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Dermatology > Skin Structure & Function (1-4) > Flashcards

Skin Structure & Function (1-4) Flashcards

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1
Q

What is the epidermis?

A

Outer layer

Wafer thin

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2
Q

What cell type is the epidermis composed of?

A

Stratified squamous epithelium

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3
Q

What is the dermis?

A

Beneath the epidermis

Connective tissue
The “leather skin”

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4
Q

From which embryological structure does the EPIDERMIS arise?

A

ECTODERM

Ectoderm cells form single layer periderm

Increase in layers of cells

Periderm cells cast off

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5
Q

From which embryological structure does the DERMIS arise?

A

MESODERM

below ectoderm

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6
Q

Melanocytes (what are they & embryological origin)

A

Originate from the NEURAL CREST

Pigment producing cells

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7
Q

What is the term for “cellular organisation into germ layers”?

A

Gastrulation

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8
Q

What are the layers of the EPIDERMIS?

A

BPGK

Basal –> Prickle –> Granular –> Keratin (or C for Cornified envelope)

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9
Q

Are epidermal cells dynamic?

A

Yes.

Constantly being replaced.
Differentiation
Many different cel types

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10
Q

Which layer of the epidermis is moving the most?

A

Prickle/spinous layer

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11
Q

What structure connects the prickle layer together?

A

Desmosomes (??? not sure at m will update)

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12
Q

Where would you find Apocrine glands? (grossly)

A

AXILLAE (main one at present time)

Additional ones//

areola and nipples of the breast, ear canal, eyelids, wings of the nostril, perianal region, and some parts of the external genitalia
(wikipedia)

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13
Q

What are APOCRINE glands? (later)

A

Function in humans still not largely known

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14
Q

What are ECCRINE/MEROCRINE glands? (later)

A

Glands
Make you sweat

Autonomc system

Thermoregulation

Whole skin surface - palms, soles and axillae in particular.

SYMPATHETIC cholinergic nerve supply

Ultrafiltration can be more than 10L per day.

Hypotonic fluid

Colling; moisten palms/soles to aid grip

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15
Q

Skin is able to reversible react to mechanical pressure by forming?

What does this mean?

A

Keratin

Callouses forming

Playing guitar a lot = thicker callous

Play it less = callous is not as thick
– hence “reversible”

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16
Q

How is turnover of skin regulated?

A

Controlled by:

Growth factors
Cell death
Hormones

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17
Q

What happens if there is a loss of control in skin regulation?

A

Skin cancer

Psoriasis

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18
Q

In normal skin, how long does it take for prickly cells to move up to the “top”?

In psoriasis?

A

28 days

5 days or so when someone has psoriasis

extremely rapid turnover

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19
Q

In psoriasis, cells have difficulty with?

A

Differentiation

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20
Q

In psoriasis, keratinous cells do not…

A

Slough off as easily as normal cells

Gives a “scaly” look

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21
Q

Where do keratinocytes migrate from?

A

The basement membrane

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22
Q

The basal layer is composed of what type of cell?

A

Small cuboidal with intermediate keratin filaments

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23
Q

Prickle cell layer is composed of?

A

Larger polyhedral cells

Desmosomes

Intermediate filaments connecting to desmosomes

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24
Q

In what direction does the prickle cell layer move in general?

A

Upwards towards apical

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25
Q

Granular layer

A 
2-3 layers of flatter cells
Lamellar bodies
High lipid content
Origin of cornified envelope
Cell nuclei lost
Keratohyalin granules (contain filaggrin & involucrin)
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26
Q

What are lamellar bodies?

A

lamellar bodies are secreted from keratinocytes, resulting in the formation of an impermeable, lipid-containing membrane that serves as a water barrier and is required for correct skin barrier function

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27
Q

Filaggrin (needs work)

A

is a filament-associated protein that binds to keratin fibers in epithelial cells

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28
Q

Involucrin

A

In binding the protein loricrin, involucrin contributes to the formation of a cell envelope that protects corneocytes in the skin.

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29
Q

Keratin layer

- composed of

A

Corneocytes (overlapping non-nucleated cell remnants) held together by filaggrin products (?)

NO NUCLEI

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30
Q

What kind of barrier does the keratin layer provide?

