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Physiology Flashcards

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Dermatology Board Prep flashcards
1
Q

Examples of skin conditions with increasing prevalence (3)

A

Skin cancers
Venous Leg Ulceration
Atopic Dermatitis

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2
Q

Examples of skin conditions with decreasing prevalence (3)

A

Leprosy
Viral Exanthem
HIV-related skin disease

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3
Q

Epidermis

A

Outer layer of the skin

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4
Q

Epidermis: Main cell type

A

Keratinocytes (95% of the layer)

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5
Q

Dermis

A

Skin layer beneath the epidermis

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6
Q

Dermis components

A

Connective tissue

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7
Q

Embryology: Epidermis origin

A

Ectoderm cells from a single layer periderm

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8
Q

Embryology: Dermis origin

A

Formed from the mesoderm below the endoderm

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9
Q

Embryology: Melanocyte Origin

A

Neural crest

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10
Q

Foetal Skin Development: What has developed at 4 weeks?

A

Periderm
Basal Layer
Dermis

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11
Q

Foetal Skin Development: Foetal term for Dermis

A

Corium

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12
Q

Foetal Skin Development: What has developed at 16 weeks?

A

Keratin layer
Granular layer
Prickle Cell layer
Basal layer
Dermis

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13
Q

Blaschko’s Lines

A

Developmental growth patterns of the skin that do not follow blood vessels, nerves or lymphatics

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14
Q

Examples of Skin Appendages (4)

A

Nails
Glands
Hair
Mucosae

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15
Q

Skin Structure: What is the sub-cutis predominantly made of?

A

Adipose tissue

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16
Q

Epidermis: Cell layer

A

Stratified squamous epithelium

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17
Q

Epidermis: Thickness

A

1.5mm

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18
Q

Epidermis: What proteins are present?

A

Structural keratins

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19
Q

Epidermis: How is movement provided?

A

By the basement membrane

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20
Q

Epidermis: Number of layers

A

4

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21
Q

Epidermis: Layers (4)

A

Keratin Layer
Granular Layer
Prickle Cell Layer
Basal Layer

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22
Q

Epidermis: Cell Types Involved (4)

A

Keratinocytes
Melanocytes
Langerhans Cells
Merkel Cells

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23
Q

Epidermis: Function of Merkel Cells

A

Sensory function

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24
Q

Epidermis: Cell variation and differentiation is controlled by what? (3)

A

Growth Factors
Cell death
Hormones

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25
Q

Epidermis: Differentiation process

A

Keratinocytes migrate from the basement membrane

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26
Q

Epidermis: How long does it take for keratinocytes to migrate from the basement membrane to the surface?

A

28 days

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27
Q

Epidermis: Difference in the sole of the foot

A

Thick keratin layer due to area of high pressure

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28
Q

Basal Layer: Cell type

A

One cell thick small cuboidal cells

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29
Q

Basal Layer: Contains what protein?

A

Intermediate keratin filaments

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30
Q

Basal Layer: Metabolic action

A

High

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31
Q

Prickle Cell Layer: Cell type

A

Large Polyhedral Cell

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32
Q

Prickle Cell Layer: What cellular structure is present?

A

Desmosomes

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33
Q

Prickle Cell Layer: What proteins are present?

A

Intermediate filaments - to connect desmosomes

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34
Q

Granular Layer: High … content

A

Lipid

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35
Q

Granular Layer: Cellular structure

A

2-3 layers of flat cells

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36
Q

Granular Layer: What are the two signature organelles?

A

Keratohyalin Granules
Odland Bodies

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37
Q

Granular Layer: Large Keratohyalin Granule function

A

Contain structural filaggrin and involucrin proteins

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38
Q

Granular Layer: Odland Body function

A

Lamellar bodies that contain lipids

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39
Q

Granular Layer: This is the origin of what?

A

Cornified envelope

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40
Q

Granular Layer: Key feature of the cells of this layer

A

No cell nuclei

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41
Q

Keratin Layer: 80% of this layer is formed of what?

A

Keratin and Filaggrin

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42
Q

Keratin Layer: Generates what type of barrier?

A

Waterproof

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43
Q

Keratin Layer: Cell type of this layer

A

Corneocytes

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44
Q

Keratin Layer: Corneocytes

A

Overlapping non-nucleated cell remnants

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45
Q

Keratin Layer: Forms what type of envelope?

A

Insoluble and Cornified

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46
Q

Keratin Layer: Lamellar granules have what function?

A

Release lipids

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47
Q

Keratin Layer: Associated Disease example

A

HPV infects keratinocytes to form warts

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48
Q

Mucosal Membranes: Highly specialised function where? (5)

A

Eyes
Mouth
Nose
Gastrointestinal tract
Genitourinary tract

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49
Q

Mucosal Membranes: Oral Mucosa example of specialised area of mucosa

A

Tongue papillae for taste

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50
Q

Mucosal Membranes: How does this benefit mastication in the oral cavity?

A

Keratinised mucosa can deal with friction and pressure

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51
Q

Mucosal Membranes: The lining mucosa of the oral cavity has what property?

A

Non-keratinised

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52
Q

Epidermal Cells: 4 Main cell types

A

Keratinocytes
Melanocytes
Langerhans Cells
Merkel Cells

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53
Q

Epidermal Cells: location of Keratinocytes

A

Epidermis

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54
Q

Location of Melanocytes

A

Basal and Suprabasal

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55
Q

Location of Langerhans cells

A

Suprabasal

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56
Q

Location of Merkel Cells

A

Basal

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57
Q

Melanocytes: Migration pattern

A

Migrate from the neural crest to the epidermis in the first 3 months of foetal development

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58
Q

Melanocytes: Location

A

Basal layer and above

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59
Q

Melanocytes

A

Pigment-producing dendritic cells

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60
Q

Melanocytes: Cellular feature of cytoplasm

A

Larger than surrounding keratinocytes

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61
Q

Melanocytes: These cells contain what main organelle?

A

Melanosomes

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62
Q

Melanocytes: Function of melanosomes

A

Produce skin pigmentation as they allow the migration of melanin to keratinocytes

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63
Q

Melanocytes: Convert … to …

A

Tyrosine to Melanin

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64
Q

Melanocytes: Eumelanin colour

A

Brown or black

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65
Q

Melanocytes: What type of melanin is brown or black?

A

Eumelanin

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66
Q

Melanocytes: Phaeomelanin colour

A

Red or Yellow

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66
Q

Melanocytes: What melanin type is red or yellow?

A

Phaeomelanin

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67
Q

Melanocytes: Function of melani

A

Acts as a neutral density filter of light as a protective function over the nucleus to protect DNA

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68
Q

Melanocytes: What wavelengths does melanin absorb?

A

All wavelengths

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69
Q

Conditions affecting Skin Colour: Vitiligo

A

Autoimmune disease associated with loss of melanocytes

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70
Q

Conditions affecting Skin Colour: Albinism

A

Genetic partial loss of pigment production

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71
Q

Conditions affecting Skin Colour: Addison’s Disease

A

Excess ACTH from the pituitary gland causes excess melanocyte stimulating hormone to cause excess pigmentation

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72
Q

Conditions affecting Skin Colour: Nelson’s Syndrome

A

Melanin Stimulating Hormone is produced in excess by the pituitary

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73
Q

Conditions affecting Skin Colour: Malignant Melanoma

A

Tumour of the melanocyte cell line

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74
Q

Langerhans Cells: Origin

A

Mesenchymal

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75
Q

Langerhans Cells: Location of origin

A

Bone marrow

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76
Q

Langerhans Cells: What level are they located in the epidermis?

