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MBChB Year 3 > Week 10 - Dermatology > Flashcards

Week 10 - Dermatology Flashcards

1
Q

For what 7 reasons is dermatology important?

A
  1. Accounts for ~20 % of GP consultations
  2. 1 of busiest Hospital OP specialties
  3. Can have significant psychological impact
  4. Skin changes can be marker of underlying systemic disease
  5. Huge increase in rates of skin cancer
  6. Research important as no cure for melanoma
  7. Need to be aware of cosmetic dermatology
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2
Q

What is the largest organ in the body?

A

Skin (15% of body weight)

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3
Q

Describe skin shedding?

A

Every 24hr skin sheds layer dead cells, renewed fully approx 28 days

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4
Q

What is the pH of skin?

A

Slightly acidic 5.4 due to Lactic & Amino acids

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5
Q

What are the 3 main functions of skin?

A
  1. Protection
  2. Regulation
  3. Sensation
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6
Q

List the 5 primary barrier functions of skin?

A
  1. Mechanical impacts
  2. Protects & detects pressure
  3. Detects variations in temperature
  4. Barrier to micro-organisms
  5. Barrier to radiation / chemicals
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7
Q

Describe the physiological regulation of the skin?

A
  • Body temperature via sweat, hair & changes in peripheral circulation
  • Fluid balance via sweat & insensible loss
  • Synthesis of Vitamin D
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8
Q

What are the 4 layers of skin?

A
  1. Epidermis
  2. Basement membrane
  3. Dermis
  4. Subcutaneous tissue
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9
Q

What 3 anatomical features does skin have?

A
  1. Glands
  2. Hair follicles
  3. Capillaries
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10
Q

What are the 4 layers of the skin epidermis?

A
  1. Stratum corneum
  2. Stratum granulosum
  3. Stratum spinosum
  4. Stratum basale
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11
Q

What 3 cells does stem cells develop into?

A
  1. Ectoderm
  2. Mesoderm
  3. Endoderm
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12
Q

Give 4 examples of what ectoderm develops into?

A
  1. Skin
  2. Hair
  3. Brain
  4. Nerves
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13
Q

Give 5 examples of what mesoderm develops into?

A
  1. Cardiac
  2. Skeletal
  3. Renal
  4. Muscle
  5. Blood
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14
Q

Give 4 examples of what endoderm develops into?

A
  1. Lung
  2. Gut
  3. Thyroid
  4. Pancreas
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15
Q

What is the epidermis early fetal period invaded by?

A

Melanoblasts, cells of the neural crest origin

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16
Q

When is hair developed on the skin?

A

3rd month as an epidermal proliferation into dermis

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17
Q

What happens to the cells of the epithelial root sheath?

A
  • Proliferate to form a sebaceous gland bud

- Sweat glands develop as downgrowths of epithelial cords into dermis

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18
Q

Describe langerhans cells (LC)?

A

Members of the dendritic cells family, residing in the basal layers

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19
Q

Describe how the skin langerhans cells specialise in antigen presentation?

A

Acquire antigens in peripheral tissues, transport them to regional lymph nodes, present to naive T cells & initiate adaptive immune response

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20
Q

What do activated T cells initiate?

A

Cytokine release cascade

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21
Q

List the 4 other things that the skin’s immune system is involved in?

A
  1. Antimicrobial immunity
  2. Skin immunosurveillance
  3. Induction hypersensitivity
  4. Pathogenesis of chronic inflammatory diseases of the skin
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22
Q

What induces langerhan cell migration & maturation in skin allergy?

A

Skin irritation by nonallergenic & allergenic compounds

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23
Q

Describe the migration of Langerhan cells?

A

Epidermis to draining lymph nodes

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24
Q

How long does the initial sensitisation in skin allergy take?

A

10-14 days from initial exposure to allergen (nickel, dye, rubber etc)

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25
Q

What happens once an individual is sensitised to a chemical?

A

Allergic contact dermatitis can then develop within hours of repeat exposure exposure

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26
Q

What are the damaging effects of ultraviolet on skin?

A
  • Direct cellular damage & alterations in immunologic function
  • Direct effects include photoaging, DNA damage & carcinogenesis
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27
Q

What is mutated by DNA damage & how is this implicated?

A
  • P53 tumour suppressor gene

- Implicated in development of melanoma & non melanoma skin cancers

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28
Q

What work together to protect cells from UV DNA damage?

A

Keratinocytes & melanocytes

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29
Q

What 5 things does chronic UV exposure in humans eventually lead to?

A
  1. Loss of skin elasticity
  2. Fragility
  3. Abnormal pigmentation
  4. Hemorrhage of blood vessels
  5. Wrinkles & premature ageing
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30
Q

What happens during exposure to sunlight?

A

Solar UVB photons are absorbed by 7-dehydrocholesterol in the skin & converted to previtamin D(3)

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31
Q

What happens to pre-vitamin D(3)?

A

Undergoes transformation within the plasma membrane to active vitamin D(3)

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32
Q

What is the skin problem during winter?

A

Minimal pre-vitamin D(3) production in the skin & few foods naturally contain Vit D

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33
Q

What are the 4 associated increased risks with Vitamin D deficiency?

A
  1. Common cancers
  2. Autoimmune diseases (MS)
  3. Infectious diseases
  4. Cardiovascular disease
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34
Q

What can cutaneous receptors be?

A

Encapsulated nerve endings such as Meissner, Pacini & Ruffini corpuscles or Free nerve endings associated with Merkel cells

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35
Q

Describe Merkel cells?

A
  • Base of the epidermis,

- Respond to sustained gentle & localised pressure, assess shape /edge

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36
Q

Describe Meissner corpuscles?

A
  • Immediately below epidermis & are particularly well represented on the palmar surfaces of the fingers and lips
  • They are especially sensitive to light touch
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37
Q

Describe Ruffini’s corpuscles?

A
  • In the dermis

- Receptors sensitive to deep pressure & stretching

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38
Q

Describe Pacinian corpuscles?

A
  • Mechanoreceptors present in the deep dermis, sensitive to deep touch, rapid deformation of skin surface and around joints for position/proprioception
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39
Q

What is a macule?

A

Flat area in the skin, usually a change in colour (pigmented)

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40
Q

What is a papule?

A

Something small raised in the skin

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41
Q

What is a pustule?

A

Raised & full of puss (infection/inflammatory cells)

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42
Q

What is a plaque?

A

Raised and tends to be big

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43
Q

What is a vesicle?

A

Tiny blisters

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44
Q

What is a bulla?

A

Giant blisters

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45
Q

What is Erythematous?

A

Redness

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46
Q

What is Ulceration?

A

The epidermis has been removed and you are left with just the deaper levels of skin

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47
Q

What are the 5 etiological stages of acne?