A

Tight waterproof barrier

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31
Q

Does the keratin layer have nuclei?

A

NO

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32
Q

What does HPV infection affect?

A

Keratinocytes

Causing warts

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33
Q

Mucosal membranes

make more concise, just guide at moment

A

Highly specialised for function
Eyes, mouth, nose, genito-urinary & GI tracts
Oral mucosa
Masticatory – keratinised to deal with friction/pressure
Lining mucosa – non-keratinised
Specialised mucosa - tongue papillae – taste
Ocular mucosa
Lacrimal glands, eye lashes, sebaceous glands

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34
Q

Why are the insides of our mouths red?

A

You can see straight through into the upper dermal vascular plexus

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35
Q

What does white indicate on the inside of the mouth?

A

Thickened skin

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36
Q

The boundary between the dermis and epidermis is not flat because…

A

The skin can withstand pressure and sideways displacement

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37
Q

Majority of epidermal cells are…

What are the 3 (main) others?

A

Keratinocytes

3 others:

  • melanocytes
  • Langerhans cells
  • Merkel cells
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38
Q

Melanocytes

  • where they originate embryologically
  • what they are
A

Migrate from neural crest to epidermis (during first 3 months of development)

They are PIGMENT-producing dendritic cells

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39
Q

What are melanocytes related to?

A

Neuronal dendritic cells

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40
Q

What organelle do melanocytes contain?

A

Melanosomes

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41
Q

Melanosomes do what?

A

Convert tyrosine –> melanin pigment

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42
Q

What are the 2 types of melanin pigment?

A
  1. Eumelanin (brown/black)

2. Phaeomelanin (red, yellow)

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43
Q

What is the function of melanin?

A

Absorbs light

neutral density filter

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44
Q

What happens to full melanin granules?

A

They are transferred to adjacent keratinocytes via dendrites

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45
Q

What does the melanin form? (hat/cap)

A

Protective cap over the nucleus

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46
Q

What do these “melanin caps” protect?

A

The nuclear DNA in basal cells

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47
Q

Are basal cells STEM cells?

A

YES

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48
Q

Vitiligo

A

Melanocytes are attacked by the immune system

Autoimmune disease

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49
Q

Albinism

A

Genetic partial loss of pigment production

Missing enzymes in enzymatic cascade

50
Q

Nelson’s syndrome

A

Melanin stimulating hormone (MSH) is produced in excess by the pituitary gland

Hyperpigmentation of the skin

51
Q

What is MSH

A

Melanin stimulating hormone

52
Q

Malignant melanoma

A

Tumour of the melanocyte cell line

53
Q

Langerhans cells

  • origin
  • where found
  • function
A

Origin - bone marrow

Found in prickle cell layer and dermis and lymph noes

Skin immune system
- antigen presenting cells

  • pick up antigen in skin and circulate to lymph nodes via lymphatics
54
Q

Langerhans cells are the outermost line of…

A

detecting cells

human burglar alarm

55
Q

Racket organelle/ Birbeck granules***

A

Specific to langerhans cells

No one knows what they do.

56
Q

Merkel cells

A

Basal membrane

Between keratinocytes and nerve fibres

Mechanoreceptors

Cushion-like –> provide touch sensation

57
Q

Merkel Cell cancer

  • cause
  • mortality
A

Rare

VIRAL infection - merkel cell polyomavirus

High mortality

58
Q

Hair follicles/ Pilosebaceous Unit

A

Epidermal component + dermal papilla

Specialised keratins

Adjacent sebaceous gland

Hair pigmentation via melanocytes above dermal papilla

The hair follicle is an invagination of epidermal tissue.

The papilla is dermal.

59
Q

What do SEBACEOUS glands secrete?

A

Sebum

Lubricates the hair follicle

60
Q

Hair follicles - stages of growth

A

There are 3 stages

Anagen = growing (3-7 yrs)

Catagen = involuting (preparing for resting phase) (3-4 wks)

Telogen = resting (each day)

Regional variations in growth patterns

Hormonal influences e.g. thyroxine, androgens

61
Q

Types of hair follicle (3)

A

Lanugo (in utero)

Vellus

Terminal

62
Q

Why can some of your come out when you put your hand through your hair?

