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year 5 > Dermatology skin biology > Flashcards

Dermatology skin biology Flashcards

1
Q

structure of the epidermis in order 5

A 
strateum corneum (horny cell layer)
granular cell layer (strateum granulosum 
spindle cell layer (stratum spinosum)
basal layer (stratum basale) 
basement membrane
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2
Q

2 layers of the skin

A

epidermis

dermis

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3
Q

what type of epithelium is skin

A

squamous epithelium

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4
Q

main cell of the epidermis is

A

keratinocytes

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5
Q

main cell of the dermis is

A

fibrolasts

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6
Q

what other cell types are in the epidermis

A
  • langerhans cells
  • melanocytes
  • merkel cells
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7
Q

what are langerhans cells

A

bone marrow derived macrophages
antigen presenting cells
immunology involved

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8
Q

what are melanocytes

A

neural crest derived pigment producing cells

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9
Q

what are merkel cells

A

neuroendocrine cells that are assoc. with particular nerve endings in the epidermis

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10
Q

what cells are in the dermis

A

fibroblasts
mast cells
inflammatory cells
vessels

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11
Q

what makes up the acellular material of the dermis

A

collagen
elastin
glycosaminoglucans

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12
Q

what are fibroblasts

A

mesenchymal derived cells

chief function is the production and remodelling of the extracellular protein collagen

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13
Q

what are mast cells

A

type of tissue basophil

contain and degranulate a range of vasoactive chemicals including histamine

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14
Q

what inflammatory cells are found in the dermis

A

lymphocytes
polymorphs
range of dermal macrophages and antigen presenting cells

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15
Q

what are the appendageal structures

A

hair follicles
sebaceous glands
eccrine glands
apocrine glands

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16
Q

from what are appendageal structures derived from

A

all epidermal derived

arise during embryonic development at end of 1st trimester

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17
Q

when do new appendageal structures stop being formed

A

cant be formed after the early second trimester

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18
Q

what is a pilosebaceous unit

A

=sweat gland and hair follicle

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19
Q

components and physiology of the basal layer in the epidermis

A
  1. basal cells are cuboidal keratinocytes that sit on the basement membrane
  2. one cell layer thick
  3. also contains stem cells which undergo division
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20
Q

process of stem cell division in basal layer

A
  1. stem cells undergo asymmetrical cell division to form another stem cell and a transient amplifying cell
  2. the transient amplifying cell can then undergo several rounds of division and finally form a terminally differentiated keratinocytes that moves into the spindle cell layer
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21
Q

where are the two pools of keratinocyte stem cells in skin and why are there two

A
  1. basal layer- interfollicular stem cell pool
  2. in the hair follicle close to where the sebaceous gland joins

the 2nd repopulates the first if the first is removed

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22
Q

spindle cell layer anatomy

A

also called prickle cell layer because the tight desmosomal attachments between cells

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23
Q

granular layer

-what is the granular layer made up of

A
  • keratohyalin= protein filaggrin and keratin
  • lipid lamellae= intraceullar membrane bodies which discharge epidermal lipids into the intercellular space in the high epidermis-lipid extrusion
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24
Q

skin keratin expression basal layer vs spindle cell layer

A
  • basal layer expresses keratin 5 and 14
  • spindle layer expresses k1 and k10
  • so when skin is wounded different keratins are expressed
  • so get different phenotypes depending on what is wounded
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25
Q

stratum corneum

what is it made up of

A

-made up of multiple layers of flattened keratinocytes called “cornified envelopes” (corneocytes)

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26
Q

process of keratinocytes death and desquammation 7

A
  1. cornified envelopes begin to form in the granular layer
  2. the plasma membrane is replaced by covalently cross linked proteins including keratins and fillagrin
  3. this is done by the enzyme transflutaminase
  4. these are dead keratinocytes with no nucleus
  5. individual (squames) dead cells of the stratum corneum eventually break off and fall into surroundings= desquammation
  6. desquammation relies on a protease mediated breaking down of the desmosomes
  7. skin then falls off
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27
Q

what do keratinocytes do 3

A

make keratin and fillagrin

make lipids

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28
Q

keratinisation

A

process of stem cell differentiation into keratinocytes

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29
Q

dead keratinocytes

A

cornoecytes

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30
Q

what aggregates keratin together

A

fillagrin

=keratohyalin granules

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31
Q

what do keratins do

A

structural proteins that provide physical support for the cell

  • they are dynamic structures that change as cells divides
  • produce keratins, fillagrin, granules and lipids
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32
Q

how do keratinocytes attach

A

-keratin attach to the desmosomes, points of cell adhesion between keratinocytes

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33
Q

how does the skin thicken in response to frictional forces

A

-frictional forces on the skin provoke thickening of the epidermis- by increase in proliferation of basal layer and an increase in daughter cells moving up into the spindle cell layer