A
  1. Accumulation of epithelial cells & keratin
  2. Androgenic accumulation of shed keratin & sebum
  3. Blockage of sebaceous gland
  4. Propionibacterium acnes proliferation & inflammation
  5. Scarring
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48
Q

List the 7 clinical features of acne?

A
  1. Papules
  2. Pustules
  3. Erythema
  4. Comedones
  5. Nodules
  6. Cysts
  7. Scarring
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49
Q

What 3 clinical features are needed to make a diagnosis of acne?

A
  1. Papules
  2. Pustules
  3. Comedones
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50
Q

What are comedones?

A

Blackheads/ whiteheads

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51
Q

What are the 4 distributions of acne?

A
  1. Face
  2. Chest
  3. Back / Shoulders
  4. Occasionally legs, scalp
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52
Q

What are 3 clinical types of acne?

A
  1. Papulopustular
  2. Nodulocystic
  3. Comedonal
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53
Q

What are the 4 subtypes of acne?

A
  1. Steroid induced
  2. Acne fulminans
  3. Acne rosacea
  4. Acne Inversus (Hidradenitis suppuritiva)
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54
Q

What are the different grades of acne?

A

Grades 1-7 (the Leeds Acne photographic grading system)

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55
Q

What are the 2 medications to reduce plugging in acne?

A
  1. Topical retinoid

2. Topical benzoyl peroxide

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56
Q

What are the 3 medications to reduce bacteria in acne?

A
  1. Topical antibiotics (erythromycin, clindamycin)
  2. Oral antibiotics (tetracyclines, erythromycin)
  3. Benzoyl peroxide reduced bacterial resistance
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57
Q

What medication can reduce sebum production in acne?

A

Hormones- anti androgen ie Dianette / OCP

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58
Q

List the 4 side effects of topical agents in acne?

A
  1. Irritant
  2. Burning
  3. Peeling
  4. Bleaching
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59
Q

What is the side effect of oral antibiotics for acne?

A

Gastro upset (esp. tetracycline)

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60
Q

What is the side effect of the oral contraceptive pill for acne?

A

Possible DVT risk

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61
Q

What is the controversial treatment option for acne?

A

Dietary modification ie. reduce glycemic load (milk, chocolate)

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62
Q

What is Oral Isotretinoin?

A
  • Licensed for severe acne vulgaris (remission in ~80% of teenagers)
  • Concentrated form of vitamin A
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63
Q

What is the effect of Oral Isotretinoin?

A

Reduces sebum, plugging and bacteria

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64
Q

What is the standard course of Oral Isotretinoin?

A
  • 16 weeks

- 1mg/kg

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65
Q

List the 9 side effects of Oral Isotretinoin?

A
  1. Dry lips
  2. Nose bleeds
  3. Dry skin
  4. Myalgia
  5. Serious side effects
  6. Deranged liver function
  7. Raised lipids
  8. Mood disturbance
  9. Teratogenicity
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66
Q

What is the program associated with Oral Isotretinoin?

A

Pregnancy Prevention program (monthly tests & contraception needed)

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67
Q

What are the 2 clinical problems with prescribing Oral Isotretinoin?

A
  1. Expensive

2. Consumes lots of clinical time

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68
Q

What is Oral Isotretinoin also known as?

A

Accutane or Roaccutane

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69
Q

What is the definition of eczema/dermatitis?

A

Inflammation of the skin

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70
Q

Describe the aetiology of eczema?

A

Combination of genetic, immune & reactivity to a variety of stimuli

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71
Q

Describe the inflammation in eczema?

A
  • Primarily due to inherited abnormalities in skin so called “barrier defect”
  • Leads to increased permeability & reduces its antimicrobial function
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72
Q

Describe the genetic problem in eczema?

A

Inherited abnormality in filaggrin expression (chromosome 1) –> disordered barrier function

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73
Q

What are filaggrins?

A

Proteins which bind to keratin fibres in the epidermal cells

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74
Q

What are the 5 endogenous types of eczema?

A
  1. Atopic
  2. Seborrhoeic
  3. Discoid
  4. Varicose
  5. Pompholyx
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75
Q

What are the 2 exogenous types of eczema?

A
  1. Contact (allergic, irritant)

2. Photoreaction (allergic, drug)

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76
Q

Describe atopic eczema?

A
  • Itchy inflammatory skin condition
  • High Ig-E immunoglobulin antibody levels
  • Genetic & immune aetiology
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77
Q

What is atopic eczema associated with?

A

Asthma, allergic rhinitis, conjunctivitis, hayfever (atopy individual)

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78
Q

Describe the prevalence of atopic eczema?

A
  • 10-15% of infants affected
  • Remission occurs in 75% by 15 years
  • 2/3 have a family history of atopy
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79
Q

Describe the presentation of infant atopic eczema?

A
  • Itchy
  • Occasionally vesicular (small blisters)
  • Often facial component
  • Secondary infection
  • Occasionally aggravated by food (ie milk)
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80
Q

Describe the prognosis of infant atopic eczema?

A

< 50% still have eczema by 18 months

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81
Q

What are the 2 complications of atopic eczema?

A
  1. Bacterial infection- staph aureus

2. Viral infection- molluscum, viral warts, eczema herpeticum

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82
Q

What are the 3 negative systemic effects of atopic eczema?

A
  1. Tiredness
  2. Growth reduction
  3. Psychological impact
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83
Q

List the 9 management techniques for atopic eczema?

A
  1. Emollients
  2. Topical steroids
  3. Bandages
  4. Antihistamines
  5. Antibiotics / anti-virals
  6. Education for parents /child
  7. National Eczema Society
  8. Avoidance of exacerbating factors
  9. Systemic drugs
  10. Newest biologic agent
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84
Q

What are the 2 systemic drugs that you can use for atopic eczema?

A
  1. Ciclosporin

2. Methotrexate

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85
Q

What is the newest biologic agent for atopic eczema?

A

IL4/13 blocker- Dupilumab

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86
Q

What is contact dermatitis?

A

Type 4 hypersensitivity reaction precipitated by an exogenous agent ie:

  1. Irritant- direct noxious effect on skin barrier
  2. Allergic - Type IV hypersensitivity reaction
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87
Q

What are the 5 common allergens for contact dermatitis?

A
  1. Nickel- Jewellery, zips, scissors, coins
  2. Chromate- Cement, tanned leather
  3. Cobalt- Pigment /dyes
  4. Colophony- Glue, adhesive tape, plasters
  5. Fragrance- Cosmetics, creams, soaps
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88
Q

What is Seborrhoeic Dermatitis?

A

Chronic, scaly inflammatory condition caused by overgrowth of Pityrosporum Ovale yeast

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89
Q

Where is typically affected by Seborrhoeic Dermatitis?

A

Face, scalp, & eyebrows occasionally the upper chest

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90
Q

What 2 things can Seborrhoeic Dermatitis occasionally be confused with?