A

Prickle cell layer

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77
Q

Langerhans Cells: Locations (3)

A

Dermis
Lymph Nodes
Prickle cell level in the Epidermis

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78
Q

Langerhans Cells: These are found alongside what structure?

A

Birbeck granules

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79
Q

Langerhans Cells: Function

A

Skin Immune System

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80
Q

Merkel Cells: Location

A

Basal cell layer

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81
Q

Merkel Cells: Located between what two structures?

A

Keratinocytes
Nerve fibres

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82
Q

Merkel Cells: Function

A

Mechanoreceptors to detect pressure

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83
Q

Merkel Cells: Merkel Cell Cancer is caused by what?

A

Viral infection

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84
Q

Hair Follicles: Scientific term for hair follicle

A

Pilosebaceous Unit

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85
Q

Hair Follicles: Adjacent to what structures?

A

Sebaceous glands

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86
Q

Hair Follicles: Hair pigmentation is determined by what?

A

Melanocytes above the dermal papilla

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87
Q

Hair Follicles: Contains specialised what?

A

Keratins

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88
Q

Hair Follicles: Develops from what structure?

A

Hair Bud

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89
Q

Hair Follicles: Anagen phase

A

Growth phase

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90
Q

Hair Follicles: Anagen phase time period

A

3-7 years

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91
Q

Hair Follicles: What is present in the Anagen phase?

A

Dermal papilla

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92
Q

Hair Follicles: Catagen phase

A

Involution or Dying Phase

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93
Q

Hair Follicles: Catagen time period

A

3-4 weeks

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94
Q

Hair Follicles: Process during Catagen phase

A

Hair bulb retracts upwards to the surface

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95
Q

Hair Follicles: Telogen Phase

A

Resting or Shedding Phase

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96
Q

Hair Follicles: Telogen Phase hair shape during this phase

A

Club shaped

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97
Q

Hair Follicles: Impact during pregnancy

A

Excess growth during pregnancy
Then excess shedding afterwards

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98
Q

Hair Follicles: How are these changed by the menopause?

A

Due to changes in oestrogen levels

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99
Q

Alopecia Areata

A

Autoimmune disease of hair loss

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100
Q

Hair Follicles: What hormones may influence growth? (2)

A

Thryoxine
Androgens

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101
Q

Hair Follicles: Lanugo

A

In utero hair state

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102
Q

Nails: Contain specialised what?

A

Keratins

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103
Q

Nails: What is the origin of growth?

A

Nail matrix or root

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104
Q

Nails: Growth rate is greater where?

A

Fingers

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105
Q

Nails: Growth rate is greatest when?

A

Summer

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106
Q

Nails: 3 parts of the nail

A

Dorsal
Intermediate
Ventral

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107
Q

Nails: Dorsal part

A

Upper layer of the nail

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108
Q

Nails: Ventral part of the nail

A

Lower part of the nail

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109
Q

Nails: Dystrophic nails can be due to what?

A

HPV

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110
Q

Nails: Sub-ungal subkeratosis can be due to what?

A

Fungal infection
Skin disorders with fast cell turnover e.g. Psoriasis

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111
Q

Nails: Tuberous Sclerosis

A

Benign tumours of the nail

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112
Q

Derma-epidermal Junction: Functions as an interface between what?

A

Epidermis and Dermis

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113
Q

Derma-epidermal Junction: Functions to stick what together?

A

Basal Keratinocytes and the papillary dermis

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114
Q

Derma-epidermal Junction: Acts as a … membrane

A

Semi-permeable

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115
Q

Derma-epidermal Junction: What disorder is due to disruption to this?

A

Bullous Pemphigoid

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116
Q

Derma-epidermal Junction: Bullous Pemphigoid Pathophysiology

A

Antibodies attack the dermo-epidermal junction to form bullae and itchiness

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117
Q

Dermis: Cells involved (5)

A

Fibroblasts
Macrophages
Mast Cells
Lymphocytes
Langerhans Cells

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118
Q

Dermis: Function of Fibroblasts

A

Generate collagen and elastin

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119
Q

Dermis: Fibres present (2)

A

Collagen
Elastin

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120
Q

Dermis: Differences in Asian/Hispanic/Latino/African dermis

A

Thicker

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121
Q

Dermis: Ethnicities with a thicker dermis

A

Asian
Hispanic
Latino
African

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122
Q

Dermis: Differences in African skin

A

Larger and more numerous fibroblasts and macrophages

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123
Q

Dermis: Darker skin types have what difference?

A

Smaller collagen fibres that are more closely stacked and run in parallel to the epidermis

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124
Q

Dermis: Intrinsic Skin Ageing description

A

Reduced collagen

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125
Q

Dermis: Extrinsic Skin Ageing is due to what?

A

Pollutants
UV
Smoking particles

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126
Q

Blood Vessels: Location of large vessels

A

Subcutaneous Fat Level

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127
Q

Blood Vessels: Location of deep vascular plexus

A

Level of the hair bulb

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128
Q

Blood Vessels: Angioma

A

Benign dilation of the blood vessels in the dermal tissue to cause bumpy red eruptions with easy bleeding

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129
Q

Lymphatic Vessels: Progress from … to ….

A

Small non-contractile vessels
Large contractile lymphatic trunks

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130
Q

Lymphatic Vessels: Function - Enables the continual drainage of what?

A

Plasma proteins
Extravasated cells
Excess interstitial fluid

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131
Q

Lymphatic Vessels: Functions - Channelling of (2)

A

Microorganisms
Toxins

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132
Q

Lymphatic Vessels: Chronic Lymphoedema

A

Recurrent episodes of cellulitis causes inflammation and dilation to cause swelling

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133
Q

Nerves: Function of Pacinian Special Receptors

A

Detect pressure

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134
Q

Nerves: Function of Meissners Corpuscles

A

Detect Vibration

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135
Q

Neurofibromatosis

A

Tumour overgrowth developments on nerve tissue

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136
Q

Pilosebaceous Unit: Composed of what 4 structures?

A

Hair follicle
Hair shaft
Erector pili muscle
Sebaceous glands

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137
Q

Pilosebaceous Unit: Upper segment name

A

Infundibulum

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138
Q

Pilosebaceous Unit: Middle segment name

A

Isthmus

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139
Q

Pilosebaceous Unit: Isthmus function

A

Region where the sebaceous glands open into the hair follicle and stem cells are present

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140
Q

Pilosebaceous Unit: Lower base segment name

A

Hair bulb

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141
Q

Pilosebaceous Unit: Asian hair structure features

A

Straight and round
Large cross-sectional area
Fastest growth rate
Strong and durable

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142
Q

Pilosebaceous Unit: African hair structure features

A

Curl or spiral
Ellipsoidal cross section
Lower hair density
Slowest growth rate
Most fragile

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143
Q

Pilosebaceous Unit: Caucasian hair structure features

A

Straight to curly hair
Round or oval cross section
Highest hair density
Most moisture content
Strong and durable

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144
Q

Alopecia Areata

A

Autoimmune disorder in which antibodies attack the hair follicles dermal root to cause fallout

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145
Q

Hirsutism

A

Hair present in excess in inappropriate locations due to genetics or imbalance in androgens

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146
Q

Skin Glands: Apocrine Glands Function

A

Discharges contents into the hair follicle

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147
Q

Sebaceous Glands: Location

A

Face and Chest

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148
Q

Sebaceous Glands: Sensitive to what?