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34
Q

what is acanthosis

A

=thickening of spindle cell layer

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35
Q

what is hyperkeratosis

A

=thickening of stratum corneum

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36
Q

what does the brick and mortar model replicate

A

brick=individual dead keratinocytes in stratum corneum cross linked and aggregated keratins
mortar= lipid
=hydrophobic barrier

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37
Q

disturbance of skin barrier- causes 3

A
  • irritant dermatitis= eg household cleaners attack the hydrophobic lipid barrier
  • atopic dermatitis =disorder of barrier function
  • mutation of filaggrin= filaggrin helps to bundle keratinocytes into the cornified envelope - so dont form a proper cornified envelope
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38
Q

why is disturbance of skin barrier a positive feedback mechanism

A

because the more the barrier is destroyed the more acids/ harmful substances can get through which cause more destruction allowing more acids through

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39
Q

why is filaggrin called filaggrin

A

filament aggregating protein- bundles up keratinocytes

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40
Q

what does transglutaminase do

A

responsible for covalently crosslinking to form the cornified envelope

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41
Q

what do mutations in transglutaminase cause

A

lamellar icthyosis-scally skin

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42
Q

how can oestrogen penetrate the skin

A

it is lipid soluble

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43
Q

what are the embyrological origins of keratinocytes and melanocytes

A

ectoderm and neural crest respectively

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44
Q

two types of melanin

A 
eumelanin= brown or black
pheomelanin= red or yellow
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45
Q

ratio between melanin means

A

determines skin and hair colour
-if mostly pheomelanin= mostly red hair
eumelanin= black hair
small amounts of both= yellow

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46
Q

how is melanin produced

A
  1. produced by melanocytes
  2. toxic to cells so made in melanosomes
  3. melanosomes are passed down the denrities of the melanocytes into the surrounding keratinocytes
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47
Q

what does melanin do

A

protects the skin from UV ratio

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48
Q

what is albinism

- main gene

A

genetic disorders in which the amount of melanin produced is reduced

  • number of melanocytes is normal
  • most common type is due to recessive mutation in the gene for tyrosinase a key enzyme in melanin production
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49
Q

other pigments contributing to skin colour are

A 
melanin
haemoglobin
bilirubin
pigment from drugs or heavy metals
foods eg carotenoids
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50
Q

what are the more common cancers derived from epidermis or dermis

A

mostly from epidermis

UVR load is higher

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51
Q

langerhans physiology

A
  • antigen presenting cells

- when there is an antigen they present it to T cells in the regional lymph node

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52
Q

what cells are involved in mechanoreception

A

merkel cells

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53
Q

what makes up the basement membrane

A

-aceullular

proteins

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54
Q

what attaches basal keratinocytes to the basement membrane

A

hemidesomosomes

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55
Q

what disease targets hemidesmosomes

A

bullous pemphigoid

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56
Q

two layers of the dermis

A

superficial papillary dermis

deeper reticular dermims

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57
Q

what vitamin is essential for normal collagen production and what disease and presentation do you get without it

A

vitamin c

scurvy= corkscrew hairs, perifollicular haemorrhage, gingivitis

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58
Q

what synthesises collagen

A

fibroblasts

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59
Q

dystrophic epidermolysis bullosa is due to

A

mutations in collagen VII

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60
Q

ehlers danlos is due to

A

mutations in a range of collagens

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61
Q

solar pupura is caused by

and pathophysiology

A

-steroids use- reduces amount of collagen
-ageing and UV exposure
due to changes in collagen biosynthesis and remodelling

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62
Q

what does solar pupura mean

A

easy bruising

reduced collagen- reduced dermal thickness

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63
Q

function of collagen in dermis

A

provides a padding around dermal vessels to help prevent bruising

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64
Q

main elastic fibres

A

fibrillin

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65
Q

main glycosaminoglycans of the skin 4

A

hyaluronic acid
heparin sulfate
chondroitin sulphate
keratin sulphate

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66
Q

function of mast cells

A
  • they contain histamine, prostaglandins, leukotrienes and cytokines
  • grouped in granules
  • tissue basophils
  • trigger causes mast cell degranulation which releases mediators such as histamine
67
Q

type 1 hypersensitivity pathophys

A

eg allergy anaphylaxis

IgE crosslinks to mast cells

68
Q

what is the archetypal clinical lesion of mast cell degranulation

A

weal

69
Q

desmographism

A

drawing on skin

70
Q

what is the triple response to histamine 3

A
  1. initial erythema close to site
  2. larger flare of erythema
  3. collection of dermal oedema= weal
71
Q

triple response what causes the initial erythema

A

direct effect of histamine on vessel walls

72
Q

triple response what causes the larger flare of erythema

A

axon reflex
stimualtion by histamine of peripheral nerves is transmitted along sensory nerve and travels backwards along other sensory nerves causing release of mediators at distal nerve endings resulting in vasodilation- antidromic stimulation