A
  1. Dandruff

2. Facial psoriasis

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91
Q

What 2 factors makes Seborrhoeic Dermatitis worse?

A
  1. Teenagers

2. Underlying HIV

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92
Q

How do you manage scalp Seborrhoeic Dermatitis?

A

Medicated anti yeast shampoo (antifungal ketoconazole -Nizoral, Selsun)

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93
Q

How do you manage face Seborrhoeic Dermatitis?

A
  • Anti-microbial, mild steroid (ie Daktacort cream)

- Simple moisturiser

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94
Q

What can Seborrhoeic Dermatitis rarely be treated with?

A

Systemic antifungals

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95
Q

What often improves Seborrhoeic Dermatitis?

A

UV/sunlight

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96
Q

Describe Venous dermatitis?

A
  • Underlying venous disease
  • Affects lower legs
  • Incompetence of deep perforating veins
  • Increased hydrostatic pressure
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97
Q

What are 4 ways to manage Venous dermatitis?

A
  1. Emollients
  2. Mild / moderate topical steroid
  3. Compression bandaging / stockings
  4. Consider early venous surgical intervention
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98
Q

What is the definition of psoriasis?

A

Chronic relapsing & remitting scaling skin disease which may appear at any age & affect any part of the skin

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99
Q

When does psoriasis often present?

A

Age onset often two peaks age 20-30y or 50-60y

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100
Q

What are 3 causes of psoriasis?

A
  1. T cell mediated autoimmune disease
  2. Abnormal infiltration of T Cells (release of inflammatory cytokines incl interferon, interleukins & TNF, increased keratinocyte proliferation)
  3. Enviromental & genetic factors
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101
Q

What are 4 things linked to psoriasis?

A
  1. Psoriatic arthritis
  2. Metabolic syndrome
  3. Liver disease / alcohol misuse
  4. Depression
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102
Q

Describe the genetic prevalence associated with psoriasis?

A
  • 1 sibling with psoriasis: risk is 24%
  • 1 parent with psoriasis: risk is 28%
  • 1 sibling & 1 parent with psoriasis: risk is 41%
  • 2 parents with psoriasis: risk is 65%
  • Both parents & a sibling have psoriasis risk is 83 %
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103
Q

What genes are related to psoriasis?

A

PSORS genes (eg PSORS1, Chromosome 6) & HLA – Cw0602 associated in certain subtypes

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104
Q

List the 5 types of psoriasis?

A
  1. Plaque
  2. Guttate
  3. Pustular
  4. Erythrodermic
  5. Flexural / Inverse
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105
Q

What type of psoriasis is now thought to NOT be psoriasis?

A

Palmar/plantar pustulosis

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106
Q

What is Koebner phenomenon?

A

Psoriasis at sites of trauma / scars ie. appendectomy

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107
Q

Describe the presentation of psoriasis?

A
  1. Well demarcated
  2. Salmon pink inflammation
  3. Plaque build up
  4. No moisture
  5. Scaled
  6. Onycholysis
  7. Nail pitting
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108
Q

What 4 factors does the management of psoriasis depend on?

A
  1. Severity
  2. What patient wants
  3. What patient can cope with
  4. If they have arthropathy
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109
Q

List 3 scoring systems for psoriasis?

A
  1. Disease life quality index- DLQI
  2. Psoriasis area severity index- PASI
  3. Patient eczema severity time- PEST
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110
Q

What do up to 20% of psoriasis patients develop?

A

Arthritis

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111
Q

What is the treatment for psoriasis in order of increasing effectiveness & toxicity?

A
  1. Topical creams & ointments
  2. Phototherapy light treatment (UV)
  3. Acitretin- retinoid drug/ vitamin A
  4. Methotrexate- decrease inflammation
  5. Ciclosporin
  6. Biologic therapies
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112
Q

What are 4 examples of biologic therapies for psoriasis?

A
  1. Adalumimab (anti TNF)
  2. Ustekinumab (anti IL12/23)
  3. Secukinumab
  4. Brodilumab
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113
Q

Give 2 examples of topical therapies for psoriasis?

A
  1. Moisturisers- help reduce dryness, flaking

2. Steroids- reduce autoimmune response, redness, itching, inflammation

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114
Q

Give 4 examples of topical therapies that slow down keratinocyte production?

A
  1. Vitamin D analogues
  2. Coal Tar
  3. Dithranol- tree bark extract
  4. Retinoid (Tazarotene) rarely used now
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115
Q

What effect does Ultraviolet Phototherpy have?

A
  • Can reduce T cell proliferations

- Encourages Vitamin D & reduces skin turnover

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116
Q

What are the 2 types of Ultraviolet Phototherpy?

A
  1. UV-B light is the most commonly used

2. UV-A with psoralen photosensitiser

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117
Q

What are the 2 risks of Ultraviolet Phototherpy?

A
  1. Short term burning

2. Longer term skin cancer

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118
Q

List the 3 potent side effects of most drugs for psoriasis?

A
  1. Liver dysfunction
  2. Hypertension
  3. Risk of infection
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119
Q

What 2 drugs would you not give for treating psoriasis?

A
  1. Azathioprine

2. Systemic steroids

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120
Q

What 2 distinct pathways interact or converge to cause skin cancer?

A
  1. Direct action of UV on target cells (keratinocytes) for neoplastic transformation via DNA damage
  2. Effects of UV on the host’s immune system
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121
Q

Describe the chain of damage that UV light has on skin?

A

DNA damage –> p53 mutation & Immune suppression & p53 induction –> Abnormal cell proliferation –> Other genetic alterations –> Skin cancer

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122
Q

What are the 3 main skin cancer types?

A
  1. Basal Cell Carcinoma
  2. Squamous Cell Carcinoma
  3. Malignant Melanoma
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123
Q

Where do melanocytes reside?

A

With the skin basal cells

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124
Q

What is the most common type of skin cancer?

A

Basal cell carcinoma

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125
Q

What is the process of creating new skin cells controlled by?

A

Basal cells DNA

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126
Q

What can a mutation in the DNA cause?

A
  • Basal cell to multiply rapidly & continue growing when it would normally die
  • Eventually the accumulating abnormal cells may form a tumour PTCH gene mutation may predispose
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127
Q

What are 80% of basal cell cancers found on?

A

Head & neck/UV exposed sites

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128
Q

What rarely happens in basal cell carcinomas?

A

Metastasis or kills

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129
Q

What are the basal cell carcinoma subtypes?

A
  1. Nodular
  2. Superficial
  3. Pigmented
  4. Morphoeic/Sclerotic
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130
Q

Describe Nodular Basal Cell Carcinoma?

A
  • Nodule ie > 0.5cm raised lesion
  • Shiny “pearly”
  • Telangectasia / blood vessels
  • Often ulcerated centrally
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131
Q

Describe superficial basal cell carcinoma?

