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Musculoskeletal Rheumatology > Intro to Dermatology > Flashcards

Intro to Dermatology Flashcards

1
Q

What are the two major embryological elements of the skin?

A
  1. Epidermis- originates from ectoderm

2. Dermis- arises from mesoderm that comes into contact with inner surface of epidermis

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2
Q

What is the mesoderm essential for?

A

-for inducing differentiation of epidermal structure e.f hair follicles

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3
Q

What is the development of the skin stages?

A
  • epidermis forms by week 4- single basal layer of cuboidal cells
  • secondary layer of squamous, non-keratinising cuboidal cells (periderm) develops in week 5& generates white, waxy protective substance- vernix caseosa
  • from week 11, basal layer of cuboidal cells (stratum germinative) proliferates to form multilayered intermediate zone - four more superficial strata Spinosum(spinous),granulosum(granular),lucidum(clear;foundon palms of hands and soles of feet), and corneum (horny).
  • Epidermal ridges protrude as troughs into developing dermis beneath neurovascular supply develops into dermal papillae
  • Weeks9-13developmentofhairfolliclesinstratumgerminativum and appearance of lanugo hair
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4
Q

What happens to melanocytes during skin development?

A
  • derived from neural crest
  • make melanoblasts
  • migrate dorsally between week 6-8 to developing epidermis (dermis) and hair follicles
  • by week 12-13, most melanoblasts have reached destination and differentiated into melanocytes
  • subset of melanoblasts from melanocyte stem cells in hair follicle bulge that replenish differentiated melanocytes
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5
Q

What is the regulation of melanocytes?

A
  1. Melanocortin 1 receptor (MC1R), a G protein-coupled receptor regulates quantity and quality of melanins produced:
    - Agonists α-melanocyte-stimulating hormone (αMSH) & adrenocorticotropic hormone (ACTH) → activation of MC1R by agonist → melanogenic cascade → synthesis of eumelanin
    - Agouti signaling protein (ASP) reverses those effects & elicit production of
    - ACTH can also up-regulate expression of MC1R gene
  2. Exposure to UV
    - increased expression of transcription factor MITF & downstream melanogenic proteins, including Pmel17, MART-1, TYR, TRP1, and DCT → increases in melanin content
    - Increased PAR2 in keratinocytes → increases uptake & distribution of melanosomes by keratinocytes
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6
Q

What are the main the structures of the skin?

A
  • epidermis
  • basement membrane/ dermal-epidermal junction
  • dermis: connective tissue
  • subcutaneous fat
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7
Q

What is the structure of the epidermis?

A
  • composed of keratinocytes
  • division of cells in basal layer
  • progressive differentiation/ flattening; Stratum spinosum, Stratum granulosum, Stratum lucidum (palms and soles only), Stratum corneum (no nuclei or organelles)
  • cellular progression from basal layer to surface in 30 days- accelerated in skin diseases (e.g psoriasis)
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8
Q

What does the filamentous cytoskeleton of keratinocytes comprise of?

A
  • actin-containing microfilaments
  • tubulin-containg microtubules
  • intermediate filaments (keratins)
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9
Q

What are the roles of keratins?

A
  • structural properties
  • cell signalling
  • stress response
  • apoptosis
  • wound healing
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10
Q

What are desmosomes?

A
  • major adhesion complex in epidermis
  • anchor keratin intermediate filaments to cell membrane and bridge adjacent keratinocytes
  • allow cells to withstand trauma
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11
Q

What are gap junction and why are they needed?

A
  • clusters of intercellular channels (connexons)
  • directly form connections between cytoplasm of adjacent keratinocytes

-essential for cell synchronisation, cell differentiation, cell growth and metabolic coordination

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12
Q

What are adherents junctions?

A
  • transmembrane structures

- engage with actin skeleton

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13
Q

What are tight junctions?

A

-role in barrier integrity and cell polarity

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14
Q

What are melanocytes?

A
  • dendritic

- distribute melanin pigment (in melanosomes) to keratinocytes

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15
Q

What are Langerhans cells?

