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
What happens once an individual is sensitised to a chemical?
Allergic contact dermatitis can then develop within hours of repeat exposure exposure
26
What are the damaging effects of ultraviolet on skin?
- Direct cellular damage & alterations in immunologic function - Direct effects include photoaging, DNA damage & carcinogenesis
27
What is mutated by DNA damage & how is this implicated?
- P53 tumour suppressor gene | - Implicated in development of melanoma & non melanoma skin cancers
28
What work together to protect cells from UV DNA damage?
Keratinocytes & melanocytes
29
What 5 things does chronic UV exposure in humans eventually lead to?
1. Loss of skin elasticity 2. Fragility 3. Abnormal pigmentation 4. Hemorrhage of blood vessels 5. Wrinkles & premature ageing
30
What happens during exposure to sunlight?
Solar UVB photons are absorbed by 7-dehydrocholesterol in the skin & converted to previtamin D(3)
31
What happens to pre-vitamin D(3)?
Undergoes transformation within the plasma membrane to active vitamin D(3)
32
What is the skin problem during winter?
Minimal pre-vitamin D(3) production in the skin & few foods naturally contain Vit D
33
What are the 4 associated increased risks with Vitamin D deficiency?
1. Common cancers 2. Autoimmune diseases (MS) 3. Infectious diseases 4. Cardiovascular disease
34
What can cutaneous receptors be?
Encapsulated nerve endings such as Meissner, Pacini & Ruffini corpuscles or Free nerve endings associated with Merkel cells
35
Describe Merkel cells?
- Base of the epidermis, | - Respond to sustained gentle & localised pressure, assess shape /edge
36
Describe Meissner corpuscles?
- Immediately below epidermis & are particularly well represented on the palmar surfaces of the fingers and lips - They are especially sensitive to light touch
37
Describe Ruffini's corpuscles?
- In the dermis | - Receptors sensitive to deep pressure & stretching
38
Describe Pacinian corpuscles?
- Mechanoreceptors present in the deep dermis, sensitive to deep touch, rapid deformation of skin surface and around joints for position/proprioception
39
What is a macule?
Flat area in the skin, usually a change in colour (pigmented)
40
What is a papule?
Something small raised in the skin
41
What is a pustule?
Raised & full of puss (infection/inflammatory cells)
42
What is a plaque?
Raised and tends to be big
43
What is a vesicle?
Tiny blisters
44
What is a bulla?
Giant blisters
45
What is Erythematous?
Redness
46
What is Ulceration?
The epidermis has been removed and you are left with just the deaper levels of skin
47
What are the 5 etiological stages of acne?
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
48
List the 7 clinical features of acne?
1. Papules 2. Pustules 3. Erythema 4. Comedones 5. Nodules 6. Cysts 7. Scarring
49
What 3 clinical features are needed to make a diagnosis of acne?
1. Papules 2. Pustules 3. Comedones
50
What are comedones?
Blackheads/ whiteheads
51
What are the 4 distributions of acne?
1. Face 2. Chest 3. Back / Shoulders 4. Occasionally legs, scalp
52
What are 3 clinical types of acne?
1. Papulopustular 2. Nodulocystic 3. Comedonal
53
What are the 4 subtypes of acne?
1. Steroid induced 2. Acne fulminans 3. Acne rosacea 4. Acne Inversus (Hidradenitis suppuritiva)
54
What are the different grades of acne?
Grades 1-7 (the Leeds Acne photographic grading system)
55
What are the 2 medications to reduce plugging in acne?
1. Topical retinoid | 2. Topical benzoyl peroxide
56
What are the 3 medications to reduce bacteria in acne?
1. Topical antibiotics (erythromycin, clindamycin) 2. Oral antibiotics (tetracyclines, erythromycin) 3. Benzoyl peroxide reduced bacterial resistance
57
What medication can reduce sebum production in acne?
Hormones- anti androgen ie Dianette / OCP
58
List the 4 side effects of topical agents in acne?
1. Irritant 2. Burning 3. Peeling 4. Bleaching
59
What is the side effect of oral antibiotics for acne?
Gastro upset (esp. tetracycline)
60
What is the side effect of the oral contraceptive pill for acne?