A
  • Grows slowly
  • Minimal tendency to be invasive
  • Erythematous
  • Well-circumscribed patch or plaque
  • Not ulcerative
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132
Q

Describe pigmented basal cell carcinoma?

A
  • Black/dark pigment
  • Curved border
  • Some ulceration
  • Raised
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133
Q

Describe Morphoeic/ Sclerotic basal cell carcinoma?

A
  • Subtle skin textural change
  • ​Slowly expanding
  • A yellow-white waxy patch with very ill-defined edges
  • Surface telangiectasia
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134
Q

What is the gold standard treatment for basal cell carcinoma?

A

Surgical excision 3-4mm margin

135
Q

What are 5 treatment options for basal cell carcinoma?

A
  1. Curettage and cautery
  2. Cryotherapy
  3. Photodynamic therapy
  4. Topical imiquimod / 5-fluorouracil cream
  5. Mohs micrographic surgery
136
Q

Where may squamous cell carcinomas occur?

A

In normal skin or in skin that has been injured (burns/UV damage) or chronically inflamed

137
Q

What does squamous cell carcinoma originate from?

A

Keratinocytes

138
Q

What are 2 pre-malignant variants of squamous cell carcinoma?

A
  1. Actinic keratoses

2. Bowens disease

139
Q

What is the % risk of high risk squamous cell carcinoma metastasis?

A

10 to 30% (high risk sites- ears, lips)

140
Q

Describe the presentation of squamous cell carcinoma?

A
  • Scaling
  • Ulceration
  • Crusting
  • Inflammation
141
Q

What are the 2 treatments for squamous cell carcinoma?

A
  1. Gold standard- Surgical excision 4mm margin

2. Curettage & cautery

142
Q

What are the 4 treatments for pre-malignant/squamous cell in-situ?

A
  1. Topical imiquimod / 5-fluorouracil cream
  2. Cryotherapy
  3. Photodynamic therapy
  4. Sun protection
143
Q

What is a melanoma?

A

Malignant tumour of melanocytes

144
Q

What are the most common sites for melanoma’s?

A

Skin (but can be bowel/ eye)

145
Q

What are the 2 phases of melanomas?

A
  1. Radial growth

2. Vertical growth

146
Q

What determines the prognosis of a melanoma?

A

Depth of presentation

147
Q

How is melanomas spread?

A

Via lymphatics

148
Q

List 11 risk factors for the development of a melanoma?

A
  1. Genetic markers (CDKN2A mutations)
  2. Family history of dysplastic nevi or melanoma
  3. UV irradiation
  4. Sunburns during childhood
  5. Intermittent burning exposure in unacclimarized fair skin
  6. Congenital nevi
  7. Atypical/dysplastic nevus syndrome
  8. High socioeconomic status
  9. Skin type I, II
  10. DNA repair defects
  11. Immunosuppression
149
Q

Describe the 5 year survival of melanomas of varying Breslow thickness?

A
  • 97% for 0-1.0 mm
  • 91% for 1.01-2.0 mm
  • 79% for 2.01-4.0 mm
  • 71% for > 4.0 mm
150
Q

List the 8 different melanoma subtypes?

A
  1. Superficial spreading malignant melanoma (most common)
  2. Nodular melanoma
  3. Acral melanoma
  4. Subungual melanoma
  5. Amelanotic melanoma
  6. Lentigo maligna
  7. Lentigo maligna melanoma
  8. Melanoma in-situ
151
Q

What 4 things should you look for when assessing a melanoma?

A
  1. Symmetry
  2. Different colours
  3. Borders
  4. Size
152
Q

Where is affected in an Acral melanoma?

A

Hands & feet

153
Q

Where is affected in a Subungual melanoma?

A

Under the nails

154
Q

What is a Amelanotic melanoma?

A

No pigment, so difficult to detect

155
Q

What are the 4 treatment options for a melanoma?

A
  1. Surgical excision
  2. Immunotherapy- ipilimumab
  3. Immune check point / MEK inhibitors
  4. Biologic antibodies eg BRAF genetic defects (debrafanib)
156
Q

What is the margin of melanoma surgical excision for a Breslow of <1mm?

A

1cm margin

157
Q

What is the margin of melanoma surgical excision for a Breslow of >1mm?

A

2cm margin

158
Q

What investigations would you do for a melanoma?

A

Imaging/ Scanning- CT/MRI/PET

159
Q

Describe the follow up of a patient with confirmed melanoma?

A
  • Long term follow up up to 5 years
  • Assessment for Lymph node / organ spread
  • Genetic testing in families, multiple primary melanomas
160
Q

Give 4 examples of cutaneous tumour syndromes?

A
  1. Gorlin’s syndrome
  2. Brook Spiegler syndrome
  3. Gardner Syndrome
  4. Cowden’s Syndrome
161
Q

Describe Gorlin’s syndrome?

A
  • Multiple BCCs
  • Jaw cysts
  • Risk of breast cancer
162
Q

Describe Brook Spiegler syndrome?

A
  • Multiple BCCs

- Trichoepitheliomas

163
Q

Describe Gardner Syndrome?

A
  • Soft tissue tumours
  • Polyps
  • Bowel cancer
164
Q

Describe Cowden’s syndrome?

A
  • Multiple hamartomas thyroid

- Breast cancer

165
Q

What are 2 superficial skin infections?

A
  1. Impetigo

2. Tinea

166
Q

What are 3 deeper examples of skin infections?

A
  1. Cellulitis
  2. Myositis
  3. Fasciitis
167
Q

What are 2 viral skin infections?

A
  1. Herpes simplex virus

2. Varicella zoster virus

168
Q

What 2 bacterial species does the skin consist of?

A
  1. Coagulase negative staphylococci

2. Corynebacterium sp.

169
Q

What 2 bacterial species reside in areas of skin with less acidic pH?

A
  1. Staphylococcus aureus

2. Streptococcus pyogenes

170
Q

Describe the microbiome of skin?

A
  • Usually not Gram negative bacteria or anearobic organisms
  • Anaerobe P. acnes dwellsin sweat & sebacious glands
  • Normal skin also colonised with fungi & mites
171
Q

Describe the appearance of Impetigo?

A

Golden encrusted skin lesions with inflammation localised to the dermis

172
Q

When is Impetigo most common?

173
Q

Describe the pathogenesis & cause of Impetigo?

A
  • Contagious and may occur in small outbreaks

- Caused by S. aureus & usually mild & self limiting

174
Q

How do you treat Impetigo?

A

Topical fusidic acid or systemic antibiotics if required

175
Q

Describe the appearance of Tinea?

A

Superficial fungal infection of the skin or nails

176
Q

Describe the prevalence of Tinea?

