Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Z YEAR 1 BRS Bones > Introduction to dermatology > Flashcards

Introduction to dermatology Flashcards

1
Q

How does the skin develop?

A

Skin arises by juxtaposition of two major embryological elements

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

Where does the epidermis originate from?

A

Ectoderm

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

Where does the dermis arise from?

A

arises from mesoderm that comes into contact with inner surface of epidermis

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

What is the mesoderm essential?

A

for inducing differentiation of epidermal structures (e.g. hair follicle)

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

When does the epidermis form? What is it?

A
  • by week 4

- single basal layer of cuboidal cells

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

What happens in week 5?

A
  • Secondary layer of squamous, non-keratinising cuboidal cells (periderm) develops
  • Generates white, waxy protective substance - vernix caseosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens in week 11?

A

basal layer of cuboidal cells (stratum germinativum) proliferates to form multilayered intermediate zone and differentiates into four more superficial strata

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

What are the four other superficial strata?

A
  1. Spinosum(spinous),
  2. granulosum(granular)
  3. lucidum(clear; found on palms of hands and soles of feet), 4.corneum(horny).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens in weeks 9-13?

A

●Weeks 9-13 development of hair follicles in stratum germinativum and appearance of lanugo hair

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

What are melanocytes?

A

-derived from neural crest → differentiate into melanoblasts → migrate dorsally between week 6-8 to developing epidermis (& dermis) and hair folliicles
●By week 12-13, most melanoblasts have reached destination and differentiated into melanocytes
●Subset of melanoblasts form melanocyte stem cells in hair follicle bulge that replenish differentiated melanocytes

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

What happens in week 10-17?

A

●Epidermal ridges protrude as troughs into developing dermis beneath neurovascular supply develops into dermal papillae

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

How are melanocytes regulated?

A

●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 pheomelanin
•ACTH can also up-regulate expression of MC1R gene

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

What happens with exposure to UV with melanocytes?

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

What is the structure of the skin?

A 
●Epidermis: 
●Basement membrane (dermal-epidermal junction)
●Dermis: 
•Connective tissue
•Subcutaneous fat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the structure of epidermis?

A

●Epidermis- > 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 → surface in ~ 30 days
●Accelerated in skin diseases (e.g. psoriasis)

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

What does the filamentous cytoskeleton of keratinocytes contain?

A
  • Actin‐containing microfilaments (7nm)
  • Tubulin‐containing microtubules (20-25nm)
  • Intermediate filaments (keratins) (7-10nm)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the role of keratins?

A
  • Structural properties
  • Cell signalling
  • Stress response
  • Apoptosis
  • Wound healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are gap junctions?

A
  • Clusters of intercellular channels (connexons)
  • Directly form connections between cytoplasm of adjacent keratinocytes
  • Essential for cell synchronization, cell differentiation, cell growth and metabolic coordination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are adherens junctions?

A
  • Transmembrane structures

* Engage with actin skeleton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are tight junctions?

A

•Role in barrier integrity and cell polarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are some other cells in the epidermis?

A 
1. Melanocytes 
•Dendritic 
•Distribute melanin pigment (in melanosomes) to keratinocytes 
2. Langerhans cells 
•Dendritic 
•Antigen‐presenting cells 
3. Merkel cells 
•Mechanosensory receptors
4. Mast cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is in the basement membrane?

A

●Aka dermal-epidermal junction
●Proteins and glycoproteins
•Collagens (IV, VII), laminin, integrins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the function of the basement membrane?

A
  • Cell adhesion

- Cell migration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does the dermis do?

A

Supporting (extracellular) matrix– provides resilience

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the papillary dermis?

A
  • Superficial
  • Loose connective tissue
  • Vascular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the reticular dermis?

A
  • Deep
  • Dense connective tissue
  • Forms bulk of dermis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the structure of the dermis?

A
  1. Proteins
    a) Collagen (80-85% of dermis) – mainly types I and III
    b) Elastic fibres (2-4%) – fibrillin, elastin
  2. Glycoproteins – fibronectin, fibulin, intregrins – facilitate cell adhesion and cell motility
  3. Ground substance – between dermal collagen and elastic tissue – glycosaminoglycan / proteoglycan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the cells in the dermis?

