Week 1 Flashcards

1
Q

The layers of skin

A

Epidermis
Glands / hairs/ nails
Dermis
Sub cutis

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2
Q

What is the layer between epidermis and dermis called

A

Dermo-epidermal junction

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3
Q

Function of dermo-epidermal junction

A

Semi permeable membrane filtering substances that crosses
Anchors the epidermis to the dermis

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4
Q

The dermis is mainly

A

Connective tissue

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5
Q

The Sub cutis layer is mainly

A

Fat

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6
Q

The layers of epidermis (from top to low)

A

Keratin layer
Granular layer
Prickle cell layer
Basal layer

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7
Q

What are basal stem cells

A

Cells that can differentiate into a specific type of cell of the epidermis and migrate through it to replace it

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8
Q

Where are basal stem cells located at

A

Basal layer of epidermis

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9
Q

What cells are in the epidermis

A

Keratinocytes
Melanocytes
Langerhans cells
Merkel cells
Basal cells

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10
Q

Which type of cells make up the most of epidermis

A

Keratinocytes

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11
Q

Function of langerhans cells

A

Dendritic cells involved in immunological functions of the skin

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12
Q

Function of Merkel cells

A

Mechanoreceptor cells

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13
Q

Function of melanocytes

A

Pigment producing dendritic cells protecting against sun damage

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14
Q

Where are langerhan cells located at

A

Prickle cell layer of epidermis

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15
Q

Where are Merkel cells located at

A

Basal layer of epidermis

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16
Q

Where are melanocytes located at

A

Basal layer of epidermis

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17
Q

Basal cells at the basal layer are which type of cells

A

Cuboidal cells

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18
Q

Features of structure of prickle cell layer

A

Large polyhedral cells
with a lot of desmosomes in between the cells acting as connections

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19
Q

Features of granular layer

A

2-3 layers of flatter cells
Cells do not have nuclei
Lamellar bodies

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20
Q

Features of keratin layer

A

Mostly corneocytes (dead keratinocytes)
Lamellar granules
Waterproof barrier

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21
Q

Function of keratin layer

A

Prevents entry of unwanted substaces
Prevents excessive loss of water

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22
Q

The cells at the outermost layer of epidermis are

A

Dead cells (corneocytes) which are continually shed and replaced from below

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23
Q

What makes the keratin layer waterproof

A

Cells are close to each other
Lamellar granules release lipids which is hydrophobic

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24
Q

How do melanocytes protect us against sun damage

A
  1. Melanocytes produce melanin
  2. Melanin absorb light and are contained in melanosomes
  3. Melanosomes are then transported to adjacent keratinocytes by dendrites of the melanocytes
  4. This induces pigmentation and protect the basal cells against UV radiation by absorbing the UV light (because it is black)
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25
Q

What causes different skin colours

A
  1. Due to different activity level of melanocytes.
    - e.g. melanocytes in black skin has higher activity level = produce more melanin = more pigmentation
  2. Ratio between eumelanin and phenomelanin
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26
Q

What is vitiligo and what causes it

A

Vitiligo = patches of skin losing colour
Due to autoimmune destruction attacking melanocytes

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27
Q

What causes albinism

A

Genetic disorder reducing melanin production

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28
Q

What causes skin hyperpigmentation in Addison’s disease

A

High ACTH stimulating melanocytes to produce more melanin

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29
Q

Structure of hair follicles

A

Specialized keratins

Hair papilla is in the dermis layer and it extends into the epidermal layer and out of the skin

Sebaceous gland next to it

Arrector pili muscle attached to the hair follicles

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30
Q

Function of arrestor pili muscle

A

It contracts to erect the hair when you’re cold to provide thermal insulation
= causes goosebumps

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31
Q

What condition affects the arrestor pili muscle

A

Leprosy

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32
Q

What causes hair to be pigmented

A

Melanocytes in epidermis

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33
Q

What are the phases of growth of hair

A

Anagen
Catagen
Telogen

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34
Q

What is anagen

A

Growth of new hair

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35
Q

What is catagen

A

end of active hair growth and cuts individual hairs off from the blood supply and from the cells that produce new hair (forms club hair)

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36
Q

What is telogen

A

resting period when strands remain in their follicles till they shed

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37
Q

Most hair at any time are in which phase

A

Anagen

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38
Q

Why can animals’ fur shed at the same time whereas human hair does not

A

Because animals have synchronous telogen phase whereas in humans the telogen phase of each hair is different