A

Very common, particularly on the feet

177
Q

What are the 3 most common causes of Tinea?

A
  1. Microsporum
  2. Epidermophyton
  3. Trichophyton
178
Q

How do you diagnose Tinea?

A

Diagnosis can be made on skin scrapings

179
Q

Describe the treatment of Tinea?

A
  • Topical therapy in non-severe cases involving skin alone: terbinafine cream
  • Systemic therapy in severe cases & those involving hair/nails: Terbinafine/Itraconazole
180
Q

Describe a Soft Tissue Abscess?

A

Infection within the dermis or fat layers with development of walled off infection & pooled pus

181
Q

Describe the treatment of a Soft Tissue Abscess?

A
  • Limited antibiotic penetration into abscess
  • Best treatment is always surgical drainage
  • Antibiotics not usually required if abscess fully drained & no surrounding cellulitis
182
Q

Describe Cellulitis?

A
  • Infection involving dermis
  • Most commonly begins on the lower limbs
  • Often tracks through the lymphatic system & may involve localised lymph nodes
183
Q

What may Cellulitis be associated with?

A

Systemic upset although bacteraemia relatively uncommon

184
Q

What is Cellulitis usually caused by?

A

β-haemolytic streptococci (Gp A Strep most common) & S. aureus

185
Q

What is the classification system for Cellulitis?

A

Enron Classification

186
Q

Describe the 4 stages of the Enron Classification system for Cellulitis?

A
  1. Not systemically unwell & no significant co-morbidites (i.e. diabetes)
  2. Systemically unwell or has significant co-morbidities which may complicate or delay resolution of infection
  3. Significant systemic upset or unstable co-morbitidies that will interfere with response to treatment or limb threatening vascular compromise
  4. Sepsis or severe, life threatening complications
187
Q

What are 2 examples of patients with stage 1 cellulitis according to the Enron Classification system?

A
  1. Patients who have not yet received antibiotics or have been on antibiotics <48 hours
  2. Patients who have failed to respond to >48 hours of appropriate oral antibiotics
188
Q

Describe the treatment for a patient with stage 1 cellulitis according to the Enron Classification system?

A
  • Oral therapy
  • Treatment to cover S. aureus & S. pyogenes:
  • 1st line: flucloxacillin 1g 6˚
  • 2nd line: doxycycline 100mg bd
  • Usual duration 7 days
189
Q

Describe the treatment for a patient with stage 2 cellulitis according to the Enron Classification system?

A
  • Initial IV therapy:
  • 1st line: flucloxacillin 2g 6˚
  • 2nd line: vancomycin based on dosing calculations
  • Usually able to be switched to oral after 48-72hrs
190
Q

Describe the treatment for a patient with stage 3 cellulitis according to the Enron Classification system?

A
  • Ambulatory care may be appropriate once daily antibiotics given in ambulatory care unit or in patient’s home
  • Usually IV ceftriaxone 2g od unless MRSA +
  • Important to be given under appropriately trained medical supervision
191
Q

Describe the prognosis for a patient with stage 4 cellulitis according to the Enron Classification system?

A
  • Regular clinical review
  • Can progress quickly to life/limb threatening complications & this is easily missed
  • Delay in surgery associated with poor outcomes
192
Q

What is Streptococcal Toxic Shock caused by?

A

Toxin producing Group A Streptococcus

193
Q

Describe the presentation of Streptococcal Toxic Shock?

A
  • Primary infection typically within the throat or skin/soft tissue
  • Present with localised infection (not necessarily severe), fever & shock
  • Often have diffuse, faint rash over body/limbs
194
Q

What are the 2 treatments for Streptococcal Toxic Shock?

A
  • Surgery: agressively seek out abscesses for drainage

- Antibiotics: penicillin may be ineffective, add clindamycin to reduce toxin production

195
Q

What treatment should you consider for Streptococcal Toxic Shock?

A

Pooled human immunoglobulin in severe cases

196
Q

Describe Necrotising Fasciitis?

A
  • Immediately life threatening soft tissueinfection with deep tissue involvement
  • Rapidly progressive, extensive tissuedamage requiring extensive surgical debridement
197
Q

What is the main factor for Necrotising Fasciitis?

A

Surgical emergency- do not delay consulting a surgeon if necrotising fasciitis suspected

198
Q

List the 4 signs/symptoms of Necrotising Fasciitis?

A
  • Rapidly progressive
  • Pain out of proportion to clinical signs
  • Severe systemic upset
  • Presence of visible necrotic tissue
199
Q

What may you see on imaging of Necrotising Fasciitis?

A

Fascial oedema & gas in soft tissues- late sign & must not be used to exclude necrotising SSTI

200
Q

Describe type 1 Polymicrobial Necrotising Fasciitis?

A
  • Usually complicates existing wounds, including surgical wounds
  • Microbiology usually a mix of Gram positives, Gram negatives & anaerobes
201
Q

Describe type 2 Group A Streptococcus Necrotising Fasciitis?

A
  • Usually occurs in previously healthy tissue, typically on the limbs
  • May follow a minor injury such as a scratch/sprain
  • Microbiology usually monobacterial infection with Streptococcus pyogenes only
202
Q

List the 5 broad spectrum antibiotics used for treating Necrotising Fasciitis?

A
  1. Flucloxacillin
  2. Benzylpenicillin
  3. Gentamicin
  4. Clindamycin
  5. Metronidazole
203
Q

What is the main treatment for Necrotising Fasciitis?

A

Experienced surgeon should review the patient without delay

204
Q

What 2 diseases can mimic cellulitis?

A
  1. Lymph disease

2. DVT

205
Q

What are 4 special dermatological circumstances?

A
  1. Bites
  2. Hospital acquired infection
  3. People who inject drugs
  4. PVL Staphylococcus aureus
206
Q

What are the 2 major considerations in bite injuries?

A
  1. Penetrating injuries often involving vulnerable structures (i.e. hands)
  2. Altered microbiology of wounds: Staphylococci, streptococci, anaerobic common
207
Q

What are 2 bugs that you would get from mammal bites?

A

Pasteurella and Capnocytophagia

208
Q

What is the antibiotic treatment for bite injuries?

A
  • 1st line: Co-amoxiclav

- 2nd line: Doxycycline & metronidazole

209
Q

What is the surgical treatment for bite injuries?

A

Need to consider early exploration & debridement of complications, i.e. tendon sheath infection

210
Q

What is the prophylactic treatment for bite injuries?

A
  • Antibiotics for high risk injuries
  • Consideration of tetanus prophylaxis
  • Rabies prophylaxis if rabies cannot be excluded: bat scratches/bites only in the UK
211
Q

Describe a hospital acquired skin infection?

A
  • Infection usually occurs at wounds & vascular access sites
  • Vascular access site infections should be preventable, need to ensure hygiene & care
212
Q

What should you consider in a hospital acquired skin infection?

