lecture 3 - skin physiology Flashcards

1
Q

What is the most common type of receptor in the skin?

A

Free nerve endings

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2
Q

Are the majority of free nerve endings in the skin myelinated or unmyelinated?

A

Majority unmyelinated with small diameter

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3
Q

What is the name for a small swelling at the distal end of a free nerve ending?

A

Sensory terminal

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4
Q

What is the sensory terminal of a free nerve ending?

A

A swelling at the distal end that acts as a receptor with cation channels

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5
Q

How do free nerve endings generate nerve signals?

A

They have cation channels that when opened lead to a local depolarisation and subsequent action potential.

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6
Q

What stimuli do free nerve endings predominantly respond to?

A

Temperature, pain, some movement/pressure, itch,

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7
Q

How do free nerve endings detect itchiness?

A

They responded to histamines

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8
Q

How do free nerve endings detect light touch from hairs bending?

A

Nerve endings wrap around hair follicles.

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9
Q

What is the name for a free nerve ending that wraps around a hair follicle to detect bending of the hair?

A

Peritrichial ending

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10
Q

What are the 5 types of touch receptors on the skin?

A

Free nerve endings, Tactile (Merkel) discs, tactile (Meissen) corpuscles, lamella (pacinian) corpuscles. bulbous corpuscles (Ruffini’s endings)

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11
Q

What is the alternative name for tactile discs?

A

Merkel discs

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12
Q

Where are tactile/merkel discs found?

A

Free nerve endings located in deepest layer of the epidermis

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13
Q

What are merkel cells?

A

Large disc shaped epidermal cells involved in sensory perception of tactile discs

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14
Q

How do merkel cells communicate?

A

Via serotonin (5HT) neurotransmitters

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15
Q

Where are tactile/merkel discs most abundant, and how does this reflect their function?

A

In fingertips and small receptive fields, as they are good for 2 point discrimination.

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16
Q

What are tactile/merkel discs sensitive to?

A

An object’s physical features: texture, shape, edges. Fine touch and light pressure

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17
Q

What is the alternative name for tactile corpuscles?

A

Meissner corpuscles

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18
Q

Where are tactile/meissner corpuscles located?

A

In the papillary layer of the dermis, especially in hairless skin (finger pads, lips, eyelids, external genitalia, soles of feet, nipples)

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19
Q

What is the structure of a tactile/meissner corpuscle?

A

Spiralling/branching unmyelinated sensory terminals surrounded by modified schwann cells then by a thin oval capsule of fibrous connective tissue.

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20
Q

Are the sensory terminals of tactile/meissner corpuscles myelinated or unmyelinated?

A

Unmyelinated - but they are surrounded by modified schwann cells

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21
Q

How are action potentials generated by tactile/meissner corpuscles?

A

Deformation of the capsule triggers entry of Na+ into a nerve terminal, triggering an action potential.

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22
Q

What type of sensation are tactile/meissner corpuscles used for?

A

Fine, discriminative touch. Sensitive to shape and texture. used for exploratory touch, e.g. braille. Detect light pressure and low frequency vibration (2-80 Hz)

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23
Q

What frequency range of vibration can be detected by tactile/meissner corpuscles?

A

2 to 80 hertz

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24
Q

What is the alternative term for lamellar corpuscles?

A

Pacinian corpuscles

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25
Q

Where are lamellar/pacinian corpuscles located?

A

Scattered deep in the dermis and hypodermis

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26
Q

What is the structure of a lamellar/pacinian corpuscle?

A

Single dendrite lying within concentric layers of collagen fibres and specialised fibroblasts, with layers separated by gelatinous interstitial fluid

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27
Q

What are the layers of collagen and fibroblasts of a lamellar/pacinian corpuscle separated by?

A

Gelatinous interstitial fluid

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28
Q

Why are lamellar/pacinian corpuscles only activated by deep pressure?

A

They are located deep in the skin, and the dendrites is isolated from light pressure by the collagen capsule.

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29
Q

How are lamellar/pacinian corpuscles rapidly adapting?