A
  • dendritic

- antigen-presenting cells

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16
Q

What are merkel cells?

A

-mechanosensory receptors

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17
Q

What are the cells in the epidermis?

A

-melanocytes
-langerhans cells
merkel cells
mast cells

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18
Q

What is the basement membrane and what are its roles?

A

-dermal-epidermal junction
-proteins and glycoproteins:
collagens (IV, VII), laminin, integrins

Roles:

  • cell adhesion
  • cell migration
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19
Q

What is the structure of the dermis?

A
  1. Papillary dermis:
    - superficial
    - loose connective tissue
    - vascular
  2. Reticular dermis:
    - deep
    - dense connective tissue
    - forms bulk of dermis

Proteins

  • collagen- TI and TIII
  • elastic fibres-fibrillin, elastin

Glycoproteins
-fibronectin, fibula, intregrins, which all facilitate cell adhesion and cell motility

Ground substance
-between dermal collagen and elastic tissue- glycosaminoglycan/ proteoglycan

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20
Q

What cells are present in the dermis?

A
  • fibroblasts
  • histiocytes
  • mast cells
  • neutrophils
  • lymphocytes
  • dermal dendritic cells
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21
Q

What is the vernix caseosa?

A

-generates white, waxy protective substances

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22
Q

What is the function of MC1R?

A

-regulates quantity and quality of melanins produced

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23
Q

Which stratum is only found in the palms and the soles?

A

-stratum lucid

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24
Q

Where are melanocytes derived from?

A

-the neural crest

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25
Q

What are the most predominant cells in the dermis?

A

-fibroblasts

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26
Q

What forms the superficial component of the dermis?

A

-the papillary dermis

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27
Q

What is the blood supply for the skin?

A
  • deep and superficial vascular plexus

- blood supply does for cross into epidermis

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28
Q

What is the sensory innervation in the skin to?

A
  • free nerve endings
  • hair follicles
  • expanded tips
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29
Q

What is the autonomic innervation in the skin to?

A

Cholinergic- eccrine

Adrenergic- eccrine and apocrine

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30
Q

What is the Pilosebaceous unit?

A

-hair follicles

-consists of the hair shaft, the hair follicle, the sebaceous gland, and the erector pili muscle

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31
Q

What are the afferent nerves in the skin?

A
  1. Corspuscular
    - encapsulated receptors e.g dermis- Pacinian, Messiners
  2. Free
    - non-encapsulated receptors e.g epidermis- Merkel cells
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32
Q

What are Meissner’s corpuscles?

A
  • aka tactile corpuscle
  • encapsulated, unmyelinated mechanoreceptors
  • light touch and slow vibration
  • sense low-frequency stimulation at level of dermal papilla
  • most concentrated in thick hairless skin- finger pads and lips
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33
Q

What are Ruffini corpuscles?

A
  • slow acting mechanoreceptor
  • sensitive to skin stretch
  • deeper in dermis
  • spindle-shaped
  • highest density round fingernails - monitors slippage of objects
34
Q

What are the Pacinian corpuscles?

A

aka lamellar corpuscles

  • encapsulated
  • rapidly adapting (phasic) mechanoreceptor
  • deep pressure and vibration (deep touch)
  • vibrational role- detects surface texture
  • ovoid
  • dermal papillae of hands and feet
35
Q

What are Merkel cells?

A
  • non-encapsulated mechanoreceptors
  • light/sustained touch, pressure
  • oval-shaped

Modified epidermal cells:

  • stratum basale, directly above basement membrane
  • most populous in fingertips
  • also in palms, soles, oral and genital mucosa
36
Q

Where are Meissner’s corpuscles most concentrated?

A

-in thick hairless skin (finger pads and lips)

37
Q

Which epidermal nerve receptors are responsive to light touch and what are the fibres?

A
  • Meissner
  • Merkel
  • Free

AB

38
Q

Which epidermal nerve receptors are responsive to touch, pressure and what are the fibres?

A
  • Merkel
  • Ruffini
  • Pacinian
  • Free

AB, AD(delta)

39
Q

Which epidermal nerve receptors are responsive to vibration and what are the fibres?

