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Charis & Ellie vs Dermatology > Physiology of the Skin > Flashcards

Physiology of the Skin Flashcards

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Dermatology Board Prep flashcards
1
Q

what are the components of skin?

A 
epidermis 
appendages (nails, hair, glands and mucosae)
dermo-epidermal junction 
dermis 
subcutis (mainly fat)
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2
Q

where does the epidermis come from embryologically?

A

periderm - starts at 4 weeks, fully developed by 26 weeks

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3
Q

where does the dermis come from embryologically?

A

mesoderm - below the ectoderm

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4
Q

where do the melanoblasts come from embryologically?

A

the neural crest - within 1st 3 months

they then go to the skin and once they are settled in the skin they for melnocytes in the basal layer

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5
Q

What are Blaschko’s lines

A

the developmental growth pattern of skin - it doesn’t follow the vessels/nerves/lymphatics

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6
Q

what is the epidermis?

A

the outer layer of stratified cellular squamous epithelium - 95% keratinocytes

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7
Q

what are the 4 layers of the epidermis - from top to bottom?

A

keratin layer
granular layer
prickle cell layer
basal layer

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8
Q

development of keratinocytes

A

formed in the basal layer and then move to the surface (takes around 28 days)
where they then shed into the environment as dead skin cells [known as epidermal turnover, this happens a lot quicker (loss of control) in psoriasis/skin cancer] - regulated by growth factors, cell death and hormones

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9
Q

What is the function of the keratin layer?

A

the keratinocytes is where vitamin D metabolism occurs

acts as a tight waterproof barrier, sole of foot/palm of hand etc. tend to have thicker keratin layers

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10
Q

what is the keratin layer composed of?

A

keratin
filaggrin and involucrin, corneocytes (type of keratinocyte, overlapping non-nucleated cell remnants)
insoluble cornified envelope and lamellar granules which release lipids

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11
Q

what is the function of the granular layer?

A

acts like glue to prevent things from coming in, (this layer is often deficient in eczema/psoriasis)
these cells lose their nuclei,
they are the origin of the cornified envelope, composed of: 2-3 layers of flatter cells, large keratohyalin granules (which contain structural filaggrin and involucrin proteins), odland [lamellar] bodies, high lipid content

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12
Q

what is the composition of the prickle cell layer?

A

larger polyhedral cells,
lots of desmosomes (connections, these are what give the spiky appearance),
intermediate filaments which connect to the desmosomes

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13
Q

what is the composition of the basal layer?

A

one cell thick
small cuboidal basal cells
highly metabolically active
composed of lots of intermediate filaments (keratins)

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14
Q

what are melanocytes?

A

pigment-producing dendritic cells - they convert tyrosine to melanin pigment
melanin absorbs light so acts as a natural density filter
absorbs UV rays to protect the DNA in the cells’ nuclei

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15
Q

types of melanin

A

eumelanin - brown/black

phaeomelanin - red/yellow

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16
Q

what are melanosomes

A

they are organelles in melanocytes

full melanosomes - melanin granules, are transferred to adjacent keratinocytes via dendrites

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17
Q

how many melanocytes do people have?

A

everyone has the same number regardless of skin tone

the melanocyte ratio = melanocyte: basal keratinocyte = 1:5 - 1:10

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18
Q

what is the MC1R gene?

A

encodes a protein which determines the balance of pigment in the hair and skin
if MC1R has 1 defective copy - freckling and if 2 defective copies - red hair and freckling

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19
Q

what are langerhan cells?

A

In the prickle cell layer of the epidermis, they are also found in the dermis and lymph nodes
They are dendritic cells, involved in the skin immune system, they are antigen-presenting cells so they pick up antigen in the skin and circulate them to lymph nodes via the lymphatic system
They have a mesenchymal origin (bone marrow)
Racket organelle (Birbeck granules) are found in Langerhans cells
There can be tumours of the Langerhans cells.

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20
Q

what are merkel cells?

A

They are found in the basal layer of the epidermis, between the keratinocytes and nerve fibres
They are mechanoreceptors (i.e. they respond to touch/sound etc.)
Merkel cell cancer is rare but very fatal (worse than melanoma), caused by viral infections.

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21
Q

What is the pilosebaceous unit?

A

a structure consisting of hair, hair follicle, arrector pili muscle and sebaceous gland

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22
Q

What are the phases of hair follicles?

A

Anagen - growing (3-7 yrs)
Catagen - involuting (3-4 weeks)
Telogen - resting (the hair that’s fallen out can be aggravated by psycho-social stress)

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23
Q

What are the types of hair?

A

lanugo - in utero
vellus - soft, fine hair, barely noticeable
terminal - thick hair e.g. armpits

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24
Q

What is telogen effluvium?

A

temporary hair loss usually after stress e.g. pregnancy/trauma and usually is lost from the top of the scalp

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25
Q

What is virilisation?

A

the development of physical male characteristics in a female - hair caused by excess androgen

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26
Q

What is alopecia?

A

hair loss, there are different types - alopecia aerate = autoimmune

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27
Q

What happens to skin appendages when there is a scar?

A

There is a permanent loss of the skin appendages

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28
Q

What is a nail made up of?

A

specialised keratins

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29
Q

What are the mucosal membranes?

A

usually not keratinised highly specialised membranes for function (eyes, mouth, nose, GU and GI tracts)

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30
Q

What is keratinised mucosal membranes a sign of?

A

skin disease

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31
Q

functions of the dermo-epidermal junction

A

support
anchorage
adhesion
growth and differentiation of basal cells
semi-permeable membrane acts as a barrier and filter

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32
Q

What is the dermo-epidermal junction made of?

A

lamina lucida - electron sparse area
lamina densa - electron dense area
sub-lamina densa zone

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33
Q

diseases of the dermo-epidermal junction

A

bullous pemphigoid - autoimmune
epidermolysis bullosa - genetic
the diseases are characterised by blisters

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34
Q

What is the dermis?

A

a connective tissue which allows movement - basically keeps the skin together

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35
Q

What is the dermis made of?

A 
ground substance 
fibroblasts
macrophages 
mast cells 
lymphocytes 
langerhans cells 
fibres (collagen and elastin)
muscles
glycoaminoglycans (GAGs)
blood vessels 
lymphatics 
nerves
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36
Q

Photo-ageing

A

when light breaks down the collagen and elastin in the dermis - causes those wrinkles

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37
Q

what is the blood vessel supply?

A

greater than metabolic need, horizontal plexus - too many can cause angioma (benign)

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38
Q

What is the order of vessels?

A 
arteriole to 
precapillary sphincters to 
capillary to 
postcapillary venules to 
collecting venules
39
Q

lymphatic vessels function

A

meshed network,
drain waste,
have important immune functions (immune surveillance by circulating lymphocytes and langerhans cells)
also channel micro-organisms/ toxins

40
Q

Chronic lymphoedema

A

may cause damaged/burst vessels - can potentially be caused by obesity

41
Q

Nerve supply

A 
somatic sensory (dermatomes) - free nerve endings
special receptors = Pacinian (pressure) and Meissner (vibration) corpuscles
42
Q

what is neurofibromatosis?

A

a genetic condition which can cause the development of benign tumours of nerve endings due to genetic defects in the chromosomes

43
Q

what are the 3 types of skin glands?

A

sebaceous glands
apocrine glands
eccrine glands

44
Q

what are the sweat glands?

A

apocrine and eccrine

45
Q

Characteristics of the sebaceous glands

A

cause acne
largest in the face and chest
hormone sensitive (glands are more active during/after puberty)
develops as part of pilosebaceous unit

46
Q

functions of the sebaceous gland

A

controls moisture loss
protects against fungal infection
holocrine secretion into pilary canal
they produce - sebum, squalene, wax, esters, triacylglycerol (TG) and free fatty acids (FFA)

47
Q

characteristics of apocrine glands

A

in the axillae and perineum

androgen dependent

48
Q

function of the apocrine glands

A

produces oily fluid

odour after bacterial decomposition

49
Q

location of the eccrine glands

A

whole skin surface - mainly palms soles and axillae, most commonly on the face
cooling by evaporation, moistens palms and soles to aid grip

50
Q

nerve supply to eccrine glands

A

sympathetic cholinergic nerve supply - mental, thermal and gustatory (taste) stimulation

51
Q

Functions of the eccrine glands

A

thermoregulation
works like a kidney (ultrafiltration)
2-4 million glands,
NaCl + HCO3 (bicarbonate) are reabsorbed resulting in hypotonic fluid

52
Q

functions of skin

A 
barrier 
thermoregulation 
immune defence 
metabolism and detoxification 
communication 
sensation
53
Q

what happens when there is failure of the barrier function?

A

fluid loss = dehydration
protein loss = hypoalbuminaemia
infection

54
Q

What is the purpose of the barrier function?

A

Physical - friction, mechanical trauma, UV radiation
Chemical - irritants, allergens and toxins
Pathogens - bacteria, viruses and fungi

55
Q

Examples of diseases of the barrier finction

A

steroid-sulphatase deficiency X linked ichthyosis
cumulative irritant hand dermatitis
Ulcer following compound fracture

56
Q

What happens when there is failure of the thermoregulation function?

A

heat loss = hypothermia

57
Q

How is the thermoregulation achieved?

A

warm/cold-sensitive thermoreceptors
behavioural changes
controls sweating/shivering/ blood supply
(too hot - blood flow increases so heat is lost, too cold - opposite)

58
Q

Diseases of the thermoregulation function

A

frostbite

59
Q

What happens when there is failure of the metabolism and detoxification function?

A

disordered thyroxine metabolism

60
Q

vitamin D metabolism is by what UV light

A

290 to 320 nm ultraviolet

61
Q

vitamin D3 converted from what by UV light

A

cholecalciferol (7-dehydrocholesterol) to Vitamin D3

62
Q

how is vitamin D3 stored?

A

As hydroxycholecaiferol in the liver

63
Q

What is hydroxycholecaiferol converted to

A

1,25-dihydroxycholecalciferol in the kidney

64
Q

Thyroid hormone metabolism

A

thyroxine (T4) - triiodothyronine (T3)

65
Q

which is the more active thyroid hormone?

A

T3 - more active than T4

66
Q

where does T4-T3 conversion occur

A

20% conversion occurs in the thyroid gland

80% occurs in the peripheral (to thyroid) tissues including the skin

67
Q

What does failure of the immune defence function do?

A

allows spread of infection

68
Q

what is the immune defence of the skin involved in?

A

protection against infection
- specific and non-specific (induces immunity responses)
sunlight responses
allergic reactions

69
Q

What cells are involved in the immune defence?

A

langerhans cells and T cells

70
Q

What does a failure in the communication function cause?

A

inability to display healthy skin = stigma

71
Q

What does the failure in the sensation function cause?

A

pain

72
Q

What are the sensory functions of the skin?

A 
touch 
pressure 
vibration 
pain 
itch 
heat 
cold
nerve endings and receptors in skin
73
Q

Examples of a disease of the sensory function of skin

A

neuropathic ulcer (leprosy)

74
Q

Immune responses of the skin

A

normal - infection is controlled
hypersensitivity - overreaction to antigen
immunodeficiency -infection not controlled, tumours may form
autoimmunity - reaction to host tissue, chronic inflammation

75
Q

what do keratinocytes (KC) do?

A

sense pathogens and help mediate an immune response
Produce AMPs - antimicrobial peptides - directly kill pathogens, high levels of AMPs in patients with psoriasis
Produce cytokines (proteins secreted from 1 cell and bind to another cell) and chemokines - recruit and regulate cells in the immune system

76
Q

Where are keratinocytes found?

A

the epidermis

77
Q

what do langerhan’s cells do?

A

the main skin resident immune cell
they process lipid antigens (Ag) and microbial fragments and present them to effector T cells
they help activate T cells

78
Q

where are langerhans cells found?

A

the epidermis

79
Q

where are the T cells found?

A

the epidermis and dermis
CD8+ cells - in the epidermis mainly
CD4+ and CD8+ cells - in the dermis
large number in healthy skin

80
Q

3 examples of CD8+ cells associated with inflammation

A

Th1 - psoriasis
Th2 - atopic dermatitis
Th17 - psoriasis and atopic dermatitis

81
Q

How are T cells developed and activated?

A

produced in the bone marrow and sensitised in the thymus

T cell receptor (TCR) and major histocompatibility complex (MHC) are involved in Ag recognition and T cell activation

82
Q

What enhances Ag recognition and T cell activation?

A

CD4 +
Th1 = activates macrophages to destroy microorganisms produces IL2 and IFNy
Th2 = helps B cells make antibody, produces IL4, IL5 and IL6

CD8 +
can kill infected cells directly, important in protection against viruses and cancer

83
Q

What are the types of dendritic cells?

A 
dermal DC = involved in Ag presenting and secreting cytokines and chemokines 
Plasmocytoid DC (pDC) = produce IFN--alpha, found in diseased skin
84
Q

What immune cells are found in the dermis?

A

dendritic cells
macrophages
neutrophils (circulating leukocytes attracted to tissue by chemokines)
mast cells

85
Q

What do activated mast cells release?

A

Preformed (really quick) - tryptase, chymase, TNF, histamine
Newly synthesised - IL, TNF, IFNy

86
Q

What activates mast cells?

A

IgE binding - allergy
physical trauma
certain drugs
micro-organisms

87
Q

What is a MHC?

A

a bunch of genes located on chromosome 6
Class 1 - found on almost all cells, they present (endogenous) Ag to Th cells
Class 2 - found on APC (B cells, macrophages), they present exogenous Ag to Th cells
very important in self and non-self recognition

88
Q

What types of immunodeficiency are there?

A

primary (genetic)
secondary (acquired)
main sign is getting lots of infections

89
Q

What is type 1 hypersensitivity?

A

antibody mediated (IgE)

90
Q

Early exposure to antigen in type 1 hypersensitivity

A

production of IgE, IgE binds to the FceR1 receptor on mast cells
very rapid, minutes, wheal and flare

91
Q

Late exposure to the antigen in type 1 hypersensitivity?

A

rapid cross linking of the receptors, signal transduction and degranulation of the mast cell
hours, cellular infiltration, nodule

92
Q

what is type 2 hypersensitivity?

A 
antibody mediated (IgG, IgM)
mechanisms are important in autoimmunity and transplantation, haemolytic disease of the newborn and blood transfusion recipients
93
Q

what is type 3 hypersensitivity?

A 
antibody mediated (IgG, IgM)
arthus reaction - slower than type 1, faster than type IV skin response 
involved in certain drug reactions
94
Q

What is type 4 hypersensitivity?

A

cell mediated (Th1 cells)
delayed response
T cell mediated response which then recruits other cells to the site
involved in tuberculin reaction and contact allergies

Charis & Ellie vs Dermatology (26 decks)

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