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Dermatology > Histology + Basic Science > Flashcards

Histology + Basic Science Flashcards

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Dermatology Board Prep flashcards
1
Q

What is the most common type of cancer in the UK?

A

Basal cell skin cancers

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2
Q

Are basal cell skin cancers malignant or benign?

A

Malignant

but rarely metastasise

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3
Q

Are melanomas malignant or benign?

A

Malignant

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4
Q

Are squamous cell carcinomas malignant or benign?

A

Melignant

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5
Q

what is the incidence trend of skin cancers?

A

increasing incidence

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6
Q

what is the incidence trend of atopic dermatitis?

A

increasing incidence

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7
Q

what is the incidence trend of venous leg ulceration?

A

staying the same

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8
Q

why are venous leg ulcerations increasing in prevalence despite incidence being the same?

A

because people with the disease are living longer

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9
Q

what is the definition of prevalence?

A

the total number of cases within the population at any one time

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10
Q

what is the definition of incidence?

A

the number of new cases of a disease (as a percentage of the population over time)

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11
Q

what type of cells make up the epidermis?

A

stratified squamous epithelium

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12
Q

what type of tissue is the dermis?

A

connective tissue

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13
Q

From what embryonic germ layer is the epidermis formed?

A

Ectoderm

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14
Q

What is the name of the single layer which is formed from ectoderm cells and goes on to become epidermis?

A

Periderm

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15
Q

From what embryonic germ layer is the dermis formed?

A

Mesoderm

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16
Q

What is the name of pigment producing cells that reside in the epidermis?

A

Melanocytes

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17
Q

Where do melanocytes come from?

A

Neural crest

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18
Q

What is the name of the embryonic phase (days 7-10) where cellular organisation into germ layers occurs?

A

Gastrulation

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19
Q

From what embryonic germ layer are endothelial linings formed?

A

Endoderm

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20
Q

At 4 weeks of foetal development, what are the 3 layers of skin that are present?

A

Periderm
Basal layer
Dermis (corium)

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21
Q

At 16 weeks of foetal development, what are the 5 layers of skin that are present?

A 
Keratin layer
Granular layer
Prickle cell layer
Basal layer
Dermis
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22
Q

What happens to the periderm as the foetus develops?

A

Gradual increase in layers of cells until keratin layer, granular layer and prickle cell layer are formed. The periderm casts off.

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23
Q

What is the name of the developmental growth pattern of skin?

A

Blaschko’s lines

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24
Q

What type of marks follow blaschko lines?

A

birth marks

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25
Q

what is the sub-cutis predominantly made of?

A

fat

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26
Q

what cells make up 95% of the epidermis?

A

keratinocytes

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27
Q

what is differentiation of a keratinocyte?

A

migration from basement membrane to keratin layer to be shed

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28
Q

what are the 4 defined layers of the epidermis?

A

keratin layer
granular layer
prickle cell layer
basal layer

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29
Q

What layer of the epidermis is noticeably thicker on the soles of feet and palms of hands?

A

keratin layer

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30
Q

what is epidermal turnover?

A

the rate of keratinocytes moving from the basement membrane to the keratin layer to be shed

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31
Q

compare epidermal turnover over of normal skin to the skin of a patient with psoriasis?

A

normal skin epidermal turnover: 28 days

psoriasis epidermal turnover: 45 days

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32
Q

what shape are the cells of the basal layer of the epidermis?

A

cuboidal

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33
Q

what shape are the cells of the prickle cell layer of the epidermis?

A

polyhedral

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34
Q

what adheres the cells of the prickle cell layer together?

A

desmosomes

+ intermediate filaments

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35
Q

what shape are the cells of the granular layer?

A

flattened cells

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36
Q

what phase in the life cycle of a keratinocyte happens in the granular layer?

A

keratinocytes start to die- cell nuclei is lost

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37
Q

what secretory organelles are released from keratinocytes in the granular layer?

A

odland bodies

lamellar bodies

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38
Q

what layer of the epidermis is not present in psoriasis?

A

granular layer

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39
Q

what are corneocytes?

A

overlapping non-nucleated cell remnants (dead keratinocytes) which make up the keratin layer

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40
Q

what forms a tight waterproof barrier within the keratin layer of the epidermis?