A
  • Meissner
  • Pacinian

AB

40
Q

Which epidermal nerve receptors are responsive to temperature and what are the fibres?

A

-Thermoreceptors

AD(delta)
C

41
Q

Which epidermal nerve receptors are responsive to pain and what are the fibres?

A

-Nociceptor (free nerve endings)

AD(delta)
C

42
Q

Which main bacteria make up the skin micro biome?

A

Actinobacteria:

  • propionibacteria
  • corynebacteria

Firmicutes

  • clostridia
  • bacilli (Staphylococcus)

Bacteroidetes
Proteobacteria

43
Q

What are the 6 functions of the skin?

A
  • immunological barrier
  • physical barrier
  • thermoregulation
  • sensation
  • metabolic function
  • aesthetic appearance
44
Q

What role do Langerhans cells play in the immune barrier of the skin?

A
  • sentinel cells in epidermis
  • innate immune response against microbial threats
  • contribute to immune tolerance
  • form dense network with which potential invaders must interact
  • specialised at “sensing” environment
  • extend dendritic processes through intercellular tight junction to sample outermost layers of the skin (stratum corneum)
  • interpret microenvironmental context to determine appropriate quality of immune response
  • in absence of danger, promote expansion and activation of skin-resident regulatory cells - Tregs
  • when sense danger (PAMP), rapid initiation of innate antimicrobial responses
  • induction of adaptive response- power and specificity of T-cell
45
Q

What do Langerhans cells do in absence of danger?

A

-promote expansion and activation of skin-resident regulatory cells - Tregs

46
Q

What are Tregs?

A

-skin-resident regulatory cells

47
Q

What do Langerhans cells do when they sense danger?

A

-rapid initiation of innate antimicrobial response

48
Q

What are PAMPs?

A

-pathogen-associated molecular patterns

49
Q

Where in the skin are the Langerhans cells found?

A

-epidermis

50
Q

Which cells carry out immune surveillance in the dermis?-

A
  • tissue-resident T-cells
  • macrophages
  • dendritic cells

-rapid, effective immunological backup if epidermis breached

51
Q

What are the endogenous antibiotics in the skin?

A

Keratinocyte-derived endogenous antibiotics:

  • defensins
  • cathelicidins

-innate immune defence against bacteria, viruses and fungi

52
Q

What are the physical barrier function of the skin?

A
  • cornified cell envelope and stratum corneum restrict water and protein loss from skin
  • extensive inflammatory skin disease leading to erythroderma can cause high-output heart failure and renal failure due to transepidermal fluid loss
  • subcutaneous fat has important roles in cushioning trauma
  • UV barrier
  • melanin in basal keratinocytes- protection against IV-induced DNA damage
53
Q

How does the skin carry out thermoregulation?

A
  • vasodilation or vasoconstriction in deep or superficial vascular plexuses to regulate heat loss
  • eccrine sweat glands for cooling effect
  • role in fluid balance
54
Q

What are the metabolic functions of the skin?

A
  • vitamin D synthesis
  • subcutanenous fat
  • calorie reserve
  • skin contains 80% of total body fat (in non-obese individuals)
  • hormone leptin release from subcutaneous fat- acts on hypothalamus- regulates hunger and energy metabolism
55
Q

How does vitamin D synthesis occur in the skin?

A
  • UVB

- 7-dehydrocholesterol to pre-vitamin D3 to 1,25(OH)2D3

56
Q

What is the aesthetic appearance of skin important to understand?

A
  • psychosexual function

- increased risk of suicide

57
Q

What are the roles of the subcutaneous fat?

A
  • calorific reserve
  • insulation
  • cushioning from trauma
  • major source of leptin (suppresses appetite)
58
Q

What are the functions of the hair?

A
  • protection against external factors
  • sebum
  • apocrine sweat
  • thermoregulation
  • social and sexual interaction
  • epithelial and melanocyte stem cells
59
Q

Where are terminal hairs found?

A

-scalp, eyebrows, eyelashes

60
Q

What type of hair is on the rest of the body?