Possible DVT risk
61
What is the controversial treatment option for acne?
Dietary modification ie. reduce glycemic load (milk, chocolate)
62
What is Oral Isotretinoin?
- Licensed for severe acne vulgaris (remission in ~80% of teenagers) - Concentrated form of vitamin A
63
What is the effect of Oral Isotretinoin?
Reduces sebum, plugging and bacteria
64
What is the standard course of Oral Isotretinoin?
- 16 weeks | - 1mg/kg
65
List the 9 side effects of Oral Isotretinoin?
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
66
What is the program associated with Oral Isotretinoin?
Pregnancy Prevention program (monthly tests & contraception needed)
67
What are the 2 clinical problems with prescribing Oral Isotretinoin?
1. Expensive | 2. Consumes lots of clinical time
68
What is Oral Isotretinoin also known as?
Accutane or Roaccutane
69
What is the definition of eczema/dermatitis?
Inflammation of the skin
70
Describe the aetiology of eczema?
Combination of genetic, immune & reactivity to a variety of stimuli
71
Describe the inflammation in eczema?
- Primarily due to inherited abnormalities in skin so called “barrier defect” - Leads to increased permeability & reduces its antimicrobial function
72
Describe the genetic problem in eczema?
Inherited abnormality in filaggrin expression (chromosome 1) --> disordered barrier function
73
What are filaggrins?
Proteins which bind to keratin fibres in the epidermal cells
74
What are the 5 endogenous types of eczema?
1. Atopic 2. Seborrhoeic 3. Discoid 4. Varicose 5. Pompholyx
75
What are the 2 exogenous types of eczema?
1. Contact (allergic, irritant) | 2. Photoreaction (allergic, drug)
76
Describe atopic eczema?
- Itchy inflammatory skin condition - High Ig-E immunoglobulin antibody levels - Genetic & immune aetiology
77
What is atopic eczema associated with?
Asthma, allergic rhinitis, conjunctivitis, hayfever (atopy individual)
78
Describe the prevalence of atopic eczema?
- 10-15% of infants affected - Remission occurs in 75% by 15 years - 2/3 have a family history of atopy
79
Describe the presentation of infant atopic eczema?
- Itchy - Occasionally vesicular (small blisters) - Often facial component - Secondary infection - Occasionally aggravated by food (ie milk)
80
Describe the prognosis of infant atopic eczema?
< 50% still have eczema by 18 months
81
What are the 2 complications of atopic eczema?
1. Bacterial infection- staph aureus | 2. Viral infection- molluscum, viral warts, eczema herpeticum
82
What are the 3 negative systemic effects of atopic eczema?
1. Tiredness 2. Growth reduction 3. Psychological impact
83
List the 9 management techniques for atopic eczema?
1. Emollients 2. Topical steroids 3. Bandages 4. Antihistamines 5. Antibiotics / anti-virals 6. Education for parents /child 6. National Eczema Society 7. Avoidance of exacerbating factors 8. Systemic drugs 9. Newest biologic agent
84
What are the 2 systemic drugs that you can use for atopic eczema?
1. Ciclosporin | 2. Methotrexate
85
What is the newest biologic agent for atopic eczema?
IL4/13 blocker- Dupilumab
86
What is contact dermatitis?
Type 4 hypersensitivity reaction precipitated by an exogenous agent ie: 1. Irritant- direct noxious effect on skin barrier 2. Allergic - Type IV hypersensitivity reaction
87
What are the 5 common allergens for contact dermatitis?
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
88
What is Seborrhoeic Dermatitis?
Chronic, scaly inflammatory condition caused by overgrowth of Pityrosporum Ovale yeast
89
Where is typically affected by Seborrhoeic Dermatitis?
Face, scalp, & eyebrows occasionally the upper chest
90
What 2 things can Seborrhoeic Dermatitis occasionally be confused with?
1. Dandruff | 2. Facial psoriasis
91
What 2 factors makes Seborrhoeic Dermatitis worse?
1. Teenagers | 2. Underlying HIV
92
How do you manage scalp Seborrhoeic Dermatitis?
Medicated anti yeast shampoo (antifungal ketoconazole -Nizoral, Selsun)
93
How do you manage face Seborrhoeic Dermatitis?