A

the insoluble cornified envelope
+
lipids, flaggrin and involucrin proteins from granules secreted from keratinocytes in granular layer

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41
Q

What 3 main components are in the keratohyalin granules?

from the keratinocytes in the granular layer

A

lipids
flaggrin
involucrin proteins

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42
Q

why does HPV commonly affect children below 6 years of age?

A

because corneocyte layer hasn’t sealed properly yet so there is no effective barrier

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43
Q

Is oral masticatory mucosa keratinised or non-keratinised?

A

keratinised

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44
Q

Is oral lining mucosa keratinised or non-keratinised?

A

non-keratinised

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45
Q

What does a white area on mucosal surfaces (eg buccal mucosa) suggest?

A

thickened epithelial lining

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46
Q

What is lost when scar tissue is formed on epidermis?

A

appendages

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47
Q

Why are appendages lost in scar tissue?

A

fyboblasts try to repair skin with collagen tissue

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48
Q

what are the 3 main other cells (apart from keratinocytes) in the epidermis?)

A

melanocytes
langerhans cells
merkel cells

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49
Q

where are melanocytes located?

A

basal and suprabasal

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50
Q

what are melanocytes?

A

pigment producing dendritic cells

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51
Q

what are the organelles within melanocytes which produce melanin?

A

melanosomes

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52
Q

what is converted by melanosomes into melanin pigment?

A

tyrosine

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53
Q

what type of melanin is brown or black?

A

eumelanin

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54
Q

what type of melanin is red or yellow?

A

phaeomelanin

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55
Q

how are melanosomes (melanin granules) transferred to adjacent keratinocytes?

A

via dendrites

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56
Q

what does melanin pigment do once inside a keratinocyte?

A

forms a protective cap from UV light over nucleus

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57
Q

what organelle within the melanocyte is the origin of the melanosome membrane?

A

golgi apparatus membranes

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58
Q

why is there a loss of colour in vitiligo?

A

due to loss of melanocytes

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59
Q

what type of disease is vitiligo?

A

autoimmune

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60
Q

what type of disease is albinism?

A

genetic

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61
Q

what is the name of the syndrome where there is excess melanin-stimulating hormone produced by the pituitray?

A

Nelson’s syndrome

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62
Q

what visual sign does Nelson’s syndrome have?

A

tanned appearance

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63
Q

what is the name of a tumour of the melanocyte cell line?

A

(malignant) melanoma

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64
Q

where do Langerhans cells originate from?

A

bone marrow

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65
Q

where do Langerhans cells reside in the epidermis?

A

pricke cell layer

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66
Q

what type of cells are langerhans cells?

A

antigen presenting cells

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67
Q

what are the names of the tennis racket shaped organelles found in langerhans cells?

A

birbeck granules

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68
Q

what are merkel cells?

A

mechanoreceptors that directly synapse with free nerve endings

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69
Q

where do merkel cells reside in the epidermis?

A

basal layer

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70
Q

why can diabetes mellitus cause reduced/loss of feeling?

A

glycation (glucose tagging) of the myelin sheath which affects function of nerve

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71
Q

what are merkel cell cancers caused by?

A

viral infection

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72
Q

what is a pilosebaceous unit?

A

a hair follicle with an adjacent sebaceous gland

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73
Q

how does pigmentation of hair occur?

A

via melanocytes above dermal papilla

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74
Q

what is the beginning of a pilosebaceous unit in embryology?

A

hair bud

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75
Q

what are the 3 phases of hair growth?

A

anagen
catagen
telogen

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76
Q

what is the telogen phase also known as?

A

shedding phase

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77
Q

what happens to the dermal papilla n the catagen phase?

A

moves away from marix leaving an epithelial column

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78
Q

what is the anagen phase also known as?

A

growth phase

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79
Q

what is the catagen phase also known as?

A

resting phase

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80
Q

what does the hair matrix become in the telogen phase?

A

club hair

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81
Q

why in autoimmune disease such as alopecia, does the hair regrow as white/grey before colour returns?

A

hair regrows before melanisation occurs

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82
Q

In humans the telogen phase is asynchronus. What does this mean?