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39
Q

List the outer structures of the nail

A

Nail plate
Nail folds
Eponychium

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40
Q

What are the nail folds

A

The skin around the nail that protects the margin of the nails

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41
Q

What is the eponychium

A

keratin layer of the skin that extends over the proximal nail plate

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42
Q

What are the structures underneath the nail plate

A

Nail bed
Germinal matrix
Hyponychium

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43
Q

What is the nail bed

A

Directly underneath the nail plate providing a smooth surface for the nail plate to glide over during growth

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44
Q

How do nail plates grow

A

Cells in germinal matrix divide and become keratinised. The continuous cell division pushes the nail plate, letting it glide over the nail bed = nail becomes longer

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45
Q

What is the hyponychium

A

The area underneath the free edge of nail plate

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46
Q

What are the 2 layers of dermis

A

Papillary dermis
Reticular dermis

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47
Q

Describe the papillary dermis and reticular dermis layers

A

Papillary dermis is thinner and it is just below the epidermis
Reticular dermis layer is thicker and contains several structures

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48
Q

What structures are in reticular dermis layer

A

Blood vessels
Pilosebaceous units (sebaceous gland + hair follicle)
Lymphatics
Nerves

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49
Q

Structures in dermis

A

Blood vessels
Lymphatics
Nerves
Collagen and elastin fibres
Hair follicles
Glands
Cells

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50
Q

What cells are present in dermis

A

Macrophage
Mast cells
Langerhans cells
Fibroblasts

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51
Q

What are the 2 types of aging

A

Intrinsic and extrinsic

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52
Q

What is intrinsic aging

A

Inevitable physiological process that causes skin to look more saggy and less firm, hollowed cheeks as you age

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53
Q

What is extrinsic aging

A

Skin aging due to external factors such as UV light, smoke particles, pollutants on top of intrinsic aging

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54
Q

If an area of skin aging is mostly due to extrinsic aging, what would the features be

A

Coarse wrinkles (deep wrinkles)
Loss of elasticity
Rough texture appearance
Hypertrophic photoaging

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55
Q

If an area of skin aging is mostly due to intrinsic aging, what would the features be

A

Fine wrinkles
Dry skin
Thin skin
Telangiectasia
Atrophic photoaging

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56
Q

Atrophic photoaging increases the risk of

A

Non melanoma skin cancer

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57
Q

What type of plexus do vessels in dermis form

A

horizontal plexuses

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58
Q

Dilation of lymphatic vessels in the dermis can cause

A

Chronic lymphoedema

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59
Q

Dilation of blood vessels in the dermis can cause

A

Angioma

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60
Q

What structures are responsible for the innervation of the skin

A

Free sensory nerve endings
Special receptors
Motor nerve fibre

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61
Q

What are the special receptors for sensory innervation of the skin

A

Pacinian corpuscle
Meissners corpuscle

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62
Q

Pacinian corpuscle is for what type of sensory

A

Pressure

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63
Q

Meissner corpuscle is for what type of sensory

A

Vibration

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64
Q

Where is Meissener’s corpuscle located at

A

Papillary layer of the dermis

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65
Q

Where is Pacinian corpuscle located at

A

Reticular layer of dermis

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66
Q

What is alopecia areata and what causes it

A

Patchy hair loss
Due to autoimmune destruction of hair papilla causing hair to fall out

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67
Q

Does hair grow back in affected areas in alopecia

A

Yes, because the stem cells are not attacked

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68
Q

What are the 3 types of glands present in skin

A

Apocrine
Eccrine
Sebaceous

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69
Q

What is eccrine gland

A

Sweat glands that open directly onto the skin surface

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70
Q

What is apocrine gland

A

glands that drain into hair follicles

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71
Q

What are sebaceous glands

A

Glands in hair follicles that secrete sebum

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72
Q

When do sebaceous glands become active and start producing sebum

A

During puberty

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73
Q

What happens when sebaceous glands are clogged because they produce too much sebum

A

Acne

74
Q

Function of sebum

A

Control moisture loss from skin
Protects against infection

75
Q

On which body parts are sebaceous glands found

A

Everywhere except Soles and palms

76
Q

On which body parts are eccrine glands found

A

Everywhere ESPECIALLY palms, soles, forehead and axillae

77
Q

Function of eccrine gland

A

Thermal regulation
Aid grip

78
Q

On which body partsare apocrine glands found

A

Axillae
Groin
Eyelids
Ears
Perineal region

79
Q

Functions of the skin

A

Barrier
Metabolism and Detoxification
Thermoregulation
Immune defense
Sensation

80
Q

What is metabolised by the skin

A

Thyroid hormones
Vitamin D

81
Q

What does the skin do to thyroid hormones

A

Converts T4 into metabolically active T3

82
Q

Around how much % of thyroid hormones are metabolised (converted) by the skin

A

80%

83
Q

Role of Vitamin D

A

To increase serum Ca2+ when there is a decrease.
By increasing absorption of Ca2+ from digested food in intestines and reabsorption of Ca2+ in kidneys