A

Hormones

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149
Q

Sebaceous Glands: When are they quiescent?

A

Pre-puberty

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150
Q

Sebaceous Glands: Produce what?

A

Sebum

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151
Q

Sebaceous Glands: Contents of sebum (4)

A

Squalene
Wax esters
Triglycerides
Free Fatty Acids

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152
Q

Sebaceous Glands: Secretion opening enters what canal?

A

Piliary

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153
Q

Sebaceous Glands: Functions (3)

A

Control moisture loss
Protect from fungal infection
Produces sticky oil to lubricate the hair follicle

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154
Q

Sebaceous Glands: What disease is distributed towards this structure?

A

Acne

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155
Q

Apocrine Glands: Develop as part of what?

A

Pilosebaceous unit

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156
Q

Apocrine Glands: Located where?

A

Axilla
Groin
Eyelids
Ears
Mammary region
Perineal region

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157
Q

Apocrine Glands: Dependent on what hormones?

A

Androgens

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158
Q

Apocrine Glands: Produces what?

A

Oily fluid

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159
Q

Apocrine Glands: Why does the oil smell at times?

A

Due to bacterial decompensation

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160
Q

Eccrine Glands: Located where?

A

Palms
Soles
Forehead
Axilla

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161
Q

Eccrine Glands: What is the nerve supply?

A

Sympathetic Cholinergic nerves

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162
Q

Eccrine Glands: Stimulated by what 3 factors?

A

Mental
Thermal
Gustatory

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163
Q

Eccrine Glands: Functions (2)

A

Discharges sweat with high water content for filtration and thermoregulation
Cool the body by evapouration
Moisten the palms and soles to aid grip

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164
Q

Skin Immunology: What structures contribute to the immunological function of the skin? (2)

A

Stratum corneum - Keratin Layer
Stratification

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165
Q

Skin Immunology: Cells contributing to the immune function of the skin (2)

A

Immune system cells
Keratinocytes

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166
Q

Keratin Layer: Rich in what?

A

Lipid

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167
Q

Keratin Layer: Features (2)

A

Tough
Physical barrier

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168
Q

Keratin Layer: Formed by what?

A

Terminal differentiation of keratinocytes to corneocytes

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169
Q

Epidermal Layer: Keratinocytes - Produce what?

A

Anti-microbial peptides

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170
Q

Epidermal Layer: Keratinocytes - Antimicrobial peptide function

A

Directly kill pathogens

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171
Q

Epidermal Layer: Keratinocytes - Role of these cells in Psoriasis

A

High antimicrobial peptide levels in the skin of psoriatic patients

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172
Q

Epidermal Layer: Keratinocytes - Produce what immune molecules?

A

Cytokines
Chemokines

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173
Q

Epidermal Layer: Langerhans Cells - Classified as what type of cell?

A

Antigen presenting cell

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174
Q

Epidermal Layer: Langerhans Cells - Located where in the epidermis?

A

Interspersed between keratinocytes

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175
Q

Epidermal Layer: Langerhans Cells - Characterised by what?

A

Birbeck Granule

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176
Q

Epidermal Layer: Langerhans Cells - Birbeck Granule functions (2)

A

Act as sentinels in the epidermis
Process antigen and microbial fragments to present them to effector T cells

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177
Q

Epidermal Layer: Langerhans Cells - Derived from what cell line?

A

Macrophage lineage

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178
Q

Epidermal Layer: Langerhans Cells - What disease are they involved in?

A

Langerhans Histiocytosis

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179
Q

Epidermal Layer: T Cells - What type is mainly found in epidermis?

A

CD8+ T cells

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180
Q

Epidermal Layer: T Cells - What type is found in the epidermis?

A

CD4+ and CD8+ T cells

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181
Q

Epidermal Layer: T Cells - What type of T cell is involved in Psoriasis?

A

TH1

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182
Q

Epidermal Layer: T Cells - What type of T cell is involved in Atopic Dermatitis?

A

TH2

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183
Q

Epidermal Layer: T Cells - What type of T cell is involved in Atopic Dermatitis and Psoriasis?

A

TH17

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184
Q

Epidermal Layer: TH1 T Cells - function

A

Activate macrophages to destroy microorganisms

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185
Q

Epidermal Layer: TH1 T Cells - secrete what? (2)

A

IL-2
IFN-gamma

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186
Q

Epidermal Layer: TH1 T Cells - Associated with what disease?

A

Psoriasis

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187
Q

Epidermal Layer: TH2 T Cells - Function

A

Help B cells to make antibody

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188
Q

Epidermal Layer: TH2 T Cells - Secrete what? (3)

A

IL-4
IL-5
IL-13

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189
Q

Epidermal Layer: TH2 T Cells - Associated with what disease?

A

Atopic Dermatitis

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190
Q

Epidermal Layer: TH17 T Cells - Function

A

Modulates skin and mucosal immunity

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191
Q

Epidermal Layer: TH17 T Cells - Secretes what?

A

IL-17

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192
Q

Dermal Layer: Dendritic Cells - Function

A

Uptakes antigens and presents them

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193
Q

Dermal Layer: Dendritic Cells - Function of Plasmacytoid Dendritic Cells

A

Main source of alpha-IFN to transmit information to T and B cells

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194
Q

Dermal Layer: Dendritic Cells - Constantly rotate between what?

A

Skin and Lymph nodes

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195
Q

Dermal Layer: Mast Cells - Preformed mediators (4)

A

Tryptase
Chymas
TNF
Histamine

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196
Q

Dermal Layer: Mast Cells - Newly Synthesised Mediators (3)

A

Interleukins
TNF
TGF-Beta

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197
Q

Skin Function: Physical Function

A

Barrier to friction, mechanical trauma and UV

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198
Q

Skin Function: Chemical function

A

Barrier to irritants, allergens and toxins

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199
Q

Steroid Sulphatase Deficiency X-Linked Ichthyosis

A

Incapacity to produce cholesterol properly in the skin so forms dry skin

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200
Q

Cumulative Irritant Hand Dermatitis

A

Flaking and scalin involving the epidermis and dermis of the skin in between fingers and on the finger tips

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201
Q

Skin Function: Metabolic Function - Process of Vitamin D metabolism

A

UV-B converts 7-dehydrocholesterol to Vitamin D23

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202
Q

Other name for Vitamin D23

A

Cholecalciferol

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203
Q

Skin Function: Metabolic Function - Vitamin B is stored in the liver as what?