A
  1. fibroblasts (primary cells)
  2. Histiocytes
  3. Mast cells
  4. Neutrophils
  5. Lymphocytes
  6. Dermal dendritic cells
30
Q

What is the blood supply?

A

Blood supply – deep and superficial vascular plexus

•Does not cross into epidermis

31
Q

What is the innervation in the skin?

A

-Innervation
•Sensory – free, hair follicles, expanded tips
•Autonomic:
1. Cholinergic – eccrine
2. Adrenergic – eccrine and apocrine
-Pilosebaceous unit
-Arrector pili muscle / arterioles / shunts

32
Q

Describe innervation in skin

A
  • One million afferent nerve fibers
  • Form branching network, often accompanying blood vessels, to form a mesh of interlacing nerves in superficial dermis
  • Distribution varies by body site
  • Face, extremities & genitalia > rest of skin
33
Q

How do the afferent nerves terminate?

A

afferent nerves:

  1. corpuscular -> encapsulated receptors (dermis e.g. Pacinina Messiners)
  2. non-encaspilated receptor (epidermis e.g. Merkel cell)
34
Q

What is the Meissnre’s corpuscle?

A

Meissner’s corpuscle (aka tactile corpuscles)
•Encapsulated, unmyelinated mechanoreceptors
•Light Touch (+slow vibration)
•Senses low-frequency stimulation at level of dermal papilla
•Most concentrated in thick hairless skin, (finger pads and lips)

35
Q

What is Ruffini corpuscle?

A 
Ruffini Corpuscule (aka Bulbous corpuscle)
•Slow acting mechanoreceptor 
•Sensitive to skin stretch
•Deeper in dermis
•Spindle-shaped 
•Highest density around fingernails 
•Monitors slippage of objects
36
Q

What is Pacinian corpuscle?

A

Pacinian corpuscle (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

37
Q

What is the Merkel cell?

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 & genital mucosa
38
Q

What is the microbiome in the skin?

A
  • Microbiota: bacteria, fungi and viruses
  • ~ 1 million bacteria /cm2 skin
  • Predominantly Actinobacteria (including Propionibacteria and Corynebacteria), Firmicutes (Clostridia and Bacilli [Staphylococcus] , Bacteroidetes & Proteobacteria
  • Composition of each niche depends on environment
  • Role in immune-modulation and epithelial health
  • Role in disease
39
Q

What is the function of skin?

A
  • Immunological barrier
  • Physical barrier
  • Thermoregulation
  • Sensation
  • Metabolic functions
  • Aesthetic appearance
40
Q

How is the skin part of the immune barrier?

A

-Langerhans cells
-Dendritic cell (DC)/macrophage family
•Sentinel cells in epidermis
-Initiate immune response against microbial threats
-Also contribute to immune tolerance
-Form dense network with which potential invaders must interact.

41
Q

What are langerhans cells?

A
  • Specialised at “sensing” environment
  • Extend dendritic processes through intercellular tight junctions to sample outermost layers of skin (stratum corneum)
  • Interpret microenvironmental context a → 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
42
Q

How is immune surveillance carried out in the the dermis?

A

•Tissue‐resident T-cells
•Macrophages
•Dendritic cells
Rapid, effective immunological backup if epidermis breached

43
Q

How is the skin a physical barrier?

A
  • Physical barrier against external environment
  • Cornified cell envelope and stratum corneum restrict water and protein loss from skin → NB high-output cardiac failure and renal failure in extensive skin disease
  • Subcutaneous fat has important roles in cushioning trauma
  • UV barrier
  • Melanin in basal keratinocytes - protection against UV-induced DNA damage
44
Q

What are some endogenous antibiotics?

A

Keratinocyte‐derived endogenous antibiotics (defensins and cathelicidins) → innate immune defence against bacteria, viruses and fungi

45
Q

How is skin used in thermoregulation?