- Anti-microbial, mild steroid (ie Daktacort cream) | - Simple moisturiser
94
What can Seborrhoeic Dermatitis rarely be treated with?
Systemic antifungals
95
What often improves Seborrhoeic Dermatitis?
UV/sunlight
96
Describe Venous dermatitis?
- Underlying venous disease - Affects lower legs - Incompetence of deep perforating veins - Increased hydrostatic pressure
97
What are 4 ways to manage Venous dermatitis?
1. Emollients 2. Mild / moderate topical steroid 3. Compression bandaging / stockings 4. Consider early venous surgical intervention
98
What is the definition of psoriasis?
Chronic relapsing & remitting scaling skin disease which may appear at any age & affect any part of the skin
99
When does psoriasis often present?
Age onset often two peaks age 20-30y or 50-60y
100
What are 3 causes of psoriasis?
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
101
What are 4 things linked to psoriasis?
1. Psoriatic arthritis 2. Metabolic syndrome 3. Liver disease / alcohol misuse 4. Depression
102
Describe the genetic prevalence associated with psoriasis?
- 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 %
103
What genes are related to psoriasis?
PSORS genes (eg PSORS1, Chromosome 6) & HLA – Cw0602 associated in certain subtypes
104
List the 5 types of psoriasis?
1. Plaque 2. Guttate 3. Pustular 4. Erythrodermic 5. Flexural / Inverse
105
What type of psoriasis is now thought to NOT be psoriasis?
Palmar/plantar pustulosis
106
What is Koebner phenomenon?
Psoriasis at sites of trauma / scars ie. appendectomy
107
Describe the presentation of psoriasis?
1. Well demarcated 2. Salmon pink inflammation 3. Plaque build up 4. No moisture 5. Scaled 6. Onycholysis 7. Nail pitting
108
What 4 factors does the management of psoriasis depend on?
1. Severity 2. What patient wants 3. What patient can cope with 4. If they have arthropathy
109
List 3 scoring systems for psoriasis?
1. Disease life quality index- DLQI 2. Psoriasis area severity index- PASI 3. Patient eczema severity time- PEST
110
What do up to 20% of psoriasis patients develop?
Arthritis
111
What is the treatment for psoriasis in order of increasing effectiveness & toxicity?
1. Topical creams & ointments 2. Phototherapy light treatment (UV) 3. Acitretin- retinoid drug/ vitamin A 4. Methotrexate- decrease inflammation 5. Ciclosporin 6. Biologic therapies
112
What are 4 examples of biologic therapies for psoriasis?
1. Adalumimab (anti TNF) 2. Ustekinumab (anti IL12/23) 3. Secukinumab 4. Brodilumab
113
Give 2 examples of topical therapies for psoriasis?
1. Moisturisers- help reduce dryness, flaking | 2. Steroids- reduce autoimmune response, redness, itching, inflammation
114
Give 4 examples of topical therapies that slow down keratinocyte production?
1. Vitamin D analogues 2. Coal Tar 3. Dithranol- tree bark extract 4. Retinoid (Tazarotene) rarely used now
115
What effect does Ultraviolet Phototherpy have?
- Can reduce T cell proliferations | - Encourages Vitamin D & reduces skin turnover
116
What are the 2 types of Ultraviolet Phototherpy?
1. UV-B light is the most commonly used | 2. UV-A with psoralen photosensitiser
117
What are the 2 risks of Ultraviolet Phototherpy?
1. Short term burning | 2. Longer term skin cancer
118
List the 3 potent side effects of most drugs for psoriasis?
1. Liver dysfunction 2. Hypertension 3. Risk of infection
119
What 2 drugs would you not give for treating psoriasis?
1. Azathioprine | 2. Systemic steroids
120
What 2 distinct pathways interact or converge to cause skin cancer?
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
121
Describe the chain of damage that UV light has on skin?
DNA damage --> p53 mutation & Immune suppression & p53 induction --> Abnormal cell proliferation --> Other genetic alterations --> Skin cancer
122
What are the 3 main skin cancer types?
1. Basal Cell Carcinoma 2. Squamous Cell Carcinoma 3. Malignant Melanoma
123
Where do melanocytes reside?