84
Q

2 forms of Vitamin D

A

Vitamin D2
Vitamin D3

85
Q

Which form of Vitamin D is more effective in raising serum vitamin D (metabolically active form)

A

Vitamin D3

86
Q

Vitamin D2 is obtained by

A

Ingestion of plants esp mushroom

87
Q

Vitamin D3 is obtained by

A

Mostly made by the skin
ingestion

88
Q

How does the skin synthesise vitamin D3

A

By the action of ultraviolet B from sunlight on 7-dehydrocholesterol

89
Q

What happens to vitamin D3 after it is synthesised in the skin

A

Stored in the liver then it is converted into its biologically active form in the kidneys

90
Q

Causes of vitamin D deficiency

A

Lack of sunlight
Lack of vitamin D in diet
Malabsorption
Kidney disorders

91
Q

Vitamin D deficiency can cause

A

Osteomalacia
Rickets in children
Secondary hyperparathyroidism

92
Q

What is rickets

A

A condition that affects the development of bones in children causing bone pain, poor growth and weak bones that can lead to bone deformities

93
Q

What can be caused if there is damage to skin barrier

A

Fluid loss
Protein loss -> hypoalbuminaemia
Infection

94
Q

What factors that contribute to skin act as an immunological defence against pathogens

A

Keratin layer
Keratinocytes
Immune cells of the epidermis and dermis

95
Q

How do keratinocytes provide immunological defence against pathogens

A

When they sense pathogens using cell surface receptors:
Produce anti-microbial peptides (AMP)
Produce cytokines and chemokine

96
Q

What are the immune cells in the epidermis

A

Langerhan cells
T cells

97
Q

What are the immune cells in the dermis

A

T cells
Dermal dendritic cell
Plasmacytoid dendritic cell
Macrophages
Neutrophils
Mast cells

98
Q

What is a characteristic feature of Langerhan cells

A

Birbeck granules

99
Q

Which type of T cell is the main T cell found in dermis layer

A

CD8+

100
Q

Which types of T cells are found in the epidermis layer

A

CD4+ and CD8+

101
Q

What are CD8+ cells

A

Differentiate into cytotoxic cells

102
Q

What are CD4+ cells

A

Helper cells that differentiate into different helper cells to produce different cytokines
They also instruct CD8+ cells and B cells

103
Q

What are the different Helper T cells differentiated from CD4+

A

Th1
Th2
Th17

104
Q

Th1 function

A

Secrete IL2 and IFNy to activate macrophages

105
Q

Th2 function

A

Secrete IL4 IL5 IL13 to stimulate B cells

106
Q

Th17 function

A

Secrete IL17 to modulate immunity

107
Q

Function of the dendritic cells in the dermis

A

To present antigens to T and B cells

108
Q

Which immune cell is responsible for allergy

A

Mast cells

109
Q

What type of disorder is psoriasis classified as

A

Autoimmune disorder

110
Q

Pathogenesis of psoriasis

A
  1. Keratinocytes under stress release AMP and cytokines that stimulate plasmacytoid dendritic cells in dermis to produce other cytokines
  2. these chemical signals causes dendritic cells to present to T cells
  3. Th1 and Th17 predominant
  4. Causing inflammation cascade
  5. Causes keratinocyte proliferation and increased epidermal turnover
111
Q

What are the 5 types of psoriasis

A

Chronic plaque psoriasis
Inverse psoriasis
Guttate psoriasis
Pustular psoriasis
Generalised psoriasis

112
Q

Which immune complex is mainly present in psoriasis

A

Th1
Th17

113
Q

Which type of psoriasis is the most common

A

Chronic plaque psoriasis

114
Q

What are the clinical features presented in chronic plaque psoriasis

A

Plaques that are :
Symmetrical
Scaly
Well demarcated
itchy

115
Q

Where are chronic plaque psoriasis usually found

A

Extensor surface distribution
Scalp
Lower back

116
Q

Where are the extensor surfaces

A

Front of the knee
Back of the elbow

117
Q

What are the clinical features caused by inverse psoriasis

A

Smooth erythematous plaques

118
Q

Where is inverse psoriasis usually found

A

Areas where the skin rubs against each other
- axilla
- groin
- gluteal cleft
- genital area