A

hairs all fall out at different times

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83
Q

what can commonly drive synchronisation of telogen phase and therefore cause hair loss?

A

psychosocial stress

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84
Q

what are the 3 patterns of male hair loss?

A

ventral
typical
anterior

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85
Q

compare nail growth in summer to winter?

A

faster nail growth in summer than in winter

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86
Q

where is the region of stem cells that become nails?

A

the nail matrix

underneath the posterior nail fold

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87
Q

what are the 3 layers of the nail plate?

A

dorsal
intermediate
ventral

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88
Q

why is the luna white and the rest of the nail plate red?

A

luna is thicker, in the rest of the nail plate you can see the blood vessels underneath

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89
Q

why can trauma cause poorly shaped/crumbly nails?

A

permanently damages stem cells causing a differentiation defect

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90
Q

What anchors the epidermis to the dermis?

A

DE junctions

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91
Q

What are the names of the keratin filaments which stick the basal cells to the papillary dermis at the DE junction?

A

hemidesmosomes

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92
Q

What is epidermolysis bullosa?

A

an inherited disease of the DE junction which causes skin fragility

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93
Q

Name 3 acquired conditions caused by auto-antibodies to proteins in the skin?

A

pemphigus
bullous pemphigoid
dermatitis herpetiformis

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94
Q

what are the main cell types in the dermis?

A 
fibroblasts
macrophages
mast cells
lymphocytes
langerhans cells
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95
Q

what are the main 2 fibres found in the dermis?

A

collagen (higher percentage)

elastin

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96
Q

what is the function of collagen in the skin?

A

strengthening

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97
Q

what is the function of elastin in the skin?

A

elastic recoil to skin

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98
Q

what is the function of fibroblasts in the dermis?

A

secrete collagen

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99
Q

What is the name for physical urticaria?

ie an exaggerated wealing tendency that occurs when skin is touched

A

dermographism

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100
Q

what cells degranulate to cause an urticarial response?

A

mast cells

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101
Q

what 2 main substances can increase wrinkling?

A

UV light

smoking

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102
Q

what happens to the collagen during aging?

A

it becomes depleted

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103
Q

what happens to the DE junctions during aging?

A

DE junctions become flatter

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104
Q

compare the supply of the skin blood vessels to the metabolic demand?

A

supply is greater than demand

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105
Q

what is the name of a localised overgrowth of blood vessels?

A

angioma

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106
Q

what is the cause of a port wine stain?

A

an angioma of the face

overgrowth of blood vessel population

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107
Q

what is the function of pacinian corpuscles?

A

pressure sensory free nerve endings

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108
Q

what is the function of meissner corpuscles?

A

vibration (light touch) sensory free nerve endings

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109
Q

what is the name of the inherited condition which causes an overgrowth of cutaneous nerve endings?

A

neurofibromatosis

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110
Q

what is the name of the benign tumour of cutaneous nerve endings?

A

neurofibromas

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111
Q

what are the 3 types of skin glands?

A

eccrine glands
sebaceous glands
apocrine glands

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112
Q

which skin glands sweat to cool you down?

A

eccrine glands

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113
Q

which skin glands secrete a feromone odour?

A

apocrine glands

114
Q

when do apocrine glands start secreting?

A

puberty

115
Q

what are the 2 main sites of apocrine glands?

A

axilla and groin

116
Q

what is the of the structure formed by a sebaceous gland and a hair follicle?

A

pilosebaceous unit

117
Q

where are the largest sebaceous glands found?

A

face and chest

118
Q

when do sebaceous glands start secreting?

A

puberty

119
Q

what are the 2 main functions of sebaceous glands?

A
  1. control moisture loss

2. protection from bacterial and fungal infection

120
Q

why do sebaceous glands protect the body from bacterial and fungal infection?

A

the sebum secreted creates a slight acidic environment

121
Q

what hormone are the apocrine sweat glands dependent on?

A

androgens

122
Q

which skin glands are the most involved in thermoregulation?

A

eccrine glands

123
Q

what nervous system controls the secretions of eccrine glands?

A

sympathetic autonomic nervous system

124
Q

where do sebaceous glands open onto?

A

hair follicles

125
Q

where do eccrine glands open onto?