With the skin basal cells
124
What is the most common type of skin cancer?
Basal cell carcinoma
125
What is the process of creating new skin cells controlled by?
Basal cells DNA
126
What can a mutation in the DNA cause?
- 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
127
What are 80% of basal cell cancers found on?
Head & neck/UV exposed sites
128
What rarely happens in basal cell carcinomas?
Metastasis or kills
129
What are the basal cell carcinoma subtypes?
1. Nodular 2. Superficial 3. Pigmented 4. Morphoeic/Sclerotic
130
Describe Nodular Basal Cell Carcinoma?
- Nodule ie > 0.5cm raised lesion - Shiny “pearly” - Telangectasia / blood vessels - Often ulcerated centrally
131
Describe superficial basal cell carcinoma?
- Grows slowly - Minimal tendency to be invasive - Erythematous - Well-circumscribed patch or plaque - Not ulcerative
132
Describe pigmented basal cell carcinoma?
- Black/dark pigment - Curved border - Some ulceration - Raised
133
Describe Morphoeic/ Sclerotic basal cell carcinoma?
- Subtle skin textural change - ​Slowly expanding - A yellow-white waxy patch with very ill-defined edges - Surface telangiectasia
134
What is the gold standard treatment for basal cell carcinoma?
Surgical excision 3-4mm margin
135
What are 5 treatment options for basal cell carcinoma?
1. Curettage and cautery 2. Cryotherapy 3. Photodynamic therapy 4. Topical imiquimod / 5-fluorouracil cream 5. Mohs micrographic surgery
136
Where may squamous cell carcinomas occur?
In normal skin or in skin that has been injured (burns/UV damage) or chronically inflamed
137
What does squamous cell carcinoma originate from?
Keratinocytes
138
What are 2 pre-malignant variants of squamous cell carcinoma?
1. Actinic keratoses | 2. Bowens disease
139
What is the % risk of high risk squamous cell carcinoma metastasis?
10 to 30% (high risk sites- ears, lips)
140
Describe the presentation of squamous cell carcinoma?
- Scaling - Ulceration - Crusting - Inflammation
141
What are the 2 treatments for squamous cell carcinoma?
1. Gold standard- Surgical excision 4mm margin | 2. Curettage & cautery
142
What are the 4 treatments for pre-malignant/squamous cell in-situ?
1. Topical imiquimod / 5-fluorouracil cream 2. Cryotherapy 3. Photodynamic therapy 4. Sun protection
143
What is a melanoma?
Malignant tumour of melanocytes
144
What are the most common sites for melanoma's?
Skin (but can be bowel/ eye)
145
What are the 2 phases of melanomas?
1. Radial growth | 2. Vertical growth
146
What determines the prognosis of a melanoma?
Depth of presentation
147
How is melanomas spread?
Via lymphatics
148
List 11 risk factors for the development of a melanoma?
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
Describe the 5 year survival of melanomas of varying Breslow thickness?
- 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
List the 8 different melanoma subtypes?
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
What 4 things should you look for when assessing a melanoma?
1. Symmetry 2. Different colours 3. Borders 4. Size
152
Where is affected in an Acral melanoma?
Hands & feet
153
Where is affected in a Subungual melanoma?
Under the nails
154
What is a Amelanotic melanoma?
No pigment, so difficult to detect
155
What are the 4 treatment options for a melanoma?
1. Surgical excision 2. Immunotherapy- ipilimumab 3. Immune check point / MEK inhibitors 4. Biologic antibodies eg BRAF genetic defects (debrafanib)
156
What is the margin of melanoma surgical excision for a Breslow of <1mm?
1cm margin
157
What is the margin of melanoma surgical excision for a Breslow of >1mm?
2cm margin
158
What investigations would you do for a melanoma?
Imaging/ Scanning- CT/MRI/PET
159
Describe the follow up of a patient with confirmed melanoma?
- Long term follow up up to 5 years - Assessment for Lymph node / organ spread - Genetic testing in families, multiple primary melanomas
160
Give 4 examples of cutaneous tumour syndromes?
1. Gorlin’s syndrome 2. Brook Spiegler syndrome 3. Gardner Syndrome 4. Cowden’s Syndrome
161
Describe Gorlin's syndrome?