A

Hydroxycholecalciferol

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204
Q

Skin Function: Metabolic Function - Hydroxycholecalciferol is converted to what and where in Vitamin D metabolism?

A

1,25-Dihydoxycholecalciferol in the kidney

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205
Q

Skin Function: Metabolic Function - Thyroid Hormone function

A

Converts Thyroxine (T4) To Triiodothyronine (T3)

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206
Q

T4

A

Thyroxine

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207
Q

T3

A

Triiodothyronine

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208
Q

Vitamin D: Soluble in what?

A

Fat

209
Q

Vitamin D

A

Pro-hormone essential for calcium and phosphorous metabolism

210
Q

Vitamin D: Function for the bone

A

Enables normal mineralization of the bone

211
Q

Vitamin D: Function with regards to Calcium

A

Increases flow of calcium into the blood stream by promoting the absorption of calcium and phosphorous from food in the intestines and reabsorption of calcium in the kidneys

212
Q

Vitamin D: D2 name

A

Calciferol

213
Q

Vitamin D: D3 name

A

Cholecalciferol

214
Q

Vitamin D: Vitamin D2 is made from what?

A

Inactive pro-vitamin ergosterol in plants by the action of sunshine

215
Q

Vitamin D: Vitamin D3 is provided by what foods?

A

Oily fish
Eggs
Meat

216
Q

Vitamin D: How is Vitamin D3 made in the skin?

A

UVB action on 7-dehydrocholesterol

217
Q

Vitamin D: 1,25-Dihydroxycholecalciferol alternate name

A

Calcitriol

218
Q

Vitamin D: Calcitriol

A

Biologically active hormonal form of Vitamin D that is used in the body to form and maintain the bones

219
Q

Vitamin D: How is calcitriol formed?

A

From cholecalciferol in the liver and kidney

220
Q

Failed Skin Functions: What happens if there is fluid loss?

A

Dehydration

221
Q

Failed Skin Functions: What happens if there is protein loss?

A

Hypoalbuminaemia

222
Q

Failed Skin Functions: What happens if there is failed barrier? (3)

A

Infection
Fluid loss
Protein loss

223
Q

Failed Skin Functions: What happens if there is failed thermoregulation

A

Hypothermia

224
Q

Failed Skin Functions: What happens if there is failed immune defences?

A

Spread of infection

225
Q

Failed Skin Functions: What happens if there is failure in metabolism?

A

Disordered thyroxine metabolism

226
Q

Failed Skin Functions: What happens if there is failed sensation? (3)

A

Pain senation
Numbness
Failure to detect changes in pressure or temperature

227
Q

Why did people evolve dark skin?

A

Protect against skin cancer

228
Q

Wound

A

Any break in the skin

229
Q

Wounds: Small surgical wounds heal by what?

A

Primary intention

230
Q

Wounds: What can compromise the healing of surgical wounds? (4)

A

Haematoma
Infection
Poor suture technique
Dehiscence

231
Q

Wounds: When is secondary intention healing used?

A

For large wounds that are too tight to stick or areas where distortion is possible

232
Q

Burns: First degree burn only affects what?

A

Epidermis

233
Q

Burns: Second degree and partial thickness burns affect what?

A

Epidermis and the Dermis

234
Q

Burns: Third Degree and full thickness burns affect what?

A

Beyond the dermis

235
Q

Burns: Superficial burn description

A

Erythematous
Wet
Extremely painful

236
Q

Burns: Deep Burn description

A

White, Black or Charred
Dry
Numb

237
Q

Secondary Intention Healing: Stage I name

A

Inflammatory Stage

238
Q

Secondary Intention Healing: Stage II name

A

Proliferation and Tissue Remodelling

239
Q

Secondary Intention Healing: Stage III name

A

Tissue remodelling

240
Q

Secondary Intention Healing: Stage I platelet role

A

Form an initial clot and release inflammatory mediators

241
Q

Secondary Intention Healing: Stage I Leucocyte role

A

Act in the wound bed by phagocytosing bacteria and scavenging cellular debris

242
Q

Secondary Intention Healing: Stage I what becomes prominent at the end of this stage?

A

Keratinocyte proliferation and new tissue formation

243
Q

Secondary Intention Healing: Stage II - Action of cells

A

Regenerate the epithelium of the wound surface

244
Q

Secondary Intention Healing: Stage II - What type of tissue formation is stimulated?

A

Granulation

245
Q

Secondary Intention Healing: Stage II - What is the role of fibroblasts?

A

Lay down matrix
Contracts the wound

246
Q

Secondary Intention Healing: Stage II - Endothelial cells generate what?

A

New blood vessels

247
Q

Secondary Intention Healing: Stage III - New tissue is converted into what?

A

Mature scar tissue

248
Q

Secondary Intention Healing: Stage III - Role of fibroblasts in this phase?

A

Lay down collagen to improve tensile strength of. the scar
Restore normal dermal matrix

249
Q

Chronic Wounds: Presents for how long?

A

> 6 weeks

250
Q

Chronic Wounds: Most common

A

Leg ulcers

251
Q

Chronic Wounds: Heal from what?

A

Edges of the wound

252
Q

Chronic Wounds: Colour

A

Yellow or Green

253
Q

Chronic Wounds: Adheres to what?

A

Underlying tissues

254
Q

Chronic Wounds: What is on the surface?

A

Slough

255
Q

Slough

A

Mixture of dead cells, polymorphs and bacteria

256
Q

Chronic Wounds: Disadvantages of slough

A

Possesses inhibitory effects on the healing ability of a wound

257
Q

Chronic Wounds: Disadvantages of slough

A

Possesses inhibitory effects on the healing ability of a wound

258
Q

Pressure Sores: Aetiology (4)

A

Prolonged pressure over a bony area
Lack of blood flow
Friction from bedding or clothing
Irritation from sweat, blood, urine or faeces

259
Q

Pressure Sores: Stage I symptoms

A

Tender
Itchy
Painful

260
Q

Pressure Sores: Stage I description

A

Unbroken skin that presents red or pink with a mild sunburn appearance

261
Q

Pressure Sores: Stage II description

A

Red, swollen and painful skin with broken or intact blisters

262
Q

Pressure Sores: Stage III description

A

Sore has broken through the skin and wound extends into the deeper layers of the skin

263
Q

Pressure Sores: Stage III what may be present?

A

Crater-like ulcers

264
Q

Pressure Sores: Stage IV description

A

Sore extends pas the skin into fat, muscle and bone tissue

265
Q

Eschar

A

Blackened dead tissue

266
Q

Pressure Sores: Management (40

A

Turn regularly
Keep skin clean and hydrated
Ensure regular skin assessment
Goof nutrition

267
Q

Give an example of a region of the skin that is impenetrable

A

Stratum cornea

268
Q

Staphylococcus aureus: Infection can present as what? (7)

A

Superficial lesions - Boils and Abscesses
Toxinoses
Carbuncle
Impetigo
Folliculitis
Rash
Scalded Skin Syndrome

269
Q

Staphylococcus aureus: Infects what areas of the skin? (2)

A

Anterior nares
Perineum

270
Q

Staphylococcus aureus: MRSA is defined by what?