A

skin surface

126
Q

what is the main cause of toxic epidermal necrolysis (acute skin failure)?

A

drugs

127
Q

why does scale cause direct protein loss?

A

scale is made of keratin

128
Q

what is a compound fracture?

A

a break in the bone AND bone exposed (direct break in skin)

129
Q

where does vitamin D metabolism occur?

A

keratinocytes in the skin

130
Q

what is the equation for vitamin D synthesis?

A

cholecalciferol –> vit D3

using UV

131
Q

what thyroid hormone is produced in the skin? (and from what hormone?)

A

T3

T4 –> T3

132
Q

what is crusted scabies?

A

scabies but with a much higher number of mites on the body than usual scabies

133
Q

what failure is usually present in individuals who get crusted scabies?

A

immune system failure

134
Q

what is tuberculoid leprosy?

A

a type of leprosy where you have few parasites but a huge immune response

135
Q

what is the name of disseminated herpes simplex virus infection?
(widespread infection instead of localised cold sores)

A

eczema herpeticum

136
Q

what type of tendency can cause eczema herpeticum to occur?

A

atopic tendency

137
Q

Are langerhans cells innate or adaptive immunity?

A

innate immunity

138
Q

What is the keratin layer made of?

A

corneocytes

139
Q

what makes corneocytes?

A

terminal differentiation of keratinocytes

140
Q

what 3 important structural proteins are found in the epidermis?

A

filaggrin
involucrin
keratin

141
Q

What do keratinocytes produce that can directly kill pathogens?

A

anti-microbial peptides

142
Q

what granules characterises langerhans cells?

A

birbeck granule

143
Q

what T cells are mainly found in the epidermis?

A

CD8+ T cells4

cytotoxic

144
Q

what peptide produced by keratinocytes is found in a high level in psoriasis lesions?

A

anti-microbial pepitides

145
Q

what type of helper T cells are associated with psoriasis?

A

Th1

Th17

146
Q

what type of helper T cells are associated with atopic dermatitis?

A

Th2

Th17

147
Q

where are T cells produced?

A

bone marrow

148
Q

where are T cells sensitised?

A

thymus

149
Q

what MHC class is found on the surface of almost all cells?

A

MHC-I

150
Q

what type of T cells do MHC-I present antigens to?

A

cytotoxic T cells

151
Q

what MHC class is found on professional antigen presenting cells?

A

MHC-II

152
Q

what type of T cells do MHC-II present antigens to?

A

helper T cells

153
Q

what mutation is associated with severe/early onset of atopic eczema?

A

mutation in fillagrin gene

154
Q

what is the function of fillagrin?

A

bind to water molecules- water retention

natural moisturiser

155
Q

in vitiligo, what cells are being attacked by autoantibodies?

A

melanocytes

156
Q

what antibodies mediate type 1 hypersensitivities?

A

IgE

157
Q

what antibodies mediate Type 2 hypersensitivities?

A

IgM and IgG

158
Q

what cell type mediates Type 4 hypersensitivities?

A

Th1 cells

159
Q

what are the 2 types of fascia?

A 
superficial fascia (subcutaneous tissue)
deep fascia
160
Q

compare the connective tissue in superficial fasca to deep fascia?

A

superficial fascia:
loose connective tissue mixed with fat

deep fascia:
dense connective tissue

161
Q

what is the name of the deep fascia that separates muscle compartments?

A

intermuscular septa

162
Q

in which fascia do the cutaneous nerves and veins run?

A

superficial fascia

163
Q

which artery of the forearm forms the deep palmar arch?

A

radial artery

164
Q

which artery of the forearm forms the superficial palmar arch?

A

ulnar artery

165
Q

what is the name of the network of veins seen on the dorsal aspect of the palms?

A

dorsal venous network

166
Q

what vein drains blood from the lateral aspect of the forearm?

A

cephalic vein

167
Q

what vein drains blood from the medial aspect of the forearm?

A

basilic vein

168
Q

what are the names of any 2 veins which accompany an artery and eventually join?

A

venae comitantes

169
Q

what connects the cephalic vein to the basilic vein?

A

median cubital vein

170
Q

what artery runs into the anterior comparment oft he leg?

