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DDT > 7 - skin disorders > Flashcards

7 - skin disorders Flashcards

1
Q

integumentary system

A

organ system made up of skin and accessory structures

- exocrine glands, hair, nails etc

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2
Q

vascularised

A

contains blood vessels

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3
Q

3 main layers of skin

A

epidermis
dermis
hypodermis - subcutaneous tissue

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4
Q

dermis structure

A

middle layer
dense, irregular connective tissue
houses blood vessels, hair follicles, sweat glands, and other structures

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5
Q

epidermis

A

outermost layer
keratinized, stratified squamous epithelium
4/5 layers of cells
avascular - no blood vessels

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6
Q

5 layers of epidermis

A 
stratum basale
stratum spinosum
stratum granulosum
stratum lucidum
stratum corneum
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7
Q

keratinocyte

A

cell that stores and produces keratin protein

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8
Q

keratin

A

intracellular fibrous protein that gives hair, nails, and skin their hardness and water-resistant properties

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9
Q

stratum basale

A

attaches epidermis to basal lamina (which lies below dermis)
keratinocytes are produced from a layer of basal cells
merkel cells and melanocytes present

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10
Q

merkel cells

A

responsible for stimulating sensory nerves that the brain perceives as touch
especially abundant on surface of hands/feet

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11
Q

melanin

A

produced by melanocyte
gives hair and skin its colour
helps protect living cells of epidermis from UV radiation damage

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12
Q

stratum spinosum

A

spiny in appearance due to the protruding cell processes that join the cells via a structure called a desmosome
langerhans cells present

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13
Q

desmosomes

A

interlock and strengthen bonds between cells

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14
Q

langerhans cell

A

type of dendritic cell

functions as a macrophage by engulfing bacteria, foreign particles, and damaged cells in stratum spinosum

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15
Q

movement of keratinocytes in the skin layers

A

As new keratinocytes are produced on top of the stratum basale, the keratinocytes of the stratum spinosum are pushed into the stratum granulosum.

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16
Q

stratum granulosum

A

middle layer - above stratum spinosum
keratinocytes are flatter
lots of fibrous keratin produced

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17
Q

stratum lucidum

A

middle layer - above stratum granulosum
only found in thick skin
keratinocytes are dead and flattened
eleiden protein present

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18
Q

stratum corneum

A

uppermost layer - above stratum lucidum - exposed to outside
dry, dead layer of keratinocytes
mechanical protection
cells are shed and replaced over a 4 week period

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19
Q

papillary layer

A

part of dermis
loose connective tissue
finger-like projections into stratum basale of epidermis

cells include: fibroblasts, adipose cells, blood vessels, phagocytes

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20
Q

reticular layer

A

under the papillary layer
much thicker
vascularized connective tissue
elastin and collagen fibres

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21
Q

hypodermis

A 
subcutaneous layer
below dermis
connects skin to bones and muscle fascia tissue
well vascularised
fat storage
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22
Q

pigments

A

influence skin colour

e.g. melanin, carotene, haemoglobin

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23
Q

increased melanin accumulation

A

protects DNA from UV damage and break down of folic acid

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24
Q

albinism

A

inability of melanocytes to produce melanin

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25
Q

dermis

A

connects epidermis to hypodermis
provides strength and elasticity (collagen/elastin)
2 layers- papillary layer and reticular layer

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26
Q

when are ROS produced

A

during mitochondrial oxidative metabolism

in response to bacterial invasion and cytokines

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27
Q

how does hydrogen peroxide cause cancer

A

causes cell damage and uncontrolled growth

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28
Q

MAPK ROS pathway

A 
ROS activates Raf in plasma membrane
Raf phosphorylates MEK
MEK phosphorylates ERK
activated ERK translocates to nucleus
transcription
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29
Q

photodynamic therapy

A

treatment of skin cancer using ROS

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30
Q

what causes the photosensitizing agent to produce ROS

A

the correct wavelength from the light source

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31
Q

how does phototherapy cause death of cancer cells

A

causes damage to blood vessels
which starves cells of nutrients
produces ROS

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32
Q

how does ROS kill cancer cells

A

highly cytotoxic

initiates cellular apoptosis and necrosis

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33
Q

red light

A

long wavelength

penetrates deeper to layers of epidermis

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34
Q

which layer of the skin absorbs the topical cream e.g. 5-ALA

A

stratum corneum

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35
Q

how do tumour cells convert 5-ALA to photosensitizer

A

via haem biosynthesis pathway

tumour cells have many enzymes for this

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36
Q

what is required if the photosensitiser is injected

A

tube needed to guide the light

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37
Q

advantages of 5-ALA

A

short-half life
diffuses over short distances
localised damage

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38
Q

what is imiquimod

A

topical cream

immunomodulator

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39
Q

what is an immunomodulator

A

stimulates immune response

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40
Q

example of non-melanoma skin cancer

A

basal cell carcinoma

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41
Q

what is imiquimod used to treat

A

non-melanoma skin cancer
genital warts
actinic keratosis

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42
Q

mechanism of imiquimod

A

binds to TLR-7 receptors of langerhans cells in epidermis
activates NF-kappaB pathway
causes production of pro-inflammatory cytokines
antigen presentation to naive t cell
effector cytokines produces by t helper cells
apoptosis of basal cell carcinoma cells