A

Flucloxacillin resistance

271
Q

Staphylococcus aureus: Those at risk to infection (5)

A

Elderly
Immunocompromised
Burns patients
Surgical patients
Patients with IV lines or Dialysis

272
Q

Staphylococcus epidermidis: Risk factors (2)

A

Foreign devices e.g. catheters
Immunocompromised patients

273
Q

Virulence Factors: Adhesin

A

Enables the binding of an organism to host tissue

274
Q

Virulence Factors: Invasin

A

Enables an organism to invade a host cell or tissue

275
Q

Virulence Factors: Impedin

A

Enables the organism to avoid host defence mechanisms

276
Q

Virulence Factors: Aggressin

A

Causes direct damage to the host

277
Q

Virulence Factors: Modulin

A

Induces damage to the host directly

278
Q

Virulence Factors: Staphylococcus aureus example of an adhesin

A

Fibrinogen Binding Protein

279
Q

Virulence Factors: Staphylococcus aureus 3 examples

A

Coagulase
Leukocidin
TSST-1 Toxin

280
Q

Toxinoses

A

Discrete diseases associated with a single protein component of a toxin or exotoxin

281
Q

Toxinoses: 3 examples

A

TSST-1
Staphylococcal Food Poisoning
SSS

282
Q

Toxinoses: Symptoms of TSST-1

A

Rapid 48 hour fever
Diarrhoea
Vomiting
Sore throat
Muscle pain

283
Q

Toxinoses: Staphylococcal food poisoning is caused by what toxin?

A

Enterotoxin Se-A, -B and -C

284
Q

Toxinoses: How does Staphylococcal Food Poisoning present?

A

Intoxication with Diarrhoea and Vomiting within 1-5 hours

285
Q

Toxinoses: SSS

A

Scalded Skin Syndrome

286
Q

Toxinoses: What causes SSS?

A

ETA and ETB Exfoliatin toxins

287
Q

Toxinoses: ETA and ETB toxins target what?

A

Desmoglein-1

288
Q

Toxinoses: SSS often affects who?

A

Neonates

289
Q

Toxinoses: SSS affects what areas?

A

Face
Axilla
Groin

290
Q

Example of a superantigen

A

TSST-1

291
Q

TSST-1

A

Toxic Shock Syndrome Toxin 1

292
Q

TSST-1: Common cause of what?

A

Toxic Shock Syndrome

293
Q

TSST-1: Activates what

A

T cells

294
Q

TSST-1: Mode of action

A

Superantigen is not processed by polymorphonuclear neutrophils but binds to the MHC-II to activate immune cells and induce a release of cytokines

295
Q

Toxic Shock Syndrome: Diagnostic Criteria (4)

A

Fever (>39 degrees) - with myalgia, headache and nausea
Diffuse macular rash with desquamation and erythema
Hypotension - <90 mmHg
>3 organ systems involved - Liver, Blood, Renal, Mucous membranes, GIT, Muscular system and. the CNS

296
Q

Adhesins

A

Extracellular matrix molecules present on the epithelial and endothelial surfaces to colonise sites of the body and a component of blood clots

297
Q

Adhesins: Type associated with streptococcus

A

CIfA or CIfB

298
Q

Adhesins: Type associated with osteomyelitis

A

CNA

299
Q

Panton-Valentine Leukocidin

A

Specific secreted proteins that form one functional complex to attack white blood cells

300
Q

Panton-Valentine Leukocidin: What toxins are involved?

A

lukS and lukF

301
Q

Panton-Valentine Leukocidin: Toxin has a specific toxicity for what?

A

Leukocytes

302
Q

Panton-Valentine Leukocidin: What skin infections are associated with PVL?

A

Recurrent furunculosis
Necrotising fasciitis

303
Q

Panton-Valentine Leukocidin: PVL with alpha toxin are linked to what?

A

CA-MRSA

304
Q

Panton-Valentine Leukocidin: What does CA-MRSA cause?

A

Necrotising pneumonia
Contagious skin infections

305
Q

Necrotising Pneumonia: Features (4)

A

Preceding influenza-like syndrome
Necrotizing haemorrhagic penumonia
Acute respiratory distress
Multi-organ failure

306
Q

Streptococcus pyogenes: Gram Stain

A

Gram positive cocci in chains

307
Q

Streptococcus pyogenes: Type of haemolysis

A

Beta Haemolysis

308
Q

Streptococcus pyogenes: What 3 skin infections can it cause?

A

Impetigo
Cellulitis
Necrotising fasciitis

309
Q

Streptococcus pyogenes: What haemolysins do they produce?

A

SLO
SLS

310
Q

Streptococcus pyogenes: What protein does it produce?

A

M protein

311
Q

Lancefield Classification

A

Surface carbohydrate classification utilised in Group A identification

312
Q

Lancefield Classification: Enables serotyping of what?

A

Cell wall carbohydrates

313
Q

Lancefield Classification: Major Serotypes (2)

A

A-H
K-V

314
Q

Group A Microorganisms: M protein subdivisions (2)

A

Major - M1 and M3
Severe Invasive Disease - M3 and M18

315
Q

Group A Microorganisms: M proteins for major division

A

M1 and M3

316
Q

Group A Microorganisms: M proteins for severe invasive disease

A

M3 and M18

317
Q

Group A Microorganisms: M proteins are encoded by what?

A

Emm gene

318
Q

Group A Microorganisms: M protein binds to what? (3)

A

Factor M
Fibronectin
Fibrinogen Albumin

319
Q

Examples of Streptococci Skin Diseases (3)

A

Impetigo
Cellulitis
Necrotising fasciitis

320
Q

Group A Streptococci Diseases: Impetigo - Infection is located where?

A

Superficial

321
Q

Group A Streptococci Diseases: Impetigo - Is this a localised or systemic?

A

Localised

322
Q

Group A Streptococci Diseases: Impetigo - Entry point

A

Small defect in the skin

323
Q

Group A Streptococci Diseases: Impetigo - Limited to what structure?

A

Stratum corneum

324
Q

Group A Streptococci Diseases: Impetigo - Often associated with what population group?

A

Children

325
Q

Group A Streptococci Diseases: Impetigo - Mechanism of spread

A

Contact with discharge on the face and scratching

326
Q

Group A Streptococci Diseases: Cellulitis - Infection of what structure?

A

Dermis and associated subcutaneous fat

327
Q

Group A Streptococci Diseases: Cellulitis - Erysipelas localised to where?

A

Upper dermis and lymphatic system

328
Q

Group A Streptococci Diseases: Cellulitis - Symptoms

A

Fevers
Rigors
Nausea

329
Q

Group A Streptococci Diseases: Necrotising Fasciitis - Pathophysiology

A

Invasive streptococci A strains penetrate the mucous membrane to develop a lesion

330
Q

Group A Streptococci Diseases: Necrotising Fasciitis - Rapidly destroys what?

A

Connective tissue

331
Q

Group A Streptococci Diseases: Necrotising Fasciitis - What is the cause of type I?

A

Clostridia species

332
Q

Group A Streptococci Diseases: Necrotising Fasciitis - What is the cause of type II?

A

S. pyogenes or aureus

333
Q

Haemolysins: Example

A

Streptolysin S

334
Q

Haemolysins: SLS forms what?