- Multiple BCCs - Jaw cysts - Risk of breast cancer
162
Describe Brook Spiegler syndrome?
- Multiple BCCs | - Trichoepitheliomas
163
Describe Gardner Syndrome?
- Soft tissue tumours - Polyps - Bowel cancer
164
Describe Cowden's syndrome?
- Multiple hamartomas thyroid | - Breast cancer
165
What are 2 superficial skin infections?
1. Impetigo | 2. Tinea
166
What are 3 deeper examples of skin infections?
1. Cellulitis 2. Myositis 3. Fasciitis
167
What are 2 viral skin infections?
1. Herpes simplex virus | 2. Varicella zoster virus
168
What 2 bacterial species does the skin consist of?
1. Coagulase negative staphylococci | 2. Corynebacterium sp.
169
What 2 bacterial species reside in areas of skin with less acidic pH?
1. Staphylococcus aureus | 2. Streptococcus pyogenes
170
Describe the microbiome of skin?
- Usually not Gram negative bacteria or anearobic organisms - Anaerobe P. acnes dwellsin sweat & sebacious glands - Normal skin also colonised with fungi & mites
171
Describe the appearance of Impetigo?
Golden encrusted skin lesions with inflammation localised to the dermis
172
When is Impetigo most common?
Children
173
Describe the pathogenesis & cause of Impetigo?
- Contagious and may occur in small outbreaks | - Caused by S. aureus & usually mild & self limiting
174
How do you treat Impetigo?
Topical fusidic acid or systemic antibiotics if required
175
Describe the appearance of Tinea?
Superficial fungal infection of the skin or nails
176
Describe the prevalence of Tinea?
Very common, particularly on the feet
177
What are the 3 most common causes of Tinea?
1. Microsporum 2. Epidermophyton 3. Trichophyton
178
How do you diagnose Tinea?
Diagnosis can be made on skin scrapings
179
Describe the treatment of Tinea?
- Topical therapy in non-severe cases involving skin alone: terbinafine cream - Systemic therapy in severe cases & those involving hair/nails: Terbinafine/Itraconazole
180
Describe a Soft Tissue Abscess?
Infection within the dermis or fat layers with development of walled off infection & pooled pus
181
Describe the treatment of a Soft Tissue Abscess?
- Limited antibiotic penetration into abscess - Best treatment is always surgical drainage - Antibiotics not usually required if abscess fully drained & no surrounding cellulitis
182
Describe Cellulitis?
- Infection involving dermis - Most commonly begins on the lower limbs - Often tracks through the lymphatic system & may involve localised lymph nodes
183
What may Cellulitis be associated with?
Systemic upset although bacteraemia relatively uncommon
184
What is Cellulitis usually caused by?
β-haemolytic streptococci (Gp A Strep most common) & S. aureus
185
What is the classification system for Cellulitis?
Enron Classification
186
Describe the 4 stages of the Enron Classification system for Cellulitis?
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
What are 2 examples of patients with stage 1 cellulitis according to the Enron Classification system?
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
Describe the treatment for a patient with stage 1 cellulitis according to the Enron Classification system?
- Oral therapy - Treatment to cover S. aureus & S. pyogenes: - 1st line: flucloxacillin 1g 6˚ - 2nd line: doxycycline 100mg bd - Usual duration 7 days
189
Describe the treatment for a patient with stage 2 cellulitis according to the Enron Classification system?
- 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
Describe the treatment for a patient with stage 3 cellulitis according to the Enron Classification system?
- 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
Describe the prognosis for a patient with stage 4 cellulitis according to the Enron Classification system?
- Regular clinical review - Can progress quickly to life/limb threatening complications & this is easily missed - Delay in surgery associated with poor outcomes
192
What is Streptococcal Toxic Shock caused by?
Toxin producing Group A Streptococcus
193
Describe the presentation of Streptococcal Toxic Shock?
- 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
What are the 2 treatments for Streptococcal Toxic Shock?
- Surgery: agressively seek out abscesses for drainage | - Antibiotics: penicillin may be ineffective, add clindamycin to reduce toxin production
195
What treatment should you consider for Streptococcal Toxic Shock?
Pooled human immunoglobulin in severe cases
196
Describe Necrotising Fasciitis?