A
  • Vasodilatation or vasoconstriction in deep or superficial vascular plexuses → regulate heat loss.
  • Eccrine sweat glands → cooling effect
  • Role in fluid balance
46
Q

How is the skin used in metabolic function?

A
  • Vitamin D synthesis
  • Subcutaneous fat
  • Calorie reserve
  • 80% of total body fat (in non-obese individuals)
  • Hormone (leptin) release - acts on hypothalamus → regulates hunger and energy metabolism
47
Q

What is the function of hair?

A
  • Protection against external factors
  • Sebum
  • Apocrine sweat
  • Thermoregulation
  • Social and sexual interaction
  • Epithelial and melanocyte stem cells
48
Q

What are terminal and velds hairs?

A
  • Terminal hairs → scalp, eyebrows and eyelashes

* Rest of body → vellus hairs (except palms, soles, mucosal regions of lips, and external genitalia.

49
Q

How is the hair cycle used in function of hair and nails?

A 
•Three components of hair cycle
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. \
50
Q

What is the structure of hair?

A
  • Human skin contains pilosebaceous follicles and sweat glands.
  • Hair follicles (pilosebaceous unit)
  • Pockets of epithelium continuous with superficial epidermis
  • Envelop a small papilla of dermis at their base.
51
Q

What is the bulge in hair?

A
  • Segment of outer root sheath located at insertion of arrector pili muscle
  • Hair follicle stem cells reside here
  • Migrate:
    1. Downward → generate lower anagen hair follicle → enter hair bulb matrix, proliferate and undergo terminal differentiation to form hair shaft and inner root sheath.
    2. Upwards (distally) → form sebaceous glands and to proliferate in response to wounding
52
Q

What is the bulb in hair?

A

•Lower most portion of hair follicle, includes follicular dermal papilla and hair matrix
-Outer root sheath (ORS)
•Extends along from hair bulb to infundibulum and epidermis
•Serves as a reservoir of stem cells
-Inner root sheath
•Guides / shapes hair
•Encloses follicular dermal papilla, mucopolysaccharide-rich strome, nerve fiber & capillary loop.

53
Q

What is the function of nails>

A
  1. Protection of underlying distal phalanx
  2. Counterpressure effect to pulp important for walking and tactile sensation
  3. Increase dexterity / manipulation of small objects
  4. Enhance sensory discrimination
  5. Facilitate scratching or grooming
54
Q

What is the structure of nails?

A 
Nail plate
•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 
•Detaches at hyponychium
•Lined laterally by lateral nail folds
55
Q

What are two parts of the hair?

A
  • Arrector pili (smooth muscle) extends at angle between surface of dermis and point in follicle wall.
  • Holocrine sebaceous glands which open into pilary canal → in axillae - follicles associated with apocrine glands.
56
Q

What are the sections of a hair follice?

A
  1. Infundibulum
    •Uppermost portion of hair follicle - from opening of sebaceous gland to surface of skin
  2. Isthmus
    •Lower portion of upper part of hair follicle between opening of sebaceous gland and insertion of arrector pili muscle
    •Epithelium keratinization begins with lack of granular layer named “trichilemmal keratinisation”
57
Q

What is the nail matrix?

A
  1. Produces nail plate
  2. Lies under proximal nail fold, above bone of distal phalanx (to which it is connected by a tendon
  3. Lunula only visible proportion
  4. Nail matrix keratinocytes differentiate → lose their nuclei and are strictly adherent - cytoplasm completely filled by hard keratins
  5. Also contains melanocytes
58
Q

What is an overview of psoriasis?

A
  • Chronic, immune-mediated disorder
  • Polygenic predisposition combined with environmental triggers, e.g. trauma, infections, or medications
  • Pathophysiology involves T-cells and their interactions with dendritic cells and cells involvement in innate immunity, including keratinocytes
  • Sharply demarcated, scaly, erythematous plaques characterise most common form of psoriasis
  • Common sites of involvement are scalp, elbows and knees, followed by nails, hands, feet and trunk (including intergluteal fold)
  • Psoriatic arthritis is most common systemic manifestation
59
Q

What is the pathophysiology of psoriasis?