A

Some of your hair is in Telogen phase (shedding)

63
Q

Telogen effluvium

A

When many hairs enter cycle at the same time – therefore hairs will enter telogen phase at the same time and will fall out

Most common cause of hair loss

64
Q

Where does pigmentation of a hair occur?

A

In the hair matrix

65
Q

Hypertrichosis

A

Too much hair at androgen receptor controlled regions - chin/chest

Female patient

66
Q

Alopecia areata

A

Autoimune hair loss

67
Q

How a nail is formed (basic, expand later)

A

Stem cells differentiate and become flat

filled with keratin

cross link - forming the nail

68
Q

Nails are sensitive to

A

Chemical or mechanical trauma

69
Q

Normal nail that becomes thick and crumbly in one area …

A

Tells you that patient has had a trauma on the nail matrix which has led to stem cells losing ability to differentiate properly

70
Q

Subungual mole

A

Under the nail

sharp brown line

71
Q

What occurs in Bullous Pemphigoid

A

Autoantibodies are attacking the hemidesmosomes within the skin.

72
Q

Requirements for healthy skin

A 
Intact epidermis - protective barrier
Keratin
Good blood supply
Melanocytes
Langerhans cells
Need the keratin to slough off properly 
Moisture 
Vitamin D 
Functioning immune system
73
Q

What are the 3 stages of wound healing

A
  1. Inflammation
  2. Proliferation
  3. Tissue remodelling
74
Q

What is Primary intention wound healing?

A

Healthy edges are brought together by sutures
Surgical

e.g. suturing, skin grafts

75
Q

What is Secondary intention wound healing?

A

Wound is left to heal on its own

76
Q

What is a CHRONIC wound?

A

A wound that hasn’t healed within 3 months

77
Q

What factors must be considered in the assessment of a chronic wound?

A
  • Infection
  • Poor arterial blood supply
  • Poor nutrition/ nutrition status
  • Impaired venous return
  • Repeated trauma/pressure
  • Systemic disease present – diabetes?
78
Q

How could pressure sores be prevented?

A

Moving about regularly
Physiotherapy
Clean sheets
Special mattress

79
Q

What is the Dermal-Epidermal junction?

What is its role?

A

Interface between the epidermis and the dermis

Key role in epithelial-mesenchymal interactions//

  • support, anchorage, adhesion, growth and differentiation of basal cells.
  • Semi-permeable membrane acting as barrier and filter
80
Q

What kind of membrane is the derma-epidermal junction?

A

Semi-permeable membrane.

81
Q

What layers does the Dermo-epidermal junction consist of?

A

Lamina lucida

Lamina densa

Sub-lamina densa zone

Proteins that link and hook together

82
Q

What occurs in bullous pemphigoid?

A

An autoantibody attacks the proteins in the DEJ

Skin slips and breaks up –> blistering and itching

83
Q

Among whom is bullous pemphigoid common?

A

Stroke and parkinson’s patients.

84
Q

Epidermolysis Bullosa is….

  • type of condition
  • presentation
  • seriousness
A

Inherited genetic condition.

Fragile skin

Friction sites slough and sheath off

Constant sloughing of skin causes some skin to merge together - leading to loss of features on the fingers.

Can be deadly in children/young babies.

85
Q

What does the dermis contain?

A

mainly fibroblasts, macrophages, mast cells, lymphocytes, Langerhans cells

collagen, elastin

Muscles, blood vessels, lymphatics, nerves

86
Q

What do fibroblasts manufacture?

A

Collagen

87
Q

What is the majority of the dermis composed of?

A

Collagen

88
Q

What occurs in photo aging?

is elastin involved( will add later)

A

Collagen have broken down

Saggier, more wrinkled

Leathery skin

89
Q

Where are the larger blood vessels in the skin located?

A

In subcutaneous fat

90
Q

Angioma

A

Overgrowth of blood vessel structure

Can dilate and can bleed

91
Q

Type of angioma in babies?

A

Strawberry nevi

92
Q

What is dermographism?

A

Dermographism is an exaggerated wealing tendency when the skin is stroked. Physical urticaria

i.e. you can “draw” on the skin with very little effort.

93
Q

Skin lymphatics

What is circulating?

Are vessels contractile?