- Immediately life threatening soft tissue infection with deep tissue involvement - Rapidly progressive, extensive tissue damage requiring extensive surgical debridement
197
What is the main factor for Necrotising Fasciitis?
Surgical emergency- do not delay consulting a surgeon if necrotising fasciitis suspected
198
List the 4 signs/symptoms of Necrotising Fasciitis?
- Rapidly progressive - Pain out of proportion to clinical signs - Severe systemic upset - Presence of visible necrotic tissue
199
What may you see on imaging of Necrotising Fasciitis?
Fascial oedema & gas in soft tissues- late sign & must not be used to exclude necrotising SSTI
200
Describe type 1 Polymicrobial Necrotising Fasciitis?
- Usually complicates existing wounds, including surgical wounds - Microbiology usually a mix of Gram positives, Gram negatives & anaerobes
201
Describe type 2 Group A Streptococcus Necrotising Fasciitis?
- 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
List the 5 broad spectrum antibiotics used for treating Necrotising Fasciitis?
1. Flucloxacillin 2. Benzylpenicillin 3. Gentamicin 4. Clindamycin 5. Metronidazole
203
What is the main treatment for Necrotising Fasciitis?
Experienced surgeon should review the patient without delay
204
What 2 diseases can mimic cellulitis?
1. Lymph disease | 2. DVT
205
What are 4 special dermatological circumstances?
1. Bites 2. Hospital acquired infection 3. People who inject drugs 4. PVL Staphylococcus aureus
206
What are the 2 major considerations in bite injuries?
1. Penetrating injuries often involving vulnerable structures (i.e. hands) 2. Altered microbiology of wounds: Staphylococci, streptococci, anaerobic common
207
What are 2 bugs that you would get from mammal bites?
Pasteurella and Capnocytophagia
208
What is the antibiotic treatment for bite injuries?
- 1st line: Co-amoxiclav | - 2nd line: Doxycycline & metronidazole
209
What is the surgical treatment for bite injuries?
Need to consider early exploration & debridement of complications, i.e. tendon sheath infection
210
What is the prophylactic treatment for bite injuries?
- Antibiotics for high risk injuries - Consideration of tetanus prophylaxis - Rabies prophylaxis if rabies cannot be excluded: bat scratches/bites only in the UK
211
Describe a hospital acquired skin infection?
- Infection usually occurs at wounds & vascular access sites - Vascular access site infections should be preventable, need to ensure hygiene & care
212
What should you consider in a hospital acquired skin infection?
MRSA infection: - Usually do not need to cover empirically - Use vancomycin for patients known to be colonised with MRSA
213
What do Vascular access site infections have a high risk for?
Bacteraemia- consider initial IV treatment if systemic illness
214
Describe the skin infections in people who inject drugs?
- Often present late with neglected soft tissue infection | - Staphylococcus aureus predominates but infections often polymicrobial
215
What do people who inject drugs have a high rate of?
Bacteraemia & disseminated infection- | Triad of S. aureus bacteraemia, DVT & multiple pulmonary abscesses
216
What should you ofter on every admission of people who inject drugs?
Blood borne virus testing
217
What is PVL Staphylococcus?
Virulence factor carried by some Staphylococcus aureus
218
What is PVL Staphylococcus associated with?
- Recurrent soft tissue boils & abscesses, often over months or even years - Rarely associated with severe necrotising pneumonia
219
Describe the spread of PVL Staphylococcus infection?
Transmissible- outbreaks occur in families & others living closely together i.e. Universities
220
How to do diagnose PVL Staphylococcus infection?
Obtain cultures & ask lab to do PVL genotyping
221
What are the 2 treatments for PVL Staphylococcus infection?
- 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
What therapy should be given to a PVL Staphylococcus patient and to household contacts?
Decolonisation therapy - Topical chlorhexidine for skin/hair - Nasal mupirocin ointment - Simultaneous washing of sheets/towels
223
Describe a primary Herpes Simplex (HSV) | infection?
- Asymptomatic in 60% - Vesicular, may be painful - Recurrent: virus latent in sensory nerve ganglia
224
What is type 1 Herpes Simplex (HSV) | infection?