A

anterior tibial artery

171
Q

what artery runs into the posterior compartment of the leg?

A

posterior tibial artery

172
Q

what artery does the fibular artery bifurcate off of?

A

posterior tibial artery

173
Q

what artery supplies the dorsal foot?

A

dorsal artery

174
Q

what arteries supplies the plantar foot?

A

lateral plantar artery

medial plantar artery

175
Q

which plantar artery forms the plantar arch?

A

lateral plantar

176
Q

what are deep veins of the leg?

A

popliteal vein

femoral vein

177
Q

what superficial vein drains directly into the femoral vein?

A

great saphenous vein

178
Q

what superficial vein drains into the popliteal vein?

A

small saphenous vein

179
Q

where does the great saphenous vein arise from?

A

dorsal venous arch

180
Q

where does the small saphenous vein arise from?

A

dorsal venous arch

181
Q

does the great saphenous vein run in front or behind the medial malleolus?

A

in front of

182
Q

does the small saphenous vein run in front or behind the lateral malleolus?

A

behind

183
Q

what aspect of the lower limb does the great saphenous vein run?

A

medial aspect of the lower limb

184
Q

what aspect of the lower limb does the small saphenous vein run?

A

posterior midline of the lower limb

185
Q

what is the name of the most common site of venous ulceration?

A

gaiter area

186
Q

where is the gaiter area?

A

medial aspect of the distal lef

187
Q

what is the route of the lymphatics in the upper limb?

A

cubital nodes
lateral axillary nodes
apical axillary nodes

188
Q

in the limbs, what blood vessels do the lymphatics tend to follow?

A

veins

189
Q

in the abdomen, what blood vessels do the lymphatics tend to follow?

A

arteries

190
Q

where do the popliteal lymph nodes drain to?

A

superficial and deep inguinal nodes

191
Q

What type of immunological reaction is pemphigus or pemphigoid?

A 
type 2 
(direct cell killing)
192
Q

what type of immunological reaction is urticaria usually?

A 
type 1
(IgE mediated)
193
Q

what type of immunological reaction is erythema/rash usually?

A 
type 4
(delayed type)
194
Q

what type of immunological reaction is purpura usually?

A 
type 3
(immune-complex mediated)
195
Q

what is purpura?

A

red/purple spots that do not blanche

196
Q

what is the cause of purpura?

A

bleeding under the skin

197
Q

what happens to an allergic reaction when the dose of drug is decreased?

A

nothing

not dose-dependent

198
Q

what happens to a non-immunologial drug reaction when the dose of drug is decreased?

A

reaction is usually less

dose-dependent

199
Q

What is a morbiliform rash?

A

a rash which looks like measels

200
Q

What is a pustular rash?

A

a rash with papules containin pus

201
Q

What is a papulosquamous rash?

A

a rash with hyperkeratosis

202
Q

is a high molecular weight drug or a low molecular weight drug more likely to be involved in drug eruptions?

A

high molecular weight

203
Q

what is the most common type of cutaneous drug eruption?

A

exanthematous

or maculopapular

204
Q

what type of hypersensitivity is an exanthematous (maculopapular) rash?

A 
type IV
(delayed type)
205
Q

what is the usual onset of an exanthematous drug reaction?

A

4-21 days after first taking drug

206
Q

what are the 6 indicators of a potential severe exanthematous drug eruption?

A
  1. involvement of mucous membranes and face
  2. facial oedema and erythema
  3. widespread confluent erythema
  4. fever (>38.5)
  5. blisters, purpura, necrosis
  6. SOB, wheeze
207
Q

what happens in a non-immunological type 1 drug reaction? (eg urticaria)

A

direct release of inflammatory mediators from mast cells due to direct effect of drug
(not IgE mediated)

208
Q

What do you see clinically on a patient with acute generalised exanthematous pustulosis? (AGEP)

A

extensive sheets of pustules

209
Q

what is the usual cause of acute generalised exanthematous pustulosis? (AGEP)

A

drug eruption

210
Q

What are the 4 main severe cutaneous adverse drug reactions?

A
  1. Stevens-Johnson syndrome (SJS)
  2. Toxic epidermal necrosis (TEN)
  3. Drug reaction with eosinophilia and systemic symptoms (DRESS)
  4. Acute generalised exanthematous pustulosis (AGEP)
211
Q

What is a positive nikolsky sign?