A

Pores

335
Q

Haemolysins: SLS is toxic to what? (3)

A

PMN
Organelles
Platelets

336
Q

Haemolysins: SLS is responsible for what?

A

Beta Haemolysis

337
Q

Hypersensitivity

A

Exaggerated immune response that causes collateral damage to the self due to exaggeration of the normal immune mechanisms

338
Q

Allergy

A

Hypersensitivity disorder of the immune system where the immune system reacts to a normally harmless substance in the environment

339
Q

Allergen

A

A substance that causes a reaction

340
Q

Type I Allergy: Mediated by what?

A

IgE

341
Q

Type I Allergy: Routes of exposure

A

Skin contact
Inhalation
Ingestion
Injection

342
Q

Type I Allergy: Reaction occurs when?

A

Within minutes to. 2hours after exposure to an allergen

343
Q

Type I Allergy: What interleukins are involved?

A

IL-4
IL-5
IL-13

344
Q

Type I Allergy: 3 potential reactions to the skin

A

Urticaria
Angioedema
Anaphylaxis

345
Q

Type I Allergy: Urticaria description

A

Itchy lesions that appear within 1 hour and last 2-24 hours

346
Q

Type I Allergy: Urticaria is caused by what?

A

Dilation of blood vessels and leakage of fluid into the tissue

347
Q

Type I Allergy: Angioedema description

A

Localised non-pitting swelling of the subcutaneous tissue or mucous membranes that isn’t itchy

348
Q

Type I Allergy: Anaphylaxis is characterised by what?

A

Rapidly developing life threatening problems
- Airway oedema - bronchospasm and tachypnoea
- Circulation complications. -Hypotension and Tachycardia

349
Q

Type I Allergy: Gastrointestinal symptoms

A

Nausea
Diarrhoea
Vomiting
Colicky abdominal pain

350
Q

Type I Allergy: Respiratory clinical presentation

A

Nasal itching
Sneezing
Rhinorrhoea
Wheezing
Asthma

351
Q

Type I Allergy: Trend in Tryptase

A

Peaks at 1-2 hours and returns to normal by 6 hours during anaphylaxis

352
Q

Type I Allergy: Adrenaline dose for adults

A

300 micrograms

353
Q

Type I Allergy: Adrenaline dose for children

A

150 micrograms

354
Q

Type I Allergy: Adrenaline Autoinjector is used when?

A

Previous anaphylaxis
Difficult allergy
Background of asthma
Live in a rural area

355
Q

Type IV Allergy: Mediated by what?

A

T Cells

356
Q

Type IV Allergy: Causes what common skin condition?

A

Allergic contact dermatitis

357
Q

Type IV Allergy: Onset of reaction

A

12-24 hours

358
Q

Type IV Allergy: Routes of exposure

A

Direct skin contact
Airborne contact
Injection

359
Q

Type IV Allergy: First phase of these reactions

A

Sensitisation Phase

360
Q

Type IV Allergy: Second phase of these reactions

A

Re-exposure Phase

361
Q

Type IV Allergy: Sensitisation - Hapten is taken up by what in the skin?

A

Langerhan Cells

362
Q

Type IV Allergy: 4 examples of this type of reaction in the skin

A

Allergic Contact Dermatitis
Photo-allergy
Skin response to microorganism
Abnormal delayed response in atopic dermatitis

363
Q

Type IV Allergy: Allergic Contact Dermatitis clinical presentation

A

Small blisters and erosions

364
Q

Type IV Allergy: Investigations

A

Patch Testing

365
Q

Type IV Allergy: Protocol of Patch Testing

A

Finn chambers containing the allergen are applied on the back and removed and read within 48-96 hours

366
Q

Irritant Contact Dermatitis: This is a … process

A

Non-immunological

367
Q

Irritant Contact Dermatitis: Due to what?

A

Contact with agents that abrade, irritate and traumatise the skin

368
Q

Irritant Contact Dermatitis: Does not require what?

A

Prior sensitisation

369
Q

Irritant Contact Dermatitis: Pattern depends on what?

A

Exposure

370
Q

Endogenous Dermatitis: Atopic Eczema - Clinical Presentation

A

Dry skin of the flexors

371
Q

Endogenous Dermatitis: Atopic Eczema - Often associated with what?

A

Asthma and Hayfever

372
Q

Endogenous Dermatitis: Two types

A

Atopic eczema
Psoriasis

373
Q

Endogenous Dermatitis: Psoriasis - Clinical presentation

A

Scaly plaques on extensor surfaces

374
Q

Management of Acute Allergic Reactions: Stage I

A

Chlorophenaomine on first sign

375
Q

Management of Acute Allergic Reactions: Stage II

A

Prednisolone if symptoms worsen over the 30 minutes

376
Q

Management of Acute Allergic Reactions: Stage III

A

Intramuscular Adrenaline if the patient becomes blue or collapses

377
Q

Management of Acute Allergic Reactions: Dose of Adrenaline

A

10mg/kg
>30kg - 300mg
15-30kg - 150mg

378
Q

How does dry skin protect the skin?

A

Desiccates microorganisms

379
Q

How does sebum protect the skin?

A

Inhibits bacterial growth by fatty acids

380
Q

Diagnosis of Bacterial Skin Infections

A

Sample taken and transported in medium

381
Q

What samples should be taken for bacterial skin infections?

A

Swab or lesion if the skin is broken
Pus or tissue if there is a deeper lesion
Blood cultures - must take aerobic, anaerobic and paediatric

382
Q

Skin Infections: Staphylococcus - Gram staining

A

Gram positive cocci in clusters

383
Q

Skin Infections: Staphylococcus - Coagulase positive

A

Staphyloccus aureus

384
Q

Skin Infections: Staphylococcus - Coagulase negative

A

Staphylococcus epidermidis
Staphylococcus saprophyticus

385
Q

Skin Infections: Staphylococcus - What is the only staphylococcus to test positive for latex agglutination?

A

Staphylococcus aureus

386
Q

Skin Infections: Staphylococcus - How does coagluase positive present?

A

Golden

387
Q

Skin Infections: Staphylococcus - How does coagulase negative present?

A

White

388
Q

Skin Infections: What is the most common human pathogen

A

Staphylococcus aureus

389
Q

Skin Infections: Staphylococcus aureus - Antibiotic of choice if MRSA negative

A

Flucocloxacillin

390
Q

Skin Infections: Staphylococcus aureus - What toxins does it produce?

A

Staphylococcal scalded skin syndrome toxin
Panton Valentine Leucocidin
Enterotoxin

391
Q

Skin Infections: Staphylococcus aureus - Treatment options for MRSA skin and soft tissue impacts (4)

A

Oral Doxycycline
Oral Co-trimoxazole
Clindamycin
Linezoid

392
Q

Contraindication for Oral Doxycycline

A

Do not treat with cations e.g. Al causes chelation

393
Q

Skin Infections: Staphylococcus aureus - Bactericidal options for MRSA

A

Vancomycin
Daptomycin

394
Q

Skin Infections: Coagulase negative are normally commensal, however they may cause infection in what situations?