A

Inner layers of the capsule that cover the axon terminal ‘relax’ quickly so that Action Potenials are discontinued.

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30
Q

What is the optimal stimulation frequency of a lamellar/pacinian corpuscle?

A

approximately 250Hz.

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31
Q

The optimal stimulation frequency (250Hz) of lamellar/pacinian corpuscles is generated by fingertip interaction with features of what size?

A

less than 1 micrometer

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32
Q

What is the alternative name for bulbous corpuscles?

A

Ruffini’s endings

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33
Q

Where are bulbous corpuscles located?

A

The dermis and subcutaneous tissue (hypodermis)

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34
Q

What is the structure of bulbous corpuscles?

A

Network of nerve endings that are continuous with those of the surrounding dermis. Surrounded by collagen capsule that transmits distortion

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35
Q

What stimulation are bulbous corpuscles sensitive to?

A

Sustained deep pressure, stretching/distortion of the skin - prolonged touch

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36
Q

What type of touch receptor is found within the joint capsule and is responsible for proprioception of joint rotation?

A

Bulbous corpuscles/Ruffini’s endings

37
Q

What is the role of bulbous corpuscles in joint capsules?

A

Help in proprioception - signal the degree at which a joint has rotated

38
Q

Why is there a high density of bulbous corpuscles around the fingernails?

A

Monitoring of slippage of objects and modulation of grip.

39
Q

How is blood flow to the skin mechanically regulated?

A

Smooth muscles in walls of arteries and pre-capillary sphincters are contracted/relaxed via innervation by the sympathetic nervous system

40
Q

What neurotransmitter is involved with triggering vascular smooth muscle contractions in the skin to regulate blood flow?

A

Noradrenaline, which acts on a1 (alpha 1) adrenergic receptors on the vascular smooth muscle in the skin

41
Q

What receptors does noradrenaline act on to produce contraction of vascular smooth muscle in the skin?

A

a1 (alpha 1) adrenergic receptors

42
Q

What is the process of vascular smooth muscle contraction, after a neurotransmitter signal have been received?

A

GPCRs (G-protein coupled receptors) are coupled to intracellular 2nd messengers, leading to an increase in intracellualr Ca2+, thereby facilitating contraction/vasoconstriction

43
Q

How is vasodilation facilitated by the skin, in terms of negative feedback?

A

Reduced sympathetic nervous system activity reduces contraction of vascular smooth muscle in the skin, increasing skin blood flow.

44
Q

What are the 2 key factors influenced by skin blood flow?

A

Thermoregulation, blood pressure

45
Q

What are the 4 heat transfer mechanisms?

A

Radiation, evaporation, convection, conduction

46
Q

What is conduction, in terms of body temperature regulation?

A

The transfer of heat between a hot/cold object and the skin

47
Q

What is evaporation, in terms of body temperature regulation?

A

Transfer of heat from skin to water, allowing it to evaporate. e.g. sweating

48
Q

What is convection, in terms of body temperature regulation?

A

Transfer of heat from skin to the surrounding air. The warmed air rises away from the skin and is replaced by cool air which is in turn warmed.

49
Q

What is radiation, in terms of body temperature regulation?

A

Transfer of heat to or from the body via infrared radiation

50
Q

How are eccrine sweat glands predominantly controlled?

A

They are innervated by the sympathetic nervous system

51
Q

What type of synapses do eccrine sweat glands receive?

A

Sympathetic cholinergic

52
Q

How do sympathetic cholinergic synapses trigger eccrine sweat glands?

A

Acetylcholine (ACh) is released onto mACHRs (muscarinic acetylcholine receptors)/GPCRs in the cell membrane.

53
Q

How are eccrine sweat glands triggered hormonally?

A

Some glands can be stimulated by adrenaline in the blood, which acts on beta receptors causing ‘nervous sweating’

54
Q

What causes ‘nervous sweating’?

A

Adrenaline in blood acting on beta receptors on eccrine sweat glands

55
Q

Where does ‘nervous sweating’ usually occur on the body?