A

-vellus hairs

61
Q

What is the hair cycle?

A
  1. Anagen - where new hair forms and grows
    - 85% of hair
    - lasts 2-6 years
  2. Catagen -regressing phase
    - 1% of hair
    - lasts 3 weeks
  3. Telogen - resting phase
    - 10-15% of hair
    - lasts 3 months

-then loss of old hair

62
Q

What is the infundibulum in regards to the structure of hair?

A
  • uppermost portion of hair follicle

- from opening of sebaceous gland to surface of skin

63
Q

What is the isthmus in regards to the structure of hair?

A

-lower portion of the hair follicle between opening of sebaceous gland and insertion of arrestor pili muscle

64
Q

What is trichilemmal keratinisation?

A

-when epithelium keratinisation begins with lack of granular layer

65
Q

What is the bulge in regards to the structure of hair?

A
  • segment of outer root sheath located at insertion of arrector pili muscle
  • lower most portion of hair follicle, includes follicular dermal papilla and hair matrix
  • hair follicle stem cells reside here
66
Q

What roles do the hair follicle stem cells have?

A
  • hair follicle stem cells migrate downwards
  • generate anlagen hair follicle
  • enter hair bulb matrix
  • proliferate and undergo terminal differentiation to form hair shaft and inner root sheath
  • upwards (distally) to form sebaceous glands and to proliferate in response to wounding.
67
Q

What is the purpose of the outer root sheath (ORS) ?

A
  • extends along from hair bulb to infundibulum and epidermis

- serves as a reservoir of stem cells

68
Q

What is the purpose of the inner root sheath (ORS) ?

A
  • guides/shapes hair

- encloses follicular dermal papilla, mucopolysaccharide-rich strome, nerve fibre & capillary loop

69
Q

What are the 5 functions of the nails?

A
  • -protection of underlying distal phalanx
  • counterpressure effect to pulp important for walking and tactile sensation
  • increase dexterity/ manipulation of small objects
  • enhance sensory discrimination
  • facilitate scratching or grooming
70
Q

What is the nail plate?

A
  • final product of proliferation and differentiation of nail matrix keratinocytes
  • emerges from proximal nail fold
  • grows at 1-3mm/month
  • firmly attached to nail bed
  • lined laterally by lateral nail folds
71
Q

What is the nail matrix?

A
  • produces the nail plate
  • lies under proximal nail fold, above bone of distal phalanx (to which it is connected by a tendon)
  • lunula only visible proportion
  • nail matrix keratinocytes differentiate- lose their nuclei and are strictly adherent- cytoplasm completely filled by hard keratins
  • also contains melanocytes
72
Q

What is psoriasis?

A
  • chronic, immune-mediated disorder
  • polygenic predispositions combined with environmental triggers
  • sharply demarcated, scaly, erythematous plaques characterise most common form of psoriasis
  • common sites of involvement are scalp, elbows, knees, nails hand, feet, trunk, intergluteal fold
73
Q

What are the possible environmental triggers for psoriasis?

A
  • trauma
  • infections
  • medications
74
Q

What is the pathophysiology of psoriasis?

A
  • -stressed keratinocytes release DNA/RNA
  • form complex with antimicrobial peptides
  • induce cytokine (TNFa, IL-1 and IFN-a) production
  • activate dermal dendritic cells (dDCs)
  • dDCs migrate to lymph nodes
  • promote Th1, Th17, Th22 cells
  • chemokine release-migration of inflammatory cells into dermis
  • cytokine release
  • keratinocyte proliferation
  • psoriatic plaque
75
Q

What are the clinical features of psoriasis?

A
  • scaly erythematous plaques in extensor distribution
  • genital psoriasis
  • flexural psoriasis
  • palmoplantar psoriasis
  • subungal hyperkeratosis
  • salmon pink patches- Onycholysis
  • pitting
  • eryhtroderma
  • guttate psoriasis
76
Q

What is the management of psoriasis?