119
Q

What clinical features are caused by guttate psoriasis

A

Sudden emergence of multiple small tear drop shaped erythematous plaques

120
Q

Guttate psoriasis usually occurs after

A

Streptococcal infection e.g. Strep throat

121
Q

What may be a common illness patients with Guttate psoriasis have a week before rashes appear

A

Tonsilitis

122
Q

What clinical features are presented in pustular psoriasis

A

Multiple red round spots (petechiae)
Multiple pustules

123
Q

Where are pustular psoriasis commonly found and what is the other name for pustular psoriasis

A

On palms and soles
Hence it is also called palmoplantar pustulosis

124
Q

What are the subtypes of generalised psoriasis

A

Erythrodermic psoriasis
Generalised pustular psoriasis

125
Q

Risk factors for developing psoriasis

A

Genetics
Obesity
Smoking
HIV

126
Q

Risk factors that can exacerbate psoriasis

A

Skin trauma (Koebner Phenomenon)
Streptococcal infection
Stress
Drugs
Withdrawal of steroids
Hormones

127
Q

What is Koebner’s phenomenon

A

Skin trauma leads to new lesions occurring at sites of skin trauma meaning it triggers psoriasis in an area that was not previously affected

128
Q

Koebner’s phenomenon can be seen in which other conditions except from psoriasis

A

Vitiligo
Lichen Planus

129
Q

What drugs can exacerbate psoriasis (BALI)

A

Beta blockers
ACEi
Antimalarials (hydroxychloroquine)
Lithium
Indomethacin (NSAID)

130
Q

Psoriasis is associated with which other conditions

A

Psoriatic arthritis
IBD
higher risk of developing other autoimmune diseases

131
Q

Apart from the skin, what other signs of psoriasis can be see

A

Nail involvement
- nail pitting
- nail onycholysis
- thickening of nail bed

132
Q

Why should patients with psoriasis avoid scratching

A

Because it can lead to skin trauma -> Koebner’s phenomenon -> psoriasis flare up

133
Q

What is a sign of psoriasis

A

Auspitz sign

134
Q

What is Auspitz sing

A

Removal of surface scale reveals tiny bleeding points

135
Q

What will a biopsy of psoriatic skin show

A

Thickened epidermis
Parakeratosis: Retention of nuclei of corneocytes at keratin layer (they should not have nuclei because they are dead cells)
Inflammatory cells

136
Q

What is parakeratosis

A

Retention of nuclei of corneocytes at keratin layer due to abnormal differentiation and proliferation of keratinocytes

137
Q

Management of chronic plaque psoriasis

A
  1. Topical therapy
  2. Phototherapy
  3. Systemic therapy
138
Q

Describe the topical therapy for psoriasis

A

Emollients with
1. Topical steroid + Topical vitamin D
2. Stop topical steroid but continue topical vitamin D twice daily
3. Stop topical vitamin D but continue topical steroid twice daily

139
Q

Examples of topical vitamin D

A

Calcipotriol
Calcitriol

140
Q

Why do you need to stop using topical steroid after certain amount of time

A

To avoid side effects such as unstable psoriasis / striae

141
Q

How long can you use a potent topical steroid for

A

4 weeks

142
Q

Mildly potent topical steroids are used in psoriasis for areas such as

A

Face
Groin
Breasts

143
Q

What are the drugs commonly used for topical steroid + topical via D therapy for psoriasis

A

Betamethasone (steroid) + calcipotriol

144
Q

What are the alternatives topical treatments for psoriasis if topical steroids + vitamin D are ineffective / contraindicated

A

Tar
Dithranol

145
Q

When is phototherapy indicated for psoriasis

A

If
- extensive psoriasis
- nail disease which cannot be treated topically
- ineffective topical therapy

146
Q

What types of phototherapies are there for psoriasis

A

UVB
PUVA (psoralen + UVA)

147
Q

When is PUVA used and why shouldn’t it be used unless necessary

A

PUVA used if UVB is ineffective
PUVA is not used unless necessary due to its side effects: increase risk in skin cancer, skin irritation

148
Q

PUVA + usage of which drug can increase risk of skin cancer

A

Ciclosporin (medication used in systemic therapy for psoriasis)

