predominant mode of apocrine secretion

A

Decapitation

= process where apical portion of secretory cell cytoplasm pinches-off & enters lumen

83
Q

Apocrine sweat

A

Consists mainly of sialomucin
= odorless initially
= as apocrine sweat comes in contact w/ normal bacterial flora on skin surface, odor develops

More viscous & produced in smaller amounts than eccrine sweat

84
Q

Function of apocrine glands

A

Exact function is unclear

Likely represent scent glands

85
Q

Chromohidrosis

A

= a disorder of apocrine glands (exclusively apocrine in origin)

  • literally translates into “colored sweat”
  • mostly reported on face, axillae, & breast areola (though apocrine glands are also in genital region)

Lipofuscin pigment
= responsible for colored sweat
= produced in apocrine gland
= its various oxidative states account for characteristic yellow, green, blue, or black secretions observed in apocrine chromhidrosis

~10% of people W/OUT true chromohidrosis have colored sweat which is regarded as minor, acceptable, and within the normal range

No fully satisfactory cure or treatment.

86
Q

Apoeccrine Glands

A

= hybrid sweat glands found chiefly in axilla
- may play role in axillary hyperhidrosis

Apocrine features:
- larger diameter portion, similar to apocrine gland

Eccrine features:

  • small diameter portion, similar to eccrine gland
  • respond mainly to cholinergic stimuli
  • ducts are long & open directly onto skin surface

May constitute up to 45% of sweat glands found in axillary region in some pts

Secrete nearly 10x as much sweat as eccrine glands, making them by far the most productive gland in the dermis.

87
Q

Localized Hyperhidrosis - defn. & source

A

= focal excessive sweating

= may be eccrine (esp. w/ “clammy hands” or “sweaty feet) or may apoeccrine (in axilla)

88
Q

Patterns in Localized Hyperhidrosis

A
  • Positive family Hx in 30%–50% of pts

Generally do not sweat during sleep
- therefore, most consider it a disease of autonomic dysfunction

89
Q

Normal vs. Hyper- Hidrosis

A

Normal (no strict defn.)
- <1 mL/m2 of sweat production per minute by eccrine glands at rest & room temp

Hyperhidrosis
- For practical purposes, any degree of sweating that interferes with ADLs should be investigated

90
Q

Qualitative documentation of perspiration

A

= for purposes of tracking treatment

  1. Apply iodine solution (1%–5%) to dry surface
  2. After a few seconds, sprinkle starch over same area.
  3. Starch & iodine interact in presence of sweat
    - –> purple-black sediment
    - Purple area IDes duct of sweat gland
91
Q

Initial treatments for focal hyperhidrosis

A

Focus on antiperspirant solutions or anticholinergic meds, which decrease eccrine & apoeccrine output

92
Q

Subsequent treatments for focal hyperhidrosis

A
  • Thoractomy w/transaction of sympathetic nerve trunk

- Botulinum toxin A (Botox)

93
Q

Thoracotomy w/ transaction of sympathetic nerve trunk to treat Focal Hyperhidrosis

A
  • Often wanted by patient, while physicians are often reluctant
  • High incidence of mild to severe compensatory hyperhidrosis (new area of increased sweating), usually involving trunk & lower limbs
  • -> occurs in up to 86% after thoracotomy
94
Q

Botulinum toxin A (Botox) to treat Focal Hyperhidrosis

A
  • When injected into dermis & subcutis, blocks release of ACh from nerves
  • –> thereby blocks stimulus for sweat production
  • Effective
  • Expensive (generally not covered by insurance)
  • Transient
  • –> limited use

Unit 3 D&D (18 decks)

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