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43
Q

which cells take up and process basal cell carcinoma antigens

A

langerhans cells

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44
Q

where do langerhans cells migrate to once they have bound to the antigens

A

regional lymph node

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45
Q

proto-oncogenes

A

genes that cause normal cells to become cancerous when they are mutated
activated version causes cancer

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46
Q

tumour-suppressors

A

genes that normally inhibit cancerous cell proliferation by terminating cell cycle or causing apoptosis

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47
Q

normal function of proto-oncogenes

A

regulating apoptosis

preventing cell differentiation

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48
Q

mutations that activate proto-oncogenes

A

dominant mutations

point mutations - inserts/deletions
gene amplification - additional copies of the gene
chromosomal translocation - gene moves to different site on chromosome

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49
Q

examples of proto-oncogenes

A

HER-2
MYC
p53
Ras

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50
Q

inactivation of tumour-suppressors

A

allows uncontrolled cell proliferation causing tumour formation

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51
Q

mutations that inactivate tumour-suppressors

A

recessive - both alleles need to be mutated

germline mutations

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52
Q

examples of tumour -suppressors

A

APC
Rb
p53
DDC

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53
Q

what are cyclins

A

family of proteins that control regulation of the cell cycle

54
Q

what does cdk stand for

A

cyclin dependent kinase

55
Q

what activates cdks

A

cyclin binding

56
Q

what are cdks important for

A

cell cycle progression

57
Q

p53 detects damaged DNA…

A

causes release of cdk inhibitor e.g p21

binds to cdk-cyclin complex and blocks activity

58
Q

G1/S cyclins

A

activate cdks in late G1

commitment to cell cycle entry

59
Q

S-cyclins

A

binds cdks and stimulate late chromosome duplication

60
Q

M-cyclins

A

activate cdks

stimulate entry into mitosis at G2/M transition

61
Q

dysregulation of Shh leads to

A

tumour formation
basal cell carcinoma

shh is important in differentiation of skin cells

62
Q

2 types of mutations in hedgehog signalling

A

tumour suppressor gene - loss-of-function mutation in Ptch 1

proto-oncogene - activating mutations in Smo

63
Q

what is the signalling transducing molecule in hedgehog signalling

A

Smo

64
Q

what happens in absence of Shh

A

Smo is blocked and cannot bind to Ptch
Gli is converted into repressor form
no transcription

65
Q

where does hedgehog signalling take place

A

primary cilium

66
Q

what happens in presence of Shh ligand

A 
Shh binds to Ptch
Shh-Ptch complex is internalised and degraded
SMo translocates to cilium 
Gli is converted into active form 
transcription initiated
67
Q

role of wnt signalling in colon cancer

A

APC gene is a tumour suppressor

mutation in APC gene inhibits GSK-3B
B-catenin is not degraded and translocates to the nucleus
uncontrolled growth and cell proliferation

68
Q

wnt signalling leads to …

A

gene transcription

69
Q

no ligand bound to frizzled receptor in wnt signalling

A

B-Catenin destruction complex gets phosphorylated and ubiquitinated
degraded in the proteosome
transcription is inhibited

70
Q

ligand bound to frizzled receptor in wnt signalling

A

dishevelled protein inhibits APC
B-catenin complex not phosphorylated/ubiquitinated
B-catenin complex translocates to nuclues
transcription initiated

71
Q

flow cytometry measures

A

how granulated cells are

size of cells

72
Q

role of laser in flow cytometry

A

excited fluorescently labelled cells to emit light at varying wavelengths

73
Q

uses of flow cytometry

A 
cell counting
cell sorting
biomarker detection 
protein engineering
diagnosis
74
Q

example of using flow cytometry as diagnostic tool

A

increased WBC count seen in leukemia

75
Q

how can you distinguish immune cells using flow cytometry

A 
graph
side scatter (granularity) on y-axis 
forward scatter (size) on x-axis

e.g. neutrophils are large and granulated

76
Q

central tolerance

A

process by which b-cells and t-cells are destroyed if they are reactive to ‘self’

77
Q

importance of immune tolerance

A

ensures immune system does not attack self peptides

78
Q

where does central tolerance take place

A

primary lymphoid organs

79
Q

peripheral tolerance

A

mechanisms that take place outside of primary lymphoid organs
aim to prevent immune system from carrying out an immune response against self tissues or harmless material e.g. food/commensal organisms

80
Q

immune response against ‘self’ causes

A

autoimmune disease

81
Q

4 mechanisms of peripheral tolerance

A
  1. clonal deletion
  2. immune ignorance
  3. anergy
  4. immune regulation
82
Q

why does peripheral tolerance occur after central tolerance

A

ensures t and b cells that have escaped central tolerance do not mount an immune response against self

83
Q

clonal deleton

A

most common mech of peripheral tolerance

apoptosis of T and B cells that have escaped central tolerance

84
Q

Anergy

A

T cells made non-responsive to antigens

85
Q

autoimmunity

A

when own immune cells recognise self-antigens and mount an immune response
- failure of central and peripheral tolerance