A

Implanted material as produces a biofilm e.g. joints, heart valves or IV catheters

395
Q

Skin Infections: What bacteria causes UTIs in women of child bearing age?

A

Staphyloccus saprophyticus

396
Q

Skin Infections: Streptococcus - Gram staining

A

Gram positive cocci in chains

397
Q

Skin Infections: Streptococcus - Survival in oxygen characteristics

A

Aerobic and facultatively anaerobic

398
Q

Skin Infections: Beta Haemolytic Streptococci - Produces what toxin?

A

Haemolysin

399
Q

Skin Infections: Beta Haemolytic Streptococci - Group A cause what?

A

Throat and severe skin infections

400
Q

Skin Infections: Beta Haemolytic Streptococci - Group B cause what?

A

Meningitis in Neonates

401
Q

Skin Infections: Streptococcus pyogenes - Involved in what skin conditions?

A

Infected eczema
Impetigo
Cellulitis
Erysipelas
Necrotising fasciitis

402
Q

Skin Infections: Alpha haemolytic streptococci - Examples (2)

A

Streptococci pneumoniae
Streptococci viridans

403
Q

Skin Infections: Alpha haemolytic streptococci - Streptococcus viridans is. acommensal of what?

A

Mouth
Throat
Vagina

404
Q

Skin Infections: Treatment of Streptococci pyogenes

A

Penicillin or Flucloxacillin

405
Q

Leg Ulcers: What microorganisms of leg ulcers are worth treating?

A

Streptococcus pyogenes
Staphylococcus aureus
Beta Haemolytic Streptococci - Groups B, C and G

406
Q

Leg Ulcers: What group of patients are anaerobes relevant to?

A

Diabetics - tells if there is dead tissue or gram negative bacteria

407
Q

Fungal Skin Infections: Examples (3)

A

Candidiasis
Tinea
Pityriasis versicolor

408
Q

Fungal Skin Infections: Candidiasis is common in what?

A

Skin fold infections

409
Q

Meaning of Tinea

A

Ringworm

410
Q

Ringworm of the scalp

A

Tinea capitis

411
Q

Ringworm of the beard

A

Tinea barbae

412
Q

Ringworm of the body

A

Tinea corporis

413
Q

Ringworm of the hand

A

Tinea manuum

414
Q

Ringworm of the nails

A

Tinea unguium

415
Q

Ringworm of the Groin

A

Tinea cruris

416
Q

Ringworm of the foot

A

Tinea pedis

417
Q

Dermatophytes: How does the fungus enter the body?

A

Via abraded or soggy skin

418
Q

Dermatophytes: Hyphae spreads into what?

A

Stratum corneum

419
Q

Dermatophytes: What spreads into the stratum corneum?

A

Hyphae

420
Q

Dermatophytes: Infects what tissue type?

A

Keratinised

421
Q

Dermatophytes: Examples of areas impacted (3)

A

Skin
Hair
Nails

422
Q

Dermatophytes: What is the cause of scaling?

A

Increased epidermal turnover

423
Q

Dermatophytes: Following an inflammatory response what is invaded?

A

Hair follicles
Shafts

424
Q

Dermatophytes: Why does it appear as a ring?

A

Lesion grows outwards. andheals in the centre

425
Q

Fungal Skin Infections: Sources of infections (3)

A

Other infected individuals - antropophillic fungi
Animals
Soil - geophilic fungi

426
Q

Fungal Skin Infections: 3 examples of causative organisms

A

Trichophyton rubrum
Trichophyton mentagraphytes
Microsporum canis

427
Q

Fungal Skin Infections: Most common causative organism

A

Trichophyton rubrum

428
Q

Fungal Skin Infections: Transmission of trichophyton rubrum

A

Human to Human Transmission

429
Q

Fungal Skin Infections: Transmission of Trichophyton mentagraphytes

A

Human to Human Transmission

430
Q

Fungal Skin Infections: Transmission of microsporum canis

A

Cats and Dogs

431
Q

Fungal Skin Infections: Diagnosis

A

Utilise skin scrapings, nail clippings and hair samples

432
Q

Fungal Skin Infections: Skin Sample Instructions

A

Take skin scrapings from the scaly edge of the lesion and send to pathology in a dermapak for microscopy and culture for 2 weeks

433
Q

Fungal Skin Infections: Management of small areas of infected skin or nails

A

Clotrimazole cream
Amorolfine topical nail paint

434
Q

Fungal Skin Infections: Management of scalp infections

A

Oral Terbinafine or Itraconazole

435
Q

Candida Skin Infections: Mainly affect what areas? (4)

A

Under breasts
Groin areas
Abdominal skin folds
Nappy area of babies

436
Q

Candida Skin Infections: Diagnosis

A

Swab for culture

437
Q

Candida Skin Infections: Treatment

A

Clotrimazole cream
Oral Fluconazole

438
Q

Parasitic Skin Infections: Scabies - Causative organism

A

Sarcoptes scabiei

439
Q

Parasitic Skin Infections: Scabies - Norweigen Scabies

A

Chronic crusted scabies that is highly infectious

440
Q

Parasitic Skin Infections: Scabies - Incubation period

A

6 weeks

441
Q

Parasitic Skin Infections: Scabies - Clinical Presentation

A

Intensely itchy rash that affects the finger webs, wrists and genital area

442
Q

Parasitic Skin Infections: Scabies - Management option (2)

A

Malathion Lotion - applied overnight and washed off the next day
Benzyl benzoate

443
Q

Parasitic Skin Infections: Scabies - When to avoid Benzyl Benzoate?

A

In children

444
Q

Parasitic Skin Infections: Lice - Causative organism of head lice

A

Pediculus capitis

445
Q

Parasitic Skin Infections: Lice - Causative organism of body lice

A

Pediculus corporis

446
Q

Parasitic Skin Infections: Lice - Causative organism of pubic lice

A

Phthirus pubis

447
Q

Parasitic Skin Infections: Lice - Management

A

Malathion

448
Q

Viral Skin Infections: Examples of causative organisms? (5)

A

Herpes Simplex Virus
Human Papilloma Virus
Pox Virus
Varicella Zoster Virus
Viral Exanthems

449
Q

Viral Skin Infections: Examples of erythematous exanthema that starts on the face (3)

A

Measles
Rubella
Erythema Infectiosum

450
Q

Viral Skin Infections: Examples. of erythematous exanthema that starts on the trunk (3)

A

Roseola
Scarlet Fever
Unilateral laterothoracic exanthem

451
Q

Viral Skin Infections: Examples of Papulo-vesicular exanthema (2)

A

Chickenpox
Gianotti Crosti Syndrome

452
Q

Viral Skin Infections: Example of Exanthema of the extremities

A

Hand Foot and Mouth Disease

453
Q

COVID Rash: Appearance

A

Morbilliform rash - this looks similar to measles

454
Q

Infection Control in Dermatology: What situations require single room isolation?

A

Group A Strep Infection
MRSA infections
Scabies patients

455
Q

Infection Control in Dermatology: What control is required for Norweigan Scabies?

A

Long-sleeved gowns

456
Q

Pruritus

A

An unpleasant poorly localised non-adapting sensation that provokes the desire to scratch

457
Q

Where is the itch sensation processed by?