73
Q

triple response what causes weal

A

transient increase in permeability in small vessels causing local oedema until fluid reabsorbed

74
Q

urticaria

A

mast cell degranulation disease

75
Q

what makes up appendageal structures

A

keratinocytes

except dermal papilla of hair follicle has specialised fibroblast

76
Q

eccrine sweat glands - where are they not present

A

lips or external ear canal

77
Q

what innervates eccrine glands

A

cholinergic post ganglionic fibres of sympathetic nervous system

78
Q

2 main functions of sweating are

A
  1. evaporative cooling

2. frictional grip - on the palms

79
Q

production of sweat

A
  • secreted into lower secretory portion of eccrine gland as an isotonic fluid
  • gradually it changes to a hypotonic fluid by selective reabsorption of salt as the duct moves through the skin
80
Q

apocrine (sweat) glands function

A
  • assoc. to sites such as axilla, nipples and groin
  • bacterial decomposition is what causes the odour
  • androgen sensitive
81
Q

sebaceous gland function

A

production of lipids that make up sebum

82
Q

what is sebum

A

made up of trig, fatty acids, squalene and cholesterol

83
Q

where are sebaceous glands mostly found

A

scalp face and upper chest

hence acne

84
Q

what increases sebum production and what decreases

A
  • androgens
  • progestogens

-oestrogens decrease sebum production

85
Q

what makes up a hair follicle

A

central medulla
cortex
outer curicle

86
Q

3 main types of hair

A

lanugo hairs
vellus
terminal hairs
-sexual hairs are subset of terminal

87
Q

lanugo hairs

A

fine hairs seen only on premature infants
no medulla
soft
no pigment

88
Q

vellus

A

hair are normally short and very thin
no medulla and lack pigment
found all over the body postnatally
comprise the majority of hairs eg most facial hair inn women

89
Q

terminal hairs

A

long thick pigmented hairs with a central medulla eg scalp and eyelashes

90
Q

what makes sexual hairs

A

androgens acting on vellus hairs

91
Q

3 phases of the hair cycle

A

anagen
catagen
telogen

92
Q

anagen is

A

growth phase which lasts about 3 years for scalp and 3-4 months for chest

93
Q

catagen

A

3 week transitory period in which each hair bulb undergoes apoptosis and regression in which the lower part of the hair moves up close to the skin surface

94
Q

telogen

A

period lasting approx 3 months in which the hair is relatively quiescent
then the new hair pushes out the old one, which is shed

95
Q

nail structure

A

nail plate
nail bed
nail matrix

96
Q

nail plate

A

hard material of nail

made up of dead keratinocytes

97
Q

nail bed

A

found under the nail plate contributes slighlty to the growth of the underside of nail

98
Q

nail matrix

A

-main growth zone of nail

extends from proximal nail fold to the end of the lunula endpoint

99
Q

sensory nerve supply to skin

-2 functions

A
  • only sympathetic nerves
  • no parasympathetic supply to the skin
  1. eccrine sweating
  2. vascular tone
100
Q

erythroderma

A

inflammatory disease where increased blood flow to the skin

  • so skin appears red all over and hot
  • but actually they have central hypothermia
  • concealed hypothermia
101
Q

arrector pilli smooth muscles function

A
  • goosebumps
  • sympathetic control
  • no function in humans
102
Q

pruritus definition

A

sensation that derives need to scratch

103
Q

itch pathway

A
  • itch receptors are found both dermis and epidermis
  • conducted along unmyelinated c fibres
  • cross over in the spinothalamic tract and synapse to neurons that mediate itch scratch reflex
  • no single itch centre in brain
104
Q

main triggers of itch 2

A

histamine

non histamine mediated pathways eg protease activated receptors PAR

105
Q

alloknesis means

A

describes how the skin around the central focus also appear to be itchy when it is lightly touched