86
Q

Treg cells function

A 
T regulatory cells
(T repressor cells)
regulate immune system
maintain immune tolerance 
prevent autoimmune disease
87
Q

treg cells in autoimmunity

A

not enough

overwhelmed

88
Q

example of systemic autoimmune disease

A

rheumatoid arthritis

89
Q

example of organ-specific autoimmune disease

A

Type 1 diabetes

immune cells attack the pancreatic insulin-producing beta cells

90
Q

what are Th17 cells

A

pro-inflammatory cytokines

produced by activated t cells

91
Q

overall effect of Th17 cell activation

A

recruitment of neutrophils via epithelial and stromal cells

92
Q

what causes Naive t cell to differentiate into Th17 cells

A

IL-23
IL-6
TGF-B

93
Q

how do epithelial cells (activated by Th17) recruit neutrophils

A

release chemokines and antimicrobial peptides

94
Q

how do stromal cells (activated by Th17) recruit neutophils

A

release chemokiens

95
Q

chemokines

A

chemotactic cytokines

96
Q

role of Th17 cells at mucosal barriers

A

maintain mucosal barriers

contribute to pathogen clearance

97
Q

Th17 cells in auto-immune disease

A

th17 cells are overactivated in autoimmune disease

cause excessive inflammation

98
Q

what do Th17 cells produce

A

IL-17

IL-22

99
Q

which layer of the skin would you find sweat glands and hair follicles

A

dermis

100
Q

where are blood vessels found in the skin

A

spread from the subcutaneous layer to rest of body

reach up to vascularise dermis

101
Q

2 layers of dermis

A

1- papillary layer

2- reticular layer

102
Q

main feature of psoriasis

A

excessive proliferation of keratinocytes in stratum basale

103
Q

what makes keratinocytes

A

basal cells in stratum basale

104
Q

what triggers psoriasis

A

inflammatory trigger

  • activation of immune langerhans cells
  • injury/infection/allergy/stress
105
Q

mechanism of psoriasis from activation of langerhans cells

A 
migrate to lymph node
differentiate into th17 cells
secrete IL-17
reduced or absent stratum granulsom 
excessive proliferation of keratinocytes
nucleated, undifferentiated cells move to top layers of skin
106
Q

what causes redness in psoriasis

A

blood vessels growth near surface of skin

107
Q

what is the problem with undifferentiated keratinocytes in the top skin layers

A

they dont secrete glycolipids - dry less waterproof

they dont stack well so form a scale

108
Q

what do keratinocytes produce

A

chemokines and antimicrobial peptides

to increase cutaneous immune response

109
Q

treatment of psoriasis

A

immunosuppressants - DMARDs
phototherapy - PUVA
topical cream
oral/injection

110
Q

main effect of antimicrobials

A

kill or inhbit growth or microorganisms

111
Q

what mediates release of AMPs

A

cytokines

112
Q

example of cytokines triggering AMP release

A

IL-17 and IL-22 produced by Th17

trigger release of AMPs in gut, skin, lungs

113
Q

3 types of AMP

A

B-defensins
cathelicidins
lysozymes

114
Q

B-defensins

A

AMP
cationic peptide
enhances resistance of epthelial surfaces
secreted at mucosal surfaces

115
Q

cathelicidins

A

found in macrophages, granulocytes, keratinocytes

punctures pathogen cell membranes

116
Q

lysozymes

A

hydrolyse bacterial cell wall

cause cell lysis

117
Q

phototheraphy

A

treatment using light

118
Q

features of UVA

A

longer wavelength
350nm
penetrates into dermis
affects fibroblasts, dendritic cells

119
Q

features of UVB

A

sshorter wavelength
around 300nm
penetrates epidermis
affects keratinocytes and langerhans cells

120
Q

3 types of phototheraphy

A

broadband UVB
narrow band UVB
PUVA

121
Q

PUVA

A

psoralen and UVA

122
Q

psoralen

A

topical or oral photosensitizer

increases sensitivity to UV radiation

123
Q

what is PUVA used to treat

A

chronic plaque psoriasis

after UVB treatment

124
Q

celllular effects of PUVA treatment

A

increases production of anti-inflammatory cytokines
increases prostaglandins - suppress langerhan cells co-stimulation
decrease cytokine-induced ICAM-1 upregulation
induce apoptosis of skin infiltration lymphocytes
module keratinocyte, cytokine and growth factor receptr ezpression

125
Q

missense

A

snp where different polypeptide is produced

126
Q

nonsense

A

snp where protein production is halted

127
Q

causes of SNPs

A

stochastic process
INDELs
substitutions
point mutations

128
Q

how do you identify SNPs

A

GWAS

129
Q

where are SNP mutations found in psoriasis

A

CARD14 gene

130
Q

what do DMARDs stand for

A

disease modifying anti-rheumatic drugs

131
Q

what are DMARDs used for

A

treatment of autoimmune disorders

eg. rheumatoid arthritis

DDT (12 decks)

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