A

MRSA infection:

  • Usually do not need to cover empirically
  • Use vancomycin for patients known to be colonised with MRSA
213
Q

What do Vascular access site infections have a high risk for?

A

Bacteraemia- consider initial IV treatment if systemic illness

214
Q

Describe the skin infections in people who inject drugs?

A
  • Often present late with neglected soft tissue infection

- Staphylococcus aureus predominates but infections often polymicrobial

215
Q

What do people who inject drugs have a high rate of?

A

Bacteraemia & disseminated infection-

Triad of S. aureus bacteraemia, DVT & multiple pulmonary abscesses

216
Q

What should you ofter on every admission of people who inject drugs?

A

Blood borne virus testing

217
Q

What is PVL Staphylococcus?

A

Virulence factor carried by some Staphylococcus aureus

218
Q

What is PVL Staphylococcus associated with?

A
  • Recurrent soft tissue boils & abscesses, often over months or even years
  • Rarely associated with severe necrotising pneumonia
219
Q

Describe the spread of PVL Staphylococcus infection?

A

Transmissible- outbreaks occur in families & others living closely together i.e. Universities

220
Q

How to do diagnose PVL Staphylococcus infection?

A

Obtain cultures & ask lab to do PVL genotyping

221
Q

What are the 2 treatments for PVL Staphylococcus infection?

A
  • Surgical treatment of abscesses
  • Antibiotics, outside UK, isolates often MRSA. Inside UK, usually MSSA. Protein synthesis inhibitors such as clindamycin reduce toxin production & may be a better choice
222
Q

What therapy should be given to a PVL Staphylococcus patient and to household contacts?

A

Decolonisation therapy

  • Topical chlorhexidine for skin/hair
  • Nasal mupirocin ointment
  • Simultaneous washing of sheets/towels
223
Q

Describe a primary Herpes Simplex (HSV)

infection?

A
  • Asymptomatic in 60%
  • Vesicular, may be painful
  • Recurrent: virus latent in sensory nerve ganglia
224
Q

What is type 1 Herpes Simplex (HSV)

infection?

A

Stomatitis “cold sore”

225
Q

What is type 2 Herpes Simplex (HSV)

infection?

A

Genital herpes

226
Q

How do you diagnose Herpes Simplex (HSV)

infection?

A
  • Clinical
  • Blood or vesicle fluid for PCR
  • Serology sometimes helpful
227
Q

What is the treatment for Herpes Simplex (HSV) infection?

A

Acyclovir (topical, oral, IV)

228
Q

What is Varicella zoster (VZV) virus also known as?

A

Chickenpox or shingles

229
Q

Describe the chickenpox Varicella zoster (VZV) virus?

A
  • Often a self limiting childhood infection
  • Highly infectious- manage in Side Room
  • Contagious from day 8-21 (before symptoms on day 10!)
230
Q

How is the chickenpox Varicella zoster (VZV) virus diagnosed?

A

PCR of vesicle fluid (or serology)

231
Q

What can be a consequence of the chickenpox Varicella zoster (VZV) virus during pregnancy?

A

Congenital abnormalities

232
Q

What can occur in adults with chickenpox Varicella zoster (VZV) virus?

A

Pneumonitis

233
Q

Varicella zoster (VZV) virus is _________ in children?

A

Self-limiting

234
Q

How do you treat the chickenpox Varicella zoster (VZV) virus at-risk adults with 48hrs of symptoms?

A

Acyclovir PO/IV

235
Q

Describe the shingles Varicella zoster (VZV) virus?

A
  • Reactivation of dormant VZV (dorsal root ganglia)
  • Dermatomal distribution
  • Transmissible: isolate until last crop of vesicles crusted
  • May be very painful
236
Q

How would you treat shingles Varicella zoster (VZV) virus?

A
  • Treat only high-risk patients (immunocompromised, disseminated) with acyclovir
  • Pain management: NSAIDS, gabapentin
237
Q

What should you consider with a presentation of shingles Varicella zoster (VZV) virus?

A

HIV testing

238
Q

What is the definition of a burn?

A

Microbial colonisation caused by loss of main protective barrier & commensal organisms

239
Q

What are the 3 distinct zones of a burn?

A
  1. Coagulation
  2. Stasis
  3. Hyperaema
240
Q

What 3 things can affect burn wounds?

A
  1. Cellulitis
  2. Necrotising fasciitis
  3. More localised infection
241
Q

What is a common organism you should be worried about with a skin burn?

A
  • Group A strep & Staphylococcus aureus
  • Enterococcus, Pseudomonas & Bacillus (opportunistic)
  • Viruses & fungi
242
Q

What is an important complication of paediatric thermal injuries?

A

Toxic shock syndrome (TSS)

243
Q

What can be particularly problematic in skin burns?

A

Biofilm forming & toxin producing organisms

244
Q

How do you treat burn wounds?

A

Debridement of dead or severely infected tissue, topical antiseptics/ antimicrobials, systemic antimicrobials

245
Q

What vaccination should you get with a burn wound?

246
Q

What 5 things can skin changes be a marker of?

A
  1. Endocrine disease
  2. Internal malignancy
  3. Nutritional deficiency
  4. Systemic infection
  5. Systemic inflammatory disease
247
Q

List 4 endocrine skin changes?

A
  1. Thyroid
  2. Diabetes
  3. Cushings / steroid excess
  4. Sex hormones
248
Q

List 3 thyroid endocrine skin changes?

A
  1. Dry skin (hypothyroidism)
  2. Thyroid dermopthy (Grave’s disease)
  3. Thyroid acropachy (Grave’s disease)
249
Q

List 5 diabetic endocrine skin changes?

A
  1. Necrobiosis lipoidica
  2. Diabetic dermopathy
  3. Scleredema (not scleroderma)
  4. Leg ulcers
  5. Granuloma annulare
250
Q

Describe Necrobiosis lipoidica?

A
  • Waxy appearance
  • Usually yellow discolouration
  • Often Shins
  • Occassionally ulcerates & scars
251
Q

Describe Diabetic dermopathy?

A
  • Small, round, brown atrophic skin lesions that occur on the shins
  • Asymptomatic & occur in up to 55% of patients withdiabetes
252
Q

Describe Scleredema?

A

Self-limiting skin condition defined by progressive thickening and hardening of the skin, usually on the areas of the upper back, neck, shoulders & face

253
Q

Describe diabetic ulcers?

A

Painless open sore or wound that are commonly located on the bottom of the feet & are typically venous ulcers

254
Q

Describe Granuloma Annulare?

A
  • Smooth discoloured plaques
  • Usually thickened & ring-shaped or annular in shape
  • Its not flaky or scaly
  • Deeper level of the skin
255
Q

What 4 skin problems can occur from cushings syndrome/ steroid excess?