  • reflects reinterpretation of light touch as an itch at the level of the spinal cord (A fibres)
  • allodynia same for pain
106
Q

interactions between pain and itch

A
  • scratching can cause pain which then masks itch

- opioids diminish pain but may provoke itch - inhibitory pathways on each other

107
Q

chronic presentation of itch 2

A
  1. lichenification

2. nodular purigo if nodules of itch

108
Q

complication of scabies infestation

A
  • strep systemic infection and death

- hence scratch to try and remove mites

109
Q

how do antihistamines help for an itch which is mediated by non-histamine mediators eg atopic dermatitis (like most are)

A
  • antihistamines are sedatives on central CNS effects which results in less scratching
  • so reduction in scratch is not due to peripheral histamine blockade but due to sedation
110
Q

can histamine induce pain and itch

A

histamine applied superficial to skin get mostly itch but if injected then get pain

111
Q

what disorders is itch mediated by histamine

A

urticaria

112
Q

what disorders is the itch not mediated by histamine

A

atopic dermatitis
psoriasis
lichen planus

113
Q

are scratch marks usually same size

A

larger on back as nerve fibre density and 2 point discrimination is not as good

114
Q

type 1 hypersensitivity reaction

A

-immediate <20 mins
-reaction is mediated by crosslinking of IgE molecules on mast cells by allergens
-results in degranulation of mast cells and the clinical lesion is urticaria
-also seen in demographisms- histamine in response to pressure
degranulation can also occur by non-immune methods

115
Q

peanut allergy patho

A

peanut antigen cross links IgE bound to mast cells in the skin and mucosae
get urticaria
peanut antigen can also provoke a response via systemic absorption or via mucosae if very sensitive

116
Q

latex allergy patho

A

eg seen in surgical gloves
IgE mast cell
intense itching and swelling of hands

117
Q

inx for hypersensitivity type 1

A
  • hx
  • serum specific IgE measurement to antigens= RAST - safer and preferred method of testing
  • skin prick testing
118
Q

pathophysiology chronic immune urticaria

A

the crosslinking of IgE is by an autoreactive IgG molecules

119
Q

type II hypersensitivity path and examples

A

IgG antibody mediated cytotoxicity

examples include pemphigoid and pemphigus and systemic vasculitis involving ANCA

120
Q

type III hypersensivity and example

A

this is where immune complexes form and deposition of these complexes in the vessel may lead to a series of changes including complement activation, and activation of polymorphs and macrophages,

and subsequent tissue damage to vessels surrounding tissue

example is leucocytoplastic vasculitis which can be response to drugs, infection, or SLE/ RA

121
Q

type IV hypersensitivity -delayed

A

T cell mediated reaction
clinically presents as eczema- dermatitis
eg nickel allergy, or allergic contact dermatitis in response to a plaster

122
Q

nickel allergy presentation

A

contact allergic eczema
type IV
20% of the population
means prior exposure to the nickel antigen to skin has resulted in presentation of t cells and development of immune memory

get eczema where skin comes into contact with nickel
24-96 hrs

123
Q

how to inx type 4 hypersensitivity

A

patch testing

-in which the skin is exposed under controlled conditions to a range of likely antigens

124
Q

type 4 vs type 1 hypersensitivity

A

type 4

  • use patch testing
  • eczema appearance

type 1

  • use skin prick test
  • urticaria appearance
125
Q

3 main types of electromagnetic radiation

A

ultraviolet radiation
visible light
infared radiation

126
Q

which condition is linked to infared and what does it look like

A

erythema ab igne
reticulated erythema, hyperpigmentation, scaling and telangiectasia
-pattern in dermal vasculature

127
Q

who commonly gets erythema ab igne 2

A
  1. shins of older people who cant afford to heat their homes adequately so they huddle close to a fire
  2. also can get it from laptops
128
Q

ultraviolet radiation 3 wavelength groups

A
  • UVA 320-400
  • UVB- 290-320
  • UVC <290
129
Q

what is UVC

A

UVC does not penetrate the atmosphere

130
Q

what wavelength is visible light

A

> 400

131
Q

what is the erythema action spectrum

A
  • ability of radiation at any wavelength to induce erythema
  • higher in UVB than UVA
  • even taking into consideration that UVA has a higher spectral output
  • most of the erythemal activity of the sunshine comes from UVB 80%
132
Q