A

gentle touching of the skin causes it to fall off

212
Q

what is the nikolsky sign for pemphigus?

A

positive

213
Q

what is the nikolsky sign for pemphigoid?

A

negative

214
Q

what is the nikolsky sign for toxic epidermal nectosis?

A

positive

215
Q

is phototoxicity an immunological or non-immunological drug reaction?

A

non-immunological

216
Q

what are the 3 acute features of phototoxic drug reactions?

A
  1. skin toxicity
  2. systemic toxicity
  3. photodegradation
217
Q

what are the 3 chronic features of phototoxic drug reactions?

A
  1. pigmentation
  2. photoageing
  3. photocarcinogenesis
218
Q

What 2 requirements are needed for a phototoxic cutaneous drug reaction?

A
  1. sufficient photo-reactive drug

2. appropriate wavelength of light

219
Q

What is the mild form of polymorphic light eruption (PLE) commonly known as?

A

prickly heat

220
Q

compare photo allergy and photoxicity in terms of immune sensitisation?

A

photo allergy requires immune sensitisation

phototoxicity does not

221
Q

compare photodermatose to photoaggravated dermatose?

A

photodermatose: condition caused by light

photoaggravated dermatose: condition not cuased by light but can be made worse by it

222
Q

What are porphyrias?

A

a group of conditions where there is a build up of porphyrin chemicals

223
Q

What is the most common skin porphyria in Scotland?

A

porphyria cutanea tarda

PCT

224
Q

what is a porphyrin?

A

normal metabolites which are part of the haem metabolic pathway

225
Q

what enzyme is defective in porphyria cutanea tarda?

A

uroporphyrinogen decarboxylase

226
Q

what porphyrin builds up in porphyria cutanea tarda?

A

uroporphyrinogen III

227
Q

where is the enzyme uroporphyrinogen decarboxylase made?

A

the liver

228
Q

what is the typical presentation of porphyria cutanea tarda?

A

blistering and fragility

also possible hyperpigmentation, hypertrichosis, solar urticaria, morphoea

229
Q

what is hirtuism?

A

increased hair growth in male pattern

230
Q

what is hypertrichosis?

A

increased hair growth generally

231
Q

what is morphoea?

A

scarring process in the dermis

232
Q

How do you investigate a possible porphyria cutanea tarda?

A

woods lamp using patients urine

233
Q

what are the 4 main causes of porphyria cutanea tarda?

A

alcohol
viral hepatitis
oestrogens
haemochromatosis

all cause decreased uroporphyrinogen decarboxylase production in the liver

234
Q

what porphyrin builds up in erythropoietic protoporphyria?

A

protoporphyrin IX

235
Q

what enzyme is deficient in erythropoietic protoporphyria?

A

ferrochelatase

236
Q

what vitamin do patients with porphyrias usually become deficient in?

A

vit D due to sun avoidance

237
Q

compare signs and symptoms of erythropoietic protoporphyria?

A

no signs only symptoms (Severe prickly burning which lasts a few days)

although eventually scars appear

238
Q

what is usually seen in a patient with a porphyria’s full blood count?

A 
reduced Hb (due to lack of haem)
--> anaemic
239
Q

what is the management of porphyria cutanea tarda?

A

treatment of underlying condition

240
Q

what is the management of erythropoietic protoporphyria?

A

visible light protection measures

241
Q

what porphyrin builds up in acute intermittent porphyria?

A

porphobillinogen (PBG)

242
Q

what enzyme is deficient in acute intermittent porphyria?

A

PBG deaminase

243
Q

What is virulence?

A

the capacity of a microbe to cause damage to the host

244
Q

What is adhesin?

A

a virulence factor which enables binding of the organism to host tissue

245
Q

what is invasin?

A

a virulence factor which enables the organism to invade a host cell/tissue

246
Q

what is impedin?

A

a virulence factor which enables the organism to avoid host defense mechanisms

247
Q

what is aggressin?

A

a virulence factor which causes damage to the host directly

248
Q

what is modulin?

A

a virulence factor which causes damage to the host indirectly

249
Q

where is S. aureus usually carried by carriers?