A
  1. Acne
  2. Striae
  3. Erythema
  4. Gynaecomastia
256
Q

What 2 skin problems can occur from Addisons disease/ steroid insufficiency?

A
  1. Hyperpigmentation

2. Acanthosis nigracans

257
Q

What does the excessive production of cortisol in Cushings disease lead to?

A
  1. Increased central adiposity
  2. Moon facies & buffalo hump
  3. Global skin atrophy, epidermal & dermal components
  4. Striae on abdominal flanks, arms, thighs
  5. Purpura with minor trauma - reduced connective tissue
258
Q

Give 3 example cases of testosterone excess?

A
  1. Polycystic Ovarian Syndrome
  2. Testicular tumours
  3. Testosterone drug therapy
259
Q

What 2 skin problems does excess testosterone cause?

A
  1. Acne

2. Hirsutism

260
Q

Give 2 example cases of progesterone excess?

A
  1. Congenital adrenal hyperplasia

2. Contraceptive treatment

261
Q

What 2 skin problems does progesterone excess cause?

A
  1. Acne

2. Dermatitis

262
Q

What 3 skin problems can indicate an internal malignancy?

A
  1. Necrolytic migratory erythema
  2. Erythema gyratum repens
  3. Acanthosis nigricans
263
Q

Describe Necrolytic migratory erythema (glucagonoma syndrome)?

A
  • Rare disease

- Erythematous, scaly plaques on acral, intertriginous & periorificial areas

264
Q

What is Necrolytic migratory erythema (glucagonoma syndrome) associated with?

A

Islet cell tumour of the pancreas

265
Q

List 4 other signs of Necrolytic migratory erythema (glucagonoma syndrome)?

A
  1. Hyperglycemia
  2. Diarrhoea
  3. Weight loss
  4. Glossitis
266
Q

How do you treat Necrolytic migratory erythema (glucagonoma syndrome)?

A

Removal of the tumour

267
Q

Describe Erythema Gyratum Repens?

A
  • Rare
  • Reddened concentric bands whorled woodgrain pattern
  • Severe pruritus & peripheral eosinophilia
268
Q

What does Erythema Gyratum Repens have a strong association with?

A

Lung cancer

269
Q

What does Erythema Gyratum Repens have a weak association with?

A

Breast, cervical, GI cancers

270
Q

How do you treat Erythema Gyratum Repens?

A

Treatment of the underlying malignancy treats skin disease

271
Q

Describe the appearance of Acanthosis nigricans?

A

Smooth, velvet-like, hyperkeratotic plaques in intertriginous areas (groin, axillae, neck)

272
Q

What are the 3 types of Acanthosis nigricans?

A
  1. Type I- malignancy ie. adenocarcinoma, esp of the GI tract (60% gastric). Sudden onset & more extensive
  2. Type II- familial, autosomal dominant. Very rare, appears at birth, no malignancy
  3. Type III- obesity & insulin resistance. Most common type
273
Q

What are 3 other skin problems that occasionally are associated with internal malignancy?

A
  1. Erythema annulare
  2. Sweet’s Syndrome
  3. Sister Mary Joseph Nodule
274
Q

What 3 nutritional deficiencies can lead to skin problems?

A
  1. Vitamin B (B6, B12 & B3)
  2. Zinc
  3. Vitamin C
275
Q

What is another form of Vitamin B6 & what can a deficiency in this result in?

A
  • ANOTHER FORM: Pyridoxine

- DEFICIENCY RESULTS IN: Dermatitis

276
Q

What is another form of Vitamin B12 & what can a deficiency in this result in?

A
  • ANOTHER FORM: Cobalamin

- DEFICIENCY RESULTS IN: Angular chelitis

277
Q

What is another form of Vitamin B3 & what can a deficiency in this result in?

A
  • ANOTHER FORM: Niacin

- DEFICIENCY RESULTS IN: Pellagra

278
Q

What is Pellagra?

A
  • Disease characterised by diarrhoea, dermatitis & dementia
  • If left untreated= death
  • It occurs as a result of niacin (vitamin B-3) deficiency
279
Q

Describe Acrodermatitis Enteropathica (Zinc deficiency)?

A
  • Inherited or acquired condition

- Pustules, bullae, scaling (acral & perioral distribution)

280
Q

Describe how Acrodermatitis Enteropathica (Zinc deficiency) is inherited?

A

Mutation in SLC39A, which encodes an intestinal zinc transporter

281
Q

Describe Acrodermatitis Enteropathica (Zinc deficiency) in infants?

A

Can follow breast-feeding, when breast milk contains low levels of zinc

282
Q

List 4 causes of Acrodermatitis Enteropathica (Zinc deficiency) in adults?

A
  1. Alcoholism
  2. Malabsorption states
  3. Inflammatory bowel disease
  4. Bowel surgery
283
Q

What are the 2 differential diagnosis for Acrodermatitis Enteropathica (Zinc deficiency)?

A
  1. Nutritional deficiencies

2. Necrolytic migratory erythema

284
Q

How do you treat Acrodermatitis Enteropathica (Zinc deficiency)?

A

Zinc supplementation

285
Q

What does a vitamin D deficiency lead to?

286
Q

List the 7 signs/symptoms of a vitamin D deficiency (scurvy)?

A
  1. Punctate purpura / bruising
  2. “Corkscrew” spiral curly hairs
  3. Patchy hyperpimentation
  4. Dry skin
  5. Dry hair
  6. Non healing wounds
  7. Inflamed gums
287
Q

List 5 causes of Erythema nodosum?

A
  1. Streptococcal infection
  2. Pregnancy / Oral contraceptive
  3. Sarcoidosis
  4. Drug induced
  5. Bacterial / Viral infection
288
Q

Describe Erythema nodosum?

A
  • Severe pain!
  • Inflammation of the subcutaneous fat, deep
  • Swells & gets tight
  • Common place is the shins
289
Q

List 3 causes of Pyoderma gangrenosum?

A
  1. Inflammatory Bowel Disease
  2. Rheumatoid arthritis
  3. Myeloma
290
Q

Describe Pyoderma gangrenosum?

A

Rare skin condition that causes painful ulcers with a purple ring around it, usually affecting shins

291
Q

Give 4 examples of dermatological hair & nail problems?

A
  1. Alopecia areata (autoimmune)
  2. Hair thinning: B12, Iron deficiency, lupus, hypothyroidism
  3. Male pattern balding- androgen excess
  4. Nail clubbing, nail fold telangectasia
292
Q

List the 10 types of skin drug reactions?

A
  1. Maculopapular
  2. Urticaria
  3. Morbilliform
  4. Papulosquamous
  5. Photo-toxic
  6. Pustular
  7. Lichenoid
  8. Fixed drug rash
  9. Bullous
  10. Itch (no rash)
293
Q

List 6 common drugs that cause acute rashes?