A

Sub-epidermal

Small non-contractile vessels -> larger contractile vessels

Continual drainage of extra fluuid, extravasated cells, debris, foreign bodies

Circulating lymphocytes and langerhans cells

Channeling of micro organisms and toxins

94
Q

Chronic lymphoedema

A

Lots of swelling

Skin thickens

COBBLESTONING
SCALING
Skin breakdown

95
Q

Nerves of the Skin

A
  1. Somatic Sensory (dermatomes)
    a) Free nerve endings

b) Special receptors:
i) Pacinian (pressure) corpuscles

ii) Meissners (vibration) corpuscles
2. Autonomic Nerve supply

  • blood vessels
  • nerves
  • Glands
96
Q

Where are meissners corpuscles located?

A

Quite high up in the dermis

Fingerpads

97
Q

Where are pacinian corpuscles located?

A

In the subcutaneous fat (?)

They look like the cross section of an onion under the microscope.

98
Q

Neurofibromatosis

A

Overgrowth of the nerve endings

Can become cancerous

Soft to the touch/ squidgy

99
Q

Hirsutism

A

Male hair growth patterns on a female.

e.g. on the chin and face

100
Q

Sebaceous Glands

Function

A

Holocrine secretion opening into pilar canal

Largest glands on the face and chest

Hormone sensitive
- quiescent pre-puberty

Control moisture loss

Protection from fungal infection

101
Q

What is Sebum composed of?

A

Composed of : squalene, wax esters, Triglycerides and Free Fatty Acids

102
Q

Main functions of the skin

A 
Barrier function 
Metabolism & detoxification
Thermoregulation
Immune defence
Communication
Sensory functions
103
Q

Toxic epidermal necrolysis

A

Acute skin failure

104
Q

Failure of the barrier function leads to…

A

Fluid loss –> dehydration

Protein loss -> hypoalbuminaemia

Infection

Dermatitis
Ulcers

105
Q

Failure of Thermoregulation

A

Heat loss –> Hypothermia

106
Q

Immune defence failure

A

Spread of infection

107
Q

Metabolic failure

A

Disordered thyroxine metabolism

108
Q

Sensation failure

A

Pain sensation working -> pain

109
Q

Skin communication failure

A

Inability to display healthy skin –> stigma

110
Q

What temperatures are good for patients whose thermoregulation has failed?

A

Warmer rooms.

Less heat loss to the environment.

111
Q

Barrier function

Physical
Chemical
Pathogens

A

Two way barrier

Physical barrier //

  • friction, mechanical trauma
  • UV radiation

Chemical//

  • irritants, allergens and toxins

Pathogens//
- bacteria, viruse, fungi

112
Q

Steroid -sulphatase deficiency X linked ichthyosis

A

Fish scales
Lack of formation of lipids in the dermiss

Cholesterol is produced properly but cannot be broken down into the lipids required for epidermal barrier to function properly

113
Q

Function of melanin?

A

It absorbs UV rays to protect DNA in the cells’ nuclei

114
Q

What metabolic processes go on in the skin?

A

Vitamin d metabolism

Thyroid hormone metabolism

Defence against chemicals, drugs, pollutants and sunlight

115
Q

Which wavelengths of light are needed for vitamin D formation?

A

290-320nm UV (i.e. UVB)

Cholecalciferol –> VitaminD3

116
Q

Where does thyroid hormone metabolism take place?

A

20% in thyroid glands

80% peripherally including skin

Thyroxine (T4) –> Triiodothyronine (T3)

117
Q

Thermoregulation

- function

A

Protects against being too hot or cold

Warm/cold-sensitive thermoreceptorrs

  • behavioural changes
  • control sweating/shivering/ blood supply
118
Q

Immune defence is important in…

cells important i the skin

A

Protection against infection

Sunlight responses

Allergic reactions (to chemicals/drugs)

Langerhans & T cells

119
Q

Crusted scabies

A

severe form of scabies

thousands of scabies mites as opposed to a dozen in “normal” scabies

120
Q

Chronic discoid lupus erythematosus

A

Autoimmune disease

Sores with inflammation and scarring favouring the face, ears, and scalp and at times on other body areas. These lesions develop as a red, inflamed patch with a scaling and crusty appearance.

Dermatology (8 decks)

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