149
Q

PUVA should be avoided in which group of people

A
  • those that are using / likely to use ciclosporin
  • young
  • light skin type (they are already prone to skin cancer)
150
Q

When is systemic therapy indicated in psoriasis

A

If psoriasis is not controlled by topical therapy
+ significant impact on wellbeing
+ extensive psoriasis / nail disease / ineffective phototherapy

151
Q

Describe the order of drugs used in systemic therapy for psoriasis

A
  1. Methotrexate
  2. Ciclosporin
  3. Acitretin
152
Q

Contraindications for methotrexate

A

Those that are pregnant / planning to be pregnant

153
Q

Advise given to patients who are going to use methotrexate

A

Contraception during treatment and 6 months after ending treatment

154
Q

When is ciclosporin used in psoriasis

A

For patients considering pregnancy
For rapid disease control
For patients with palmoplantar pustulosis

155
Q

What does atopy mean

A

When a patient has predisposition to abnormally exaggerated IgE response to allergen

156
Q

Atopic individuals are at risk of developing which conditions

A

Atopic dermatitis
Asthma
Allergic rhinitis
Food allergy

157
Q

Atopic dermatitis is most common in

A

Children, most present symptoms by the age of 5

158
Q

Causes of atopic dermatitis

A

Multifactorial - genetics, environment, immunological

159
Q

What genetic factor contributes to causing atopic dermatitis

A

Mutation in FLG gene which codes for filaggrin protein. Filaggrin protein is required for effective skin barrier hence mutation in FLG gene -> ineffective skin barrier

160
Q

How does ineffective skin barrier contribute to atopic dermatitis

A

Ineffective skin barrier allows antigens to enter the skin more easily which causes sensitization of the allergen then trigger inflammation in allergen stage

161
Q

Which immune complexes are mainly present in atopic dermatitis

A

Th2
Mast cells

162
Q

Patients with atopic dermatitis are more likely to have

A

Food allergy
Allergic rhinitis
Asthma

163
Q

What can trigger flares of atopic dermatitis

A

Certain chemicals in soaps / detergents / shampoo / perfume
Stress
Food
Fabrics
Hormones
Dry weather

164
Q

Symptoms of atopic dermatitis

A

Pruritus
Erythema
Scaling
Dry skin
Nodular pruigo
Flexural distribution of symptoms in older children / adults

165
Q

What is the distribution of atopic dermatitis in infants

A

Extensor surfaces
Face - cheeks
Neck
Scalp
Eyelids

166
Q

What are nodular pruigo

A

Very itchy nodules most commonly present in black people with atopic dermatitis

167
Q

What can you see in skin biopsy of atopic eczema

A

Spongiosis - intraepidermal oedema

168
Q

Diagnostic criteria for atopic dermatitis

A

Pruritus + 3 or more of the following:
- flexural dermatitis (or extensor dermatitis in infants)
- PMH of flexural dermatitis
- PMH of asthma / allergic rhinitis
- Dry skin in the last 12 months

169
Q

What is the first line treatment for atopic dermatitis

A

Identify and avoid triggers

170
Q

Management for mild atopic dermatitis

A

Emollients
Mild potency topical steroids (hydrocortisone)

171
Q

Management for moderate atopic dermatitis

A

Emollients
Moderate potency topical steroids
Topical calcineurin
Bandages

172
Q

Management for severe atopic dermatitis

A

Emollients
Potent topical steroids
Topical Calcineurin
Phototherapy
Systemic therapy

173
Q

What drugs are used in the systemic therapy for atopic dermatitis

A

Methotrexate
Azathioprine
Prednisolone

174
Q

Which drugs that are used in systemic therapy for atopic dermatitis are not safe in pregnancy

A

Methotrexate
Azathioprine

175
Q

Complications of atopic dermatitis

A

Infection due to ineffective skin barrier
Mental health

176
Q

What infections are at increased risk due to atopic dermatitis

A

S aureus
Eczema herpeticum

177
Q

What symptoms does S aureus infection cause in a patient with eczema

A

Oozing rash (weeping eczema) fluid seeping onto skin surface due to blood vessel dilatation causing fluid to leak out

Oedema

178
Q

Eczema herpeticum is caused by

A

Herpes simplex virus

179
Q

Treatment of eczema herpeticum

A

IV aciclovir

180
Q

What does acanthosis mean

A

Increased thickness of epithelium

181
Q

What does parakeratosis mean and in which condition is it present

A

Persistence of nuclei in the keratin layer
Present in psoriasis

182
Q

What does hyperkeratosis mean

A

Increased thickness of keratin layer