A
  1. Antibiotics ie. penicillins, trimethoprim
  2. NSAIDs
  3. Chemotherapeutic agents
  4. Psychotropic ie. chlorpromazine
  5. Anti-epileptic ie. lamitrigine, carbamaz
  6. Cardiac
294
Q

Describe a Morbilliform rash?

A
  • Looks like measles

- Macular lesions that are red & usually 2–10 mm in diameter but may be confluent in places

295
Q

Describe a penicillin rash?

A
  • Generalised redness
  • Urticaria
  • Swollen & puffy
296
Q

Describe Urticaria /

Angiooedema?

A
  • Deep dermal histamine release
  • If you scratch them it makes it worse
  • Mucosal surfaces affected ie. Lips
297
Q

What 2 drugs can cause a Photo-toxic drug rash?

A

Quinine & bendroflumethiazide

298
Q

What drugs commonly cause pustular rashes?

A

Antibiotics

299
Q

Describe a Lichenoid rash?

A
  • Purple, itchy rash & can be triggered off by drugs

- Tends to have a white network pattern on the top

300
Q

List 3 triggers of vasculitis?

A
  1. Infection
  2. Drugs
  3. Connective tissue disease ie RA
301
Q

What should you check for with vasculitis?

A

Systemic vasculitis ie renal BP / Urinalysis

302
Q

Describe vasculitis?

A
  • Often localised & not rapidly progessive
  • Less unwell than in meningococcal rash
  • Inflammation of blood vessels ie. Small vessels in the skin
303
Q

Describe drug induced psoriasiform rash?

A
  • Psoriasis–like well demarcated pink erythema with scale

- Sudden onset, no FHx

304
Q

What 2 drugs can cause drug induced psoriasiform rash?

A
  1. Lithium

2. Beta blockers

305
Q

Describe a fixed drug rash?

A

Same area, same drug

306
Q

What drug can cause a fixed drug rash?

A

Paracetamol

307
Q

List 2 drug induced blistering disorders?

A
  1. Steven Johnson Syndrome

2. Toxic epidermal necrolysis

308
Q

List 2 Immunobullous disease causing blistering?

A
  1. Bullous pemphigoid

2. Pemphigus vulgaris

309
Q

Describe Steven Johnson Syndrome?

A
  • Blistering around mouth, eyes & sometimes on the skin

- Haemorrhagic crusting in the lips

310
Q

What is Toxic epidermal necrolysis (TEN)?

A
  • Dermatological emergency
  • Majority drug induced
  • Disease spectrum
  • Most severe mucous membrane involvement
  • Stop suspect drug
311
Q

In Toxic epidermal necrolysis (TEN) what is the condition if there is <10% of skin involved?

A

Steven Johnson Syndrome (SJS)

312
Q

Describe the appearance of Toxic epidermal necrolysis (TEN)?

A
  • Necrotic skin
  • Falling off
  • Looks like a 3rd degree burn
  • Extremely painful
313
Q

Describe the management of Toxic epidermal necrolysis (TEN)?

A
  • Analgesia
  • Fluid balance SCORTEN severity scale
  • Special mattress, sheets
  • Infection control / prophylaxis
  • Non adherent dressings
  • Urology, Gynae, Ophthalmology input
314
Q

What is the prognosis for Toxic epidermal necrolysis (TEN)?

A

> 50% mortality rate

315
Q

Describe Staphlococcal scalded skin syndrome?

A
  • Patient’s are not usually that unwell
  • Scaling
  • Temperature
  • No mucosal involvement
316
Q

Describe Erythema multiforme?

A
  • Self-limiting allergic reaction
  • HSV, EBV, occassionally drug
  • No or mild prodrome
  • Target lesions
  • Never –> TEN
317
Q

What is the appearance of Erythema multiforme?

A

Dartboard appearance (3 rings together)

318
Q

List 5 Immunobullous disorders (not triggered by drugs)?

A
  1. Bullous pemphigoid
  2. Mucous membrane pemphigoid
  3. Paraneoplastic pemphigoid
  4. Pemphigus
  5. Dermatitis herpetiformis (coeliac disease)
319
Q

Describe the difference between Bullous pemphigoid & Pemphigus vulgaris?

A
  • Bullous pemphigoid: skin split is at the bottom, so the whole epidermis rises up ie. distinct intact blister
  • Pemphigus vulgaris: skin is split superficially so does not form a distinct blister
320
Q

Describe the treatment of Immunobullous disorders?

A
  • Oral steroids
  • Steroid sparing agents ie azathioprine
  • Burst any blisters
  • Dressings and infection control
321
Q

What should you check for with Immunobullous disorders?

A

Oral / mucosal involvement

322
Q

What should you consider doing for patients with Immunobullous disorders?

A

Screen for underlying malignancy

323
Q

List the 3 treatments for Dermatitis herpetiformis (coeliac disease)?

A
  1. Topical steroids
  2. Gluten free diet
  3. Oral dapsone
324
Q

Describe the appearance of Dermatitis herpetiformis (coeliac disease)?

A
  • Intensely itchy, even when only appearing as a mild rash

- Small blisters on extensor surfaces

325
Q

Describe Urticaria?

A
  • Itchy, wheals (hives)
  • Lesions last < 24 hours
  • Non-scarring
326
Q

How long is acute & chronic Urticaria?

A
  • Acute <6 weeks

- Chronic >6 weeks

327
Q

What are the 2 types of Urticaria?

A
  1. Immune-mediated: type 1 allergic IgE response

2. Non-immune-mediated: direct mast cell degranulation eg opiates, antibiotics, contrast media, NSAIDs

328
Q

List the 4 treatments for Urticaria?

A
  1. Antihistamines
  2. Steroids
  3. Immunosuppression
  4. Omiluzimab
329
Q

List 5 causes of Acute Urticaria?

A
  1. Viral infections
  2. Medication- NSAIDS, Aspirin, ACE
  3. Foods & food additives
  4. Parasitic infections
  5. Physical stimulants- cold, pressure, solar, cholinergic, aquagenic
330
Q

What is Dermographism?

A
  • Exaggerated wealing tendency when the skin is stroked

- Commonest form of physical urticaria

331
Q

What is erythroderma?

A

Descriptive term for “Bright red”

332
Q

List 4 causes of erythroderma?

A
  1. Psoriasis
  2. Eczema
  3. Drug reaction
  4. Cutaneous lymphoma
333
Q

How do you treat erythroderma?

A
  • Treat underlying skin disorder, supportive

- Fluid / temperature balance

334
Q

Describe Pustular Psoriasis?

A
  • Uncommon form of psoriasis
  • Defined, raised bumps filled with white, thick fluid composed of WBCs (purulent exudate/ pus)
  • The skin under & around these bumps is red

MBChB Year 3 (15 decks)

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