A
  1. Stressed keratinocytes release DNA / RNA → form complex with antimicrobial peptides → induce cytokine (TNFα, IL-1 and IFN-α) production → activate dermal dendritic cells (dDCs)
  2. dDCs migrate to lymph nodes → promote Th1, Th17, Th22 cells → chemokine release - migration of inflammatorycells into dermis → cytokine release → keratinocyte proliferation → psoriatic plaque
60
Q

What are the clinical features of psoriasis?

A
  • Scaly erythematous plaques in extensor distribution
  • Erythroderma
  • Guttate psoriasis
  • Genital psorisasis
  • Flexural psoriasis
  • palmoplntar psoriasis
  • subungual hyperkeratosis
  • Onycholysis (salmon pink patches)
  • pitting
61
Q

What is the lifestyle management of psoriasis?

A

Lifestyle
•Alcohol
•Smoking
•Co-morbidities

62
Q

What is the therapy ladder for psoriasis?

A
  • Topical therapies
  • Vitamin D analogues
  • Topical corticosteroids
  • Retinoids
  • Topical tacrolimus / pimecrolimus
  • Phototherapy
  • Narrowband UVB
  • PUVA (Psoralen + UVA)
63
Q

What is the overview of atopic eczema?

A
  • Intensely pruritic chronic inflammatory condition
  • Complex genetic disease with environmental influences
  • Typically beings during infancy or early childhood
  • Often associated with other ‘atopic’ disorders 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, seborrhoiec dermatitis, venous stasis eczema, allergic contact dermatitis, irritant contact dermatitis
64
Q

What is the treatment of psoriasis?

A

-Retinoids (hand dermatitis)
1. Systemic immunosuppression
•Methotrexate
•Ciclosporin
•Fumaric acid esters
•Apremilast
2. Advanced therapies
•Biologics (anti-TNF, anti-IL17, anti-IL23)
•JAK inhibitors

65
Q

What is the barrier defect is eczema pathophysiology?

A
  • Filaggrin - bind and aggregate keratin bundles and intermediate filaments to form cellular scaffold in corneocytes
  • Reduced extracellular lipids and impaired ceramide production
  • Increased transepidermal water loss (TEWL)
  • Impaired protection against microbes and environmental allergens
66
Q

What is the immune dysregulation in eczema pathophysiology?

A
  • Staphylococcal superantigens stimulate Th2 lymphocyte responses and subvert T‐reg
  • T-cell infiltrate - bias towards Th2 responses
  • Role of microbiome?
  • Eosinophils
67
Q

What are the clinical features of atopic eczema?

A
  1. Infantile phase atopic dermatitis: erythematous, oedematous papule & plaques ± vesiculation
  2. Lichenification, crusting and excoriation and dyspigmentation postinflammatorydyspigmentation pigmentation. (c) Flexural dermatitis causing hypopigmentation. (d) Flexural dermatitis. dyspig
  3. Fissuring
  4. Allergic contact dermatitis
  5. Impetiginisation
    Gold crust
    Staphylococcus aureus
  6. Venous stasis eczema
    7.Eczema
    herpeticum
  7. emergency
    HSV
68
Q

What is the lifestyle management of atopic eczema?

A 
•Emollients
•Omission of soap
-Clinical Nurse Specialist involvement
•Topical application technique
•Day treatment
•Habit reversal
-Co-morbidities
-Patch testing
-Biopsy
69
Q

What is the therapeutic ladder for atopic eczema?

A 
1. Topical therapies
•Topical corticosteroids - correct potency for correct site
•Retinoids (hand dermatitis)
•Topical tacrolimus / pimecrolimus
2. Phototherapy
•Narrowband UVB
•PUVA (hand dermatitis)
70
Q

What is the treatment of atopic eczema?

A
  1. Retinoids (hand dermatitis)
  2. Systemic immunosuppression
    •Methotrexate
    •Ciclosporin
    •Azathioprine
    •Mycophenolate mofetil
  3. Advanced therapies
    •Biologics (anti-IL-4α, anti-IL13)
    •JAK inhibitors

Z YEAR 1 BRS Bones (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions