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Dermatology > skin structure and function > Flashcards

skin structure and function Flashcards

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Dermatology Board Prep flashcards
1
Q

what is the largest organ

A

skin

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2
Q

how many skin diseases are there

A

> 2000

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3
Q

what percentage of the population suffers from a skin condition

A

25%

1:5

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4
Q

describe the epithelium of the dermis

A

stratified squamous epithelium-1.5mm

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5
Q

where did the epidermis come from

A

it came from the Ectoderm cells form single layer periderm

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6
Q

what is the biggest component of the epidermis

A

keratinocytes

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7
Q

what other cells are present in the epidermis

A

o Melanocytes (basal & suprabasal)
o Langerhans cells (suprabasal)
o Merkel cells (basal)

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8
Q

what are the 4 layers of the epidermis

A

Keratin layer
Granular layer
prickle cell layer
basal layer

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9
Q

where did the dermis come from

A

mesoderm bellow ectoderm

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10
Q

what is the dermis

A

connective tissue

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11
Q

what are the cells present in the dermis

A 
fibroblasts, 
macrophages, 
mast cells, 
lymphocytes, 
Langerhans cells
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12
Q

what are the fibres in the dermis

A

collagen
fibrin
^ produced by the fibroblast
elastin

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13
Q

what other parts are present in the dermis

A

Muscles,
blood vessels,
lymphatics,
nerves

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14
Q

what skin type is the stronger

A

dark skin

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15
Q

what is the basal layer for

A

stem cells

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16
Q

true or false: keratinocytes have no nucleus

A

TRUE

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17
Q

what are Appendages

A 
nails 
hair 
glands 
muscles 
nerves 
blood vessels 
ect
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18
Q

what junctions are present in the prickle cell layer

A

desmosomes that attach and un attach

* they contain intermediate filament

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19
Q

what are the Blaschko’s lines

A

the developmental pattern of skin

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20
Q

describe skin conditions that follow the Blaschko’s lines

A

congenital conditions

mosaic

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21
Q

what are the layers of the skin

A 
•	Epidermis
•	Appendages
o	Nails
o	Hair
o	Glands
o	Mucosae
•	Dermo-epidermal junction
•	Dermis: connective tissue, less cellular 
•	Sub-cutis: predominantly fat
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22
Q

what is the name of the muscle that lifts the hair shaft

A

Arrector pili muscle

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23
Q

what is the regulation of skin turnover

A

• Balance between cells in/out

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24
Q

what is the skin turnover controlled by

A
  • Growth factors
  • Cell death
  • Hormones
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25
Q

what happens when the regulation of the skin is lost

A
  • Skin cancer

* Psoriasis

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26
Q

what are the steps of differentiation

A
  • Keratinocytes migrate from basement membrane
  • Continuous regeneration of epidermis
  • 28 days from bottom to top
  • This period can change in disease
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27
Q

describe the thickness of the basal layer

A

one cell thick

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28
Q

describe the cell types in the basal layer

A

small cuboidal

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29
Q

true or false: there are Lots of intermediate filaments (keratin) in the basal layer

A

TRUE

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30
Q

true or false the basal layer is Highly metabolically active

A

TRUE

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31
Q

describe the cell types in the Prickle cell layer

A

Larger polyhedral cells

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32
Q

describe the cell types in the Granular layer

A

2-3 layers of flatter(squamous) cells

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33
Q

what does the Granular layer contain

A

• Large keratohyalin granules – contain structural filaggrin & involucrin proteins

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34
Q

How do you retain the water in your skin

A
  • the granular cells rupture and release granules. containing filaggrin.
  • Enzymes take the filaggrin protein and snip it into short pieces. So you have groups of 2 or 3 amino acids. These amino acids bind water molecules therefore they are hydroscopic.
  • This means that there is a sudden massive accumulation of tinny substances that bind water (emollient- it prevent water from leaving the body).
  • If we don’t have the filaggrin mechanism the skin gets very dry and this for example leads to eczema in atopic dermatitis
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35
Q

what are Corneocytes

A

Corneocytes are terminally differentiated keratinocytes and compose most if not all of the stratum corneum, the outermost part of the epidermis. They are regularly replaced through desquamation and renewal from lower epidermal layers, making them an essential part of the skin barrier property.

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36
Q

true or falses keratine layer contains non-overlaping nucleated cells

A

false

• overlapping non-nucleated cell remnants

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37
Q

true or falses keratine layer contains Insoluble cornified envelope

A

true

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38
Q

true or falses Lamellar granules in keratine layer release ions

A

false they release lipids

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39
Q

give an example of viral infection affecting keratinocyte

A

Human papillomavirus infection of keratinocytes causes warts.

• HPV thrives in the keratin and epidermis layers as they can’t handle the heat in the dermis

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40
Q

explain why keratinocytes are waterproof

A
  • Tight waterproof barrier
  • Mechanical protection
  • They bind fatty acids and cross-link them. This is why water doesn’t enter your body.
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41
Q

how do Viral warts change the epidermis

A

the epidermis thickens and becomes round and inflamed. They are not transmitted to other people unless they have a breached barrier.

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42
Q

true or false Mucosal membranes varies depending on the area

A

true

43
Q

Masticatory Mucosal

A

keratinised to deal with friction/pressure

44
Q

Lining mucosa

A

non-keratinised

45
Q

Specialised mucosa

A
  • tongue papillae – taste
46
Q

Ocular mucosa

A

Lacrimal glands, eye lashes, sebaceous glands

47
Q

why is the oral mucosa red

A

In the mouth because the keratin layer is so thin the vascular plexus shines through giving it the red layers. If we have thickening it look white and that is bad news

48
Q

what does the Hypodermis (subcutaneous) consist of

A

it mostly consist of fat lobules and droplets each with a membrane.

49
Q

why is the Hypodermis important

A

This is important as it allows all of the dermis and all of the epidermis to move across

50
Q

what happens if you block the Spacious glands

A

skin becomes dry

51
Q

how does acne occur

A

bacteria feeds on the oil produced by spacious glands.

it breaks down the fatty acid causing inflation.

These break down lipids trigger inflammation and the buildup of pus

52
Q

what is the commonest side effect of acne treatment

A

to treat acne you have to dry the oil, this results in the skin becoming dry and can cause eczema.

53
Q

what are milia

A

oil trapped underneath the skin due to a block in the skin follicle.

54
Q

describe Melanocyte migration

A

• Migrate from the neural crest to the epidermis in the first 3 months of foetal development.

55
Q

why do melanocytes look like brain cells

A

they migrate from the same neural crest

56
Q

true or false melanocytes have synapse and synaptic functions.

A

True

57
Q

where are melanocytes present

A

basal layer

58
Q

what are melanocytes described as

A

They are described as pigment-producing dendritic cells

59
Q

what are melanosomes’

A

melanocyte organelles that contain pigments

• Full melanosomes (‘melanin granules’) transferred to adjacent keratinocytes via dendrites

60
Q

melanocytes convert tyrosine to what

A

to melanin pigment

61
Q

what colour is Eumelanin

A

brown or black

62
Q

what colour is Phaeomelanin

A

red, yellow

63
Q

why is Melanin described as a neutral density filter

A

as it absorbs light

64
Q

true or false melanocytes Form a protective cap over the nucleus

A

TRUE

Melanin caps protect the nuclear DNA in basal cells

65
Q

how do melanocytes transport melanin

A

melanin gets transported through the axon of the melanocyte to the keratinocyte

66
Q

what is the other name for the keratine layer

A

stratum corneum

67
Q

true or false Hair does some protections against sunlight

A

true

For examples animals who have lots of hair tend to not have lots of melanin in their skin

68
Q

Describe VITILIGO

A
  • Vitiligo represents an autoimmune disease with loss of melanocytes
  • Melanocytes are being attacked by cytotoxic lymph cells
  • Self-limited
69
Q

Describe ALBINISM

A

In this disorder, there is a genetic partial loss of pigment production.

70
Q

Describe NELSON’S SYNDROME

A

In this disorder, melanin production stimulating hormones are produced in excess by the pituitary glands.

71
Q

what are Langerhans cells

A

Tissue-resident macrophages

72
Q

what is the origin of Langerhans cells

A

Mesenchymal origin – bone marrow

73
Q

where are Langerhans cells resident

A

Prickle cell level in epidermis

• Also found in dermis and lymph nodes

74
Q

what appearance do Langerhans cells have

A
  • Tennis racket appearance

* Antigen-presenting cells

75
Q

where are Merkel cells found

A
  • basal

* between keratinocytes & nerve fibres

76
Q

what type of receptors are Merkel cells

A

• mechanoreceptors

77
Q

what is the function of Merkel cells

A
  • connects 2 nerve endings
  • direct entry point to the central nervous system.
  • Sense of feeling
78
Q

what is the cause of Merkel cell cancer

A

• caused by viral infection (polyomavirus)

79
Q

describe Hair follicles “Pilosebaceous unit”

A

• Epidermal component plus dermal papilla

80
Q

where does hair pigment come from

A

• Hair pigmentation via melanocytes above the dermal papilla

81
Q

where does the hair follicle grow from

A
  • Hair branches out from the epidermis and becomes a bud
  • Then at the same time, something else also buds out to the side and becomes the sebaceous gland.
  • The papilla comes in from the dermis (comes from the mesoderm)
  • The stem cells come from the bulge on the side
82
Q

Phases of growth

A 
Anagen 	=  growing
Catagen 	=  involuting (around a month) 
Telogen  =  resting
83
Q

which hormones influence the growth of haiur

A

thyroxine, androgens

84
Q

types of hair growth

A

Lanugo (in utero),
vellus, childhood
terminal, adult

85
Q

true or false • In humans the telogen phase is asynchronous

A

true

it doesn’t occur at the same time unlike animals

86
Q

what is Telogen effluvium

A

Telogen effluvium occurs when there is a marked increase in the number of hairs shed each day.
eg during chemotherapy
it grows back afterwards
it usually occurs because of a sharp drastic change in the levels of hormones

After Childbirth is an example or a contraceptive. Stress is also a cause.

87
Q

Describe Virilisation

A

is a condition in which a female develops characteristics associated with male hormones (androgens), or when a new-born has characteristics of male hormone exposure at birth. due to excess androgen from a tumour

88
Q

Nails

A 
•	Specialised keratins
•	Nail matrix / root similar to hair bulb
•	Growth rate  0.1mm  per day
–	Fingers > toes
–	Summer > winter
•	Some drugs increase nail / hair growth
•	Hyponychium–secures the free nail edge
89
Q

what is the function of Dermo- epidermal Junction

A

• Interface between epidermis and dermis
• Key role in epithelial–mesenchymal interactions:
– Support, anchorage, adhesion, growth and differentiation of basal cells
– Semi-permeable membrane acting as barrier and filter
– Important in terms of structure and what can go wrong in diseases
– Complex structure filled with protein desmosomes and collagen.

90
Q

what are the layers of Dermo- epidermal Junction

A

Lamina lucida
lamina densa
sub-lamina densa zone

91
Q

describe Bullous Pemphigoid

A
  • Occurs in older patients
  • It occurs when an antibody is created by immune cells against the junction
  • Its an inflammatory response causing Bulli
92
Q

how can we treat Bullous Pemphigoid

A

steroids

93
Q

describe Epidermolysis Bullosa

A
  • Rare
  • Children usually
  • No cure
  • Inheritance where there is a defect in the proteins that make the junction
  • Can be life threatening
  • Causes deformities and scarring
94
Q

Describe Intrinsic ageing

A

Happens to everyone and everywhere

95
Q

Describe Extrinsic ageing

A

caused by UV light, smoking, pollution, heat

96
Q

Describe Hypertrophic photoaging

A

this is characterised by deep furrows and a leathery appearance

97
Q

Describe Atrophic photoaging

A

this is characterised by telangiectasia, a smooth, relatively unwrinkled appearance, and the development of a variety of benign and malignant skin lesions.

98
Q

what are the 2 types of Extrinsic ageing

A

Hypertrophic photoaging

Atrophic photoaging

99
Q

what type of plexuses of blood vessels are present in the dermis

A

Horizontal plexuses

100
Q

describe angioma

A
  • When the blood vessels go wrong in the dermis.
  • Its benign dilatation of the blood vessels
  • Can bleed easy and hard to stop
101
Q

what are the treatments of Angioma

A

laser -for large areas
surgery -for small areas
topical beta blockers

102
Q

true or false lymphatic vessels follow vertical plexus

A

false they follow the horizontal plexus of the blood vessels.

103
Q

what is the function of the lymphatics

A

• Smaller non-contractile vessels drain into larger contractile lymphatic trunks.
• Continual drainage of plasma proteins, extravasated cells and excess interstitial fluid
• Have no muscle so they require external help to pump fluid around.
• Important immune functions:
- immune surveillance by circulating
o lymphocytes and Langerhans cells
- channelling of micro-organisms / toxins

Dermatology (9 decks)

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