what is larger UVA or UVB- spectral output

A

most radiation comes from UVA

133
Q

when and where is UVR higher

A
  • UVR peaks at midday for both UVA and UVB
  • close to the equator UVR is compressed into a shorter day - so avoid midday!
  • as the sun lowers in the sky -radiation from a fixed solar angle is distributed over a larger area - this reduces wavelengths especially those <320 the main sunburn wavelenths
  • clouds attenuate UV due to scattering and also infared- but they attenuate infared more than UV- hence temperature is a bad proxy for UVR as can underestimate amount of UVR
  • UVR passes through water
  • snow reflects up to 90% of UVR
  • annual exposure- annual UVR rises on where people holiday…
  • lifestyle eg gamer vs athlete
134
Q

what is a monochromator used for

A

solar urticaria to test erythema response to UV

135
Q

what is sunburn

A

dilatation of the vasculature in response to damage from UV radiation

  • tends to peak between 8 and 24 hours and disappears a few days later
  • can use laser doppler to detect it before 8 hours
136
Q

what drug can inhibit suburn erythema

A

indomethacin- cyclooxygenase inhibitor

-inhibitor production of NO- reduce vasodilation

137
Q

what is xeroderma pigmentosa

A
  • abnormal freckling
  • abnormal response to UV light -develop more erythema with trivial amounts of UV exposure and it is prolonged erythema
  • autosomal recessive disorder
  • rare
  • develop skin cancers
  • inability to repair DNA damage due to UV radiation exposure - mutations and skin cancer
138
Q

why do people develop skin cancers

A
  • whilst there is DNA damage repair from UV radiation
  • even in normal people not all the damage is completely repaired and the accumulations of the damage over time results in accumulation of multiple mutations which lead to skin cancers
139
Q

mode of inheritance of xeroderma pigmentosa

A

autosomal recessive

140
Q

number of skin cancers patients with xeroderma pigmentosum develop varies why

A
  1. XP is heterogenous and different genes contribute to DNA repair so severity varies depending on which gene is mutated
  2. difference in skin exposure eg living in Africa vs living in Scotland
  3. skin type- dark skin type melanin protects more
141
Q

what do freckles represent

A

focal overproduction of melanin in the skin

  • number of melanocytes are the same
  • good at photoprotection
  • related to gene and environment
142
Q

constitutive pigmentation vs facultative pigmentation

A

constitutive pigmentation= baseline
facultative pigmentation= tanning - increase from baseline pigmentation as a response of UV radiation on melanin production

143
Q

how does melanin protect against UVR

A
  • melanocytes are not uniformly distributed in skin- they are focused in the basal layer
  • melanosomes cluster around the nucleus on top of it to protect the DNA in the nucleus against UVR- melanin cap
  • melanin absorbs visible light and some UVR
144
Q

what controls the production of melanin

A

range of enzymes including tyrosinase

145
Q

eumelanin are

A

black/ brown

146
Q

pheomelanin

A

are red/ yellow

147
Q

control of melanin ratio is under

A

melanocortin 1 receptor

-mutations of this gene cause red hair so get a high pheomelanin to eumelanin

148
Q

skin type 1

A

pale skin
red/ blonde hair and light eyes
rarely if ever tans, always burns

149
Q

skin type 2

A

beige
darkish blonde/ lightbrown
occasionally tans, usually burns

150
Q

skin type 3 olive

A

brown hair, brown eyes

usually tans, sometimes burns

151
Q

skin type 4

A

medium brown
dark hair , brown eyes
easily tans, burns minimally

152
Q

skin type 5

A

dark
dark brown, black hair
always tans, rarely burns

153
Q

skin type 6

A

always tans, never burns

deep dark colour

154
Q

ways in which the skin responds to UVR

A
  • tanning- facultative pigmentation although is less effective
  • stratum corneum thickens in response to UVR so it blocks more photons
155
Q

use of phototherapy

A

psoriasis

eczema

156
Q

what is vitiligo

A

autoimmune

melanocytes are destroyed in discrete areas -white patches

157
Q

albinism pathophysiology

A

melanocytes are present but dont synthesise normal amounts of melanin

158
Q

commonest cancer uk

A

skin cancer 20%

159
Q

% of eczema

A

15%

160
Q

% psorisais

A

2%

161
Q

moderate or severe acne %

A

20%

162
Q

main causes of skin disease death are

A

skin cancers
blistering eg pemphigoid and pemphigus
cutaneous adverse drugs- toxic epidermal necrolysis

163
Q

what are infectious skin diseases

A 
viral warts
impetigo
herpes simplex- lips
herpes zoster- shingles 
-candida
-ringworm 
-staph
-scabies
164
Q

haematuria and purpuric rash suggests

A

glomerulonephritis

year 5 (9 decks)

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