A

Forebrain and Hypothalamus

458
Q

What nerves carry the itch sensation?

A

Unmyelinated C fibres

459
Q

Where do the nerves subserving the itch and pain sensation originate in the skin?

A

Epidermis

460
Q

The itch sensation uses what CNS tract?

A

Lateral Spinothalamic Tract

461
Q

Pre-formed Mast Cell Products (3)

A

Proteases
Heparin
Histamine

462
Q

Newly Formed Mast Cell Products (3)

A

Prostaglandin D2
Leukotrienes C4, D4 and E4
Platelet Activating Factor

463
Q

Itch: Pruitoceptive is usually associated with what?

A

Inflammation or Dryness

464
Q

Itch: Psychogenic aetiology

A

Pscyhological cause with no CNS damage

465
Q

Itch: Examples of Pruitoceptive causes (5)

A

Asteatotic Eczema
Insect bite reactions
Lichen plants
Chronic plaque psoriasis
Prurigo nodularis

466
Q

Lichen plants cause an itch how?

A

Associated with Hepatitis C

467
Q

Asteatotic Eczema

A

Direct exposure of itch-associated unmyelinated C fibres in the bases of microfissures and inflammation with release of mediators in the skin

468
Q

Itch: Examples of a neuropathic cause of itch

A

Herpes Simplex Virus

469
Q

Itch: Examples of Itch Managements (5)

A

Sedative anti-histamines
Emollients e.g. methanol cooled
Anti-depressants
Phototherapy
Opiate Antagonists

470
Q

Itch: When are non-sedative anti-histamines not used?

A

When excess histamine is in the skin

471
Q

Itch: Examples of Anti-depressants used for management

A

Doxepin
SSRIs

472
Q

Itch: Example of an opiate antagonist used for management

A

Ondansetron

473
Q

Hyperkeratosis

A

Increased thickness of the keratin layer

474
Q

Parakeratosis

A

Persistence of nuclei in the keratin layer

475
Q

Acanthosis

A

Increased thickness of the epithelium

476
Q

Papillomatosis

A

Irregular epithelial thickening

477
Q

Spongiosis

A

Oedema fluid goes between squares appear to increase the prominence of intercellular prickles

478
Q

4 Main reaction patterns of inflammatory skin disease

A

Spongiotic Intraepidermal Oedema
Psoriasiform elongation of the rete ridges
Lichenoid-basal layer damage
Vesiculobullous blistering

479
Q

Example of spongiotic intraepidermal oedema

A

Eczema

480
Q

Example of psoriasiform elongation of the rete ridges

A

Psoriasis

481
Q

Examples of lichenoid-basal layer damage (2)

A

Lichen Planus
Lupus

482
Q

Where can skin tumours arise from? (5)

A

Epidermis
Melanocytes
Dermis
Appendages
Lymphoid elements

483
Q

Oncogene

A

Overactive form of a gene that positively regulates cell deivision and therefore drives tumour formation when activity or copy number is increased

484
Q

Proto-oncogene

A

Normal, not yet mutated form of an oncogene

485
Q

Tumour suppressor

A

Inactive or non-functional form of a gene that negatively regulates cell division

486
Q

Oncogenic Ras Signalling

A

In the absence of Growth Factor, Ras is still active to cause cell division and proliferation

487
Q

Normal p53 function

A

In the presence of DNA damage, p53 is activated to halt the G1 checkpoint to repair DNA or trigger apoptosis

488
Q

Oncogenic p53

A

In the presence of DNA damage, p53 cannot bind to DNA therefore progresses through the cell cycle

489
Q

UV: wavelength of UVC

A

200-290nm

490
Q

UV: wavelength of UVB

A

290-320nm

491
Q

UV: wavelength of UVA

A

320-400nm

492
Q

UV: Which is the highest exposure?

A

UVA

493
Q

UV: UVA - How does this cause cancer?

A

Causes indirect DNA damage via oxidative damage

494
Q

UV: UVA - causes damage to what skin structures?

A

Collagen
Elastic Fibres

495
Q

UV: UVB - How does this cause cancer?

A

Direct DNA damage

496
Q

UV: UVB - When are we most at risk?

A

When the sun is overhead

497
Q

UV: UV exposure has what property?

A

Immunosuppressive

498
Q

UV: UVB - Induces the secretion of what from where?

A

IL-10 from keratinocytes

499
Q

UV: UVB - Causes a reduction in function of what cells of the epidermis?

A

Langerhan Cells - reduced APC function

500
Q

UV: UVB - Causes a reduction in function of what cells of the dermis?

A

Dendritic Cells

501
Q

DNA Damage: Two major types of UVB-induced DNA lesions

A

Cyclobutane Pyrimidine Dimers
Pyrimidine-Pyrimidone (6-4) Photo Products

502
Q

DNA Damage: UVB-induced DNA lesions are formed how?

A

Covalent bonding between adjacent pyrimidines of the same DNA strand

503
Q

Examples of acute skin effects of UV (2)

A

Erythema
Immunosuppression

504
Q

Chronic skin effects of UV (2)

A

Photoageing
Photocarcinogenesis

505
Q

Indications for skin biopsy (2)

A

Rash
Tumour of the skin

506
Q

Dermoscopy function

A

Recognises morphological structures not visible to the eye to aid diagnosis

507
Q

5 layers of the scalp

A

Skin
Connective Tissue
Aponeurosis
Loose Connective Tissue
Periosteum

508
Q

What is the sensory nerve to the face?

A

Trigeminal Nerve

509
Q

What are the three divisions of the Trigeminal Nerve?

A

V1 - Opthalamic division
V2 - Maxillary
V3 - Mandibular

510
Q

How do you assess the sensory function of the face?

A

Ask the patient to close their eyes
Gently brush the skin in each dermatome with a fine tip of cotton woolAsk the patient where they feel sensation - compare the two sides

511
Q

What impacts can fracture of the lateral aspect of the mandible have?

A

Damage V3 supply to the chin and lower limb to make them numb

512
Q

What nerve supplies the muscle of the face?

A

Facial (VII) Nerve

513
Q

How is the Facial nerve assessed?

A

Get. thepatient to frown, close their eyes and smile
Then get them to puff out their cheeks - if the sphincter is intact there will be no air leakage from the mouth

514
Q

Anaesthesia: What are the 4 main options?

A

Topical
Local infiltration
Nerve block
Field block

515
Q

Anaesthesia: What type of anaesthetic is Lignocaine?

A

Amide type

516
Q

Anaesthesia: Lignocaine excretion is reduced in what patients?

A

Liver, Renal and Cardiac failure patients
Young
Elderly

517
Q

Anaesthesia: Impact of adrenaline?

A

Prolongs anaesthesia and reduced bleeding

518
Q

Anaesthesia: Maximum safe dose of Lignocaine

A

50ml 1% Lignocaine with adrenaline

519
Q

Anaesthesia: Avoid adrenaline where?

A

Fingers and Toes

520
Q

Anaesthesia: Avoid in patients with what?

A

Cardiac disease
On psychotropic drugs

521
Q

When may electrosurgery be used?

A

Haemostasis
Treatment of minor skin lesions

Dermatology (5 decks)

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