A

Therapeutic ladder

  1. Topical therapies:
    - vitamin D analogues
    - topical corticosteroids
    - retinoids
    - topical tacrolimus/ pimecrolimus
  2. Phototherapy:
    - narrowband UVB
    - PUVA (psoralen + UVA)
  3. Retinoids (hand dermatitis)
  4. Systemic immunosuppression:
    - methotrexate
    - ciclosporin
    - fumaric acid esters
    - apremilast
  5. Advanced therapies:
    - biologics (anti-TNF, anti-IL17, anti-IL23)
    - JAK inhibitors
77
Q

What is atopic eczema?

A
  • intensely pruritic chronic inflammatory condition
  • complex genetic disease with environmental influences
  • typically begins during infancy or early childhood
  • often associated with other ‘atopic’ disorder e.g asthma, rhinoconjunctivitis
  • acute inflammation of cheeks, scalp and extensors in infants
  • flexural inflammation and lichenification in children and adults
  • daily emollients and anti-inflammatory therapy are cornerstone of management
  • eczema (dermatitis)- umbrella term: atopic eczema, seborrhoea dermatitis, venous stasis eczema, allergic contact dermatitis, irritant contact dermatitis
78
Q

What is the pathophysiology of eczema?

A

Barrier defect:

  • reduced extracellular lipids and impaired ceramide production
  • increased transepidermal water loss (TEWL)
  • impaired protection against microbes and environmental allergens

Immune dysregulation:

  • staphylococcal superantigens stimulate Th2 lymphocyte responses and subvert T-regg
  • T-cell infiltrate- bias towards Th2 response
  • role of micro biome ?
  • eosinophils
79
Q

What is the function of filaggrins?

A

-binds and aggregate certain bundles and intermediate filaments to form cellular

80
Q

What are the clinical features of atopic eczema?

A

-infantile phase atopic dermatitis: erythematous, oedematous papule & plaques +- vesiculation

  • lichenification, crusting and excoriation and dyspigmentation postinflammatorydyspigmentation pigmentation
  • flexural dermatitis causing hypo pigmentation
  • flexural dermatitis
  • fissuring
  • allergic contact dermatitis
  • impetiginisation
  • gold crust
  • staphylococcus aureus
  • venous stasis eczema
  • eczema herpeticum
  • patients with atopic eczema are predisposed towards HSV infection that can spread rapidly, involve internal organs and be fatal
81
Q

What is the management of atopic eczema?

A

Lifestyle:

  • emollients
  • omission of soap

Clinical Nurse Specilaist involvement:

  • topical application technique
  • day treatment
  • habit reversal
  • co-morbidites
  • patch-testing
  • biopsy (e.g resistant nipple eczema should undergo biopsy to exclude Paget’s disease of the nipple)

Therapeutic ladder:

  1. Topical therapies:
    - topical corticosteroids- correct potency for correct site
    - retinoids (hand dermatitis)
    - topical tacrolimus/pimecrolimus
  2. Phototherapy:
    - narrowband UVB
    - PUVA (hand dermatitis)

-retinoids (hand dermatitis)

Systemic immunosuppression:

  • methotrexate
  • ciclosporin
  • azathioprine
  • mycophenolate mofetil

Advanced therapies:

  • biologics (anti-IL-4a, anti-IL13)
  • JAK inhibitors
82
Q

lecture slides

A

https://d3c33hcgiwev3.cloudfront.net/WDPKWv0bTE2zylr9G9xNpQ_1310a535ae8544ddabcb2fb28dbbe6a4_SV_Final_Derm_LE01Introduction_to_dermatology.pdf?Expires=1581206400&Signature=K4o82cbpgd9OPSPKzMtglQoq0SbRT4YRIV-FtbSJay5tI1Fyb9PGLde-26O8IXIU9oBl2FteAwfvSNu1gobvNQw21Puiy0rK7HIMmVKOjY1aOYpVMgcuYBFYGLd6yF-2Yf1k2uLVzKzc1YL16LoXLVGudIOjW8ZzR6Z62KXABVo&Key-Pair-Id=APKAJLTNE6QMUY6HBC5A

Musculoskeletal Rheumatology (6 decks)

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