A

Palms and soles, axilla (armpit)

56
Q

What is the axilla?

A

The armpit

57
Q

What part of the brain detects body temperature?

A

The pre optic area of the hypothalamus, which contains central thermoreceptors

58
Q

What are mAChRs?

A

muscarinic acetylcholine receptors

59
Q

What are GPCRs?

A

G protein coupled receptors

60
Q

What are central thermoreceptors?

A

Heat and cold sensitive neurons found in the pre optic area of the hypothalamus

61
Q

How is the body’s heat loss centre activated?

A

If the hypothalamus detects the blood temperature exceeding the set point

62
Q

When the heat loss centre is activated, what happens to the skin blood flow?

A

Less SNS activation of alpha 1 receptors on skin blood vessels leads to vasodilation

63
Q

When the heat loss centre is activated, what happens to sweat production?

A

Increased SNS cholinergic activation of mAChRs on eccrine sweat glands.

64
Q

What happens to respiratory rate when the heat loss centre is activated?

A

Increased respiratory rate

65
Q

What mechanisms are activated by the heat loss centre (4)?

A

Vasodilation, sweating, increased respiratory rate, behavioural changes

66
Q

What activates the heat gain centre?

A

Central thermoreceptors detect blood temperature going below set point, and activate the hypothalamus

67
Q

What are key heat generation mechanisms (3)?

A

Shivering, non-shivering thermogenesis, increased thyroxine release

68
Q

How is shivering initiated?

A

Skeletal muscle tone is increases until it rises above a critical level, causing oscillatory contractions of agonist and antagonist muscles mediated by muscle spindles/stretch receptors

69
Q

What is non-shivering thermogenesis?

A

Increased sympathetic nerve activity, releasing noradrenaline/adrenaline from the adrenal medulla to increase cellular metabolism

70
Q

What cellular processes does non-shivering thermogenesis induce?

A

Increased cellular metabolism - e.g. glyocgenolyis in liver and muscle.

71
Q

What hormones increase cellular metabolism in non-shivering thermogenesis?

A

Adrenaline and noradrenaline

72
Q

What is the role of thyroxine in heat generation?

A

Increased thyroxine/T4 is released as a result of TRH and TSH release. This increases the basal metabolic rate.

73
Q

What is thyroxine?

A

T4 thyroid hormone.

74
Q

What is the long term heat generation mechanism?

A

Thyroxine release - increases metabolic rate after lengthy exposure to cold .

75
Q

What are the arrector pili muscles activated by?

A

They are smooth muscle, activated by SNS at alpha 1 receptors.

76
Q

What do the arrector pili muscles attach?

A

Hair follicle to upper dermis

77
Q

How do arrector pili muscles affect sebaceous glands?

A

They compress them, allowing them to release sebum to lubricate the skin

78
Q

How are the arrector pili muscles involved in thermoregulation?

A

They causes goosebumps which allow the hairs to trap a layer of warm air around the skin, preventing heat loss.

79
Q

What does fluid replacement in burn victims depend on?

A

The percentage of total body surface that is involved.

80
Q

What rule is used in burn fluid replacement?

A

‘Rule of 9’s’ (in adults)

81
Q

In burn fluid replacement, what percentage of the body is given by the head?

A

9%

82
Q

In burn fluid replacement, what percentage of the body is given by the upper limbs?

A

9% each

83
Q

In burn fluid replacement, what percentage of the body is given by the trunk (front and back)?

A

36%

84
Q

In burn fluid replacement, what percentage of the body is given by the genitalia?

A

1%

85
Q

In burn fluid replacement, what percentage of the body is given by the lower limbs?

A

18% each

86
Q

What are the complications of severe burns that are directly related to skin function?

A

Dehydration/hypovolemic shock, infection/sepsis, hypothermia

87
Q

What complications of severe burns are not directly related to skin function?

A

Electrolyte imbalances, hypermetabolism, gastrointestinal ulceration, renal failure, respiratory dysfunction

88
Q

What is an example of an electrolyte imbalance caused by severe burns?

A

Hyperkalaemia (high K+ conc.)