A 
anterior nares (in the nose)
perineum
250
Q

what is haemolysin?

A

a virulence factor which breaks down clots

251
Q

what adhesin increases the chance of a specific S. aureus strain being able to infect a joint?

A

collagen binding protein

252
Q

what impedin, found in some strains of S. aureus is associated with severe skin infections?

A

Panton Valentine Leukocidin

253
Q

compare PVL toxin percentage of hospital acquired MRSA strands to community acquired strands?

A

higher percentage of community acquired MRSA contain PVL than hospital acquired strands

254
Q

what is refractory hypoxaemia?

A

oxygen is reduced but because the tissue is dead this cannot be improved by using an oxygen mask

255
Q

What are superantigens?

A

antigens which causes immune system to respond with an inappropriate immune response that causes host damage

256
Q

Why do superantigens cause a massive release of cytokines and an inappropriate immune response? (which leads to huge scale inflammation)

A

because they don’t go through the normal reaction between receptor and presenting antigen

257
Q

What superantigen found in S. aureus is associated with Toxic Shock Syndrome?

A

TSST-1

toxic shock syndrome toxin 1

258
Q

what are the 3 main skin infections caused by Strep pyogenes? (GAS)

A

impetigo
cellultis (erysipelas)
necrotising fasciitis

259
Q

what is the lancefield system?

A

a system which serotypes the cell wall carbohydrate of a bacteria

260
Q

what Strep infection has a lancefield classification of A?

A

Strep pyogenes

GAS

261
Q

what is celulitis?

A

skin infection of the dermis

no necrosis

262
Q

Why is there no bacteremia in S. aureus Toxic Shock Syndrome?

A

because the superantigen goes through the blood stream causing host destruction, the infection itself is localised

263
Q

What acts as the brick and mortar in the brick and mortar model of the stratum corneum?

A

bricks- corneocytes

mortar- intercellular lipids

264
Q

what are the corneocytes held together by?

A

corneodesmosomes

265
Q

what are the 2 entry routes of drug through the skin?

A 
intercellular route (through intercellular lipids)
transcellular route (through corneocytes)
266
Q

why is the intercellular route of drug entry through the skin highly tortuous?

A

it has to weave between the corneocytes

267
Q

what is Fick’s law?

A 
J = Kp x Cv
J = Rate of Absorption (flux)
Kp = permeability coefficient
Cv = concenration of drug in vehicle
268
Q

what is the best combination of drug and base to allow a good partition across the stratum corneum?

A

lipophilic drug in hydrophilic base

269
Q

why does a lipophilic drug in a lipophilic base not allow a good partition across the stratum corneum?

A

lipophilic vehicle will retain the drug

270
Q

what are excipents?

A

molecules which are included in the drug vehicle to increase solubility and enhance absorption

271
Q

what are 2 ways to improve partitioning of the drug across the stratum corneum?

A
  1. hydration of the skin by occlusion

2. addition of excipients

272
Q

what receptors do glucocorticoids signal via?

A

nuclear receptors

273
Q

how do glucocorticoids enter cells?

A

by diffusion across the plasma membrane

274
Q

when glucorticoids are within the cytoplasm what do they combine with?

A

GRalpha molecules

275
Q

what has to dissociate from the GRalpha molecules in order to let glucocorticoids combine?

A

inhibitory heat shock proteins

276
Q

what allows the activated GRalpha receptor to translocate to the nucleus once it has binded with a glucocorticoid?

A

importins

277
Q

what must form before the GRalphas can bind to glucorticoid response elements in the nucleus?

A

GRalpha monomers must become homodimers

278
Q

where are glucocorticoid response elements found in genes?

A

in the promoter regions

279
Q

what is the main disadvantage of subcutaneous administration?

A

injection volume limited

280
Q

what is iontophoresis?

A

application of low voltage electrical pulses to the skin via a surface electrode in order to drive low molecular weight molecules of the same charge through the skin

281
Q

what is electroporation?

A

very brief high voltage pulses which lead to pore formation in order to deliver hydrophilic and charged molecules into the skin

282
Q

what is sonophoresis?

A

use of ultrasound to increase skin permeability

Dermatology (4 decks)

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