Stomatitis “cold sore”
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What is type 2 Herpes Simplex (HSV) | infection?
Genital herpes
226
How do you diagnose Herpes Simplex (HSV) | infection?
- Clinical - Blood or vesicle fluid for PCR - Serology sometimes helpful
227
What is the treatment for Herpes Simplex (HSV) infection?
Acyclovir (topical, oral, IV)
228
What is Varicella zoster (VZV) virus also known as?
Chickenpox or shingles
229
Describe the chickenpox Varicella zoster (VZV) virus?
- Often a self limiting childhood infection - Highly infectious- manage in Side Room - Contagious from day 8-21 (before symptoms on day 10!)
230
How is the chickenpox Varicella zoster (VZV) virus diagnosed?
PCR of vesicle fluid (or serology)
231
What can be a consequence of the chickenpox Varicella zoster (VZV) virus during pregnancy?
Congenital abnormalities
232
What can occur in adults with chickenpox Varicella zoster (VZV) virus?
Pneumonitis
233
Varicella zoster (VZV) virus is _________ in children?
Self-limiting
234
How do you treat the chickenpox Varicella zoster (VZV) virus at-risk adults with 48hrs of symptoms?
Acyclovir PO/IV
235
Describe the shingles Varicella zoster (VZV) virus?
- Reactivation of dormant VZV (dorsal root ganglia) - Dermatomal distribution - Transmissible: isolate until last crop of vesicles crusted - May be very painful
236
How would you treat shingles Varicella zoster (VZV) virus?
- Treat only high-risk patients (immunocompromised, disseminated) with acyclovir - Pain management: NSAIDS, gabapentin
237
What should you consider with a presentation of shingles Varicella zoster (VZV) virus?
HIV testing
238
What is the definition of a burn?
Microbial colonisation caused by loss of main protective barrier & commensal organisms
239
What are the 3 distinct zones of a burn?
1. Coagulation 2. Stasis 3. Hyperaema
240
What 3 things can affect burn wounds?
1. Cellulitis 2. Necrotising fasciitis 3. More localised infection
241
What is a common organism you should be worried about with a skin burn?
- Group A strep & Staphylococcus aureus - Enterococcus, Pseudomonas & Bacillus (opportunistic) - Viruses & fungi
242
What is an important complication of paediatric thermal injuries?
Toxic shock syndrome (TSS)
243
What can be particularly problematic in skin burns?
Biofilm forming & toxin producing organisms
244
How do you treat burn wounds?
Debridement of dead or severely infected tissue, topical antiseptics/ antimicrobials, systemic antimicrobials
245
What vaccination should you get with a burn wound?
Tetanus
246
What 5 things can skin changes be a marker of?
1. Endocrine disease 2. Internal malignancy 3. Nutritional deficiency 4. Systemic infection 5. Systemic inflammatory disease
247
List 4 endocrine skin changes?
1. Thyroid 2. Diabetes 3. Cushings / steroid excess 4. Sex hormones
248
List 3 thyroid endocrine skin changes?
1. Dry skin (hypothyroidism) 2. Thyroid dermopthy (Grave’s disease) 3. Thyroid acropachy (Grave’s disease)
249
List 5 diabetic endocrine skin changes?
1. Necrobiosis lipoidica 2. Diabetic dermopathy 3. Scleredema (not scleroderma) 4. Leg ulcers 5. Granuloma annulare
250
Describe Necrobiosis lipoidica?
- Waxy appearance - Usually yellow discolouration - Often Shins - Occassionally ulcerates & scars
251
Describe Diabetic dermopathy?
- Small, round, brown atrophic skin lesions that occur on the shins - Asymptomatic & occur in up to 55% of patients with diabetes
252
Describe Scleredema?
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
Describe diabetic ulcers?
Painless open sore or wound that are commonly located on the bottom of the feet & are typically venous ulcers
254
Describe Granuloma Annulare?
- Smooth discoloured plaques - Usually thickened & ring-shaped or annular in shape - Its not flaky or scaly - Deeper level of the skin
255
What 4 skin problems can occur from cushings syndrome/ steroid excess?
1. Acne 2. Striae 3. Erythema 4. Gynaecomastia
256
What 2 skin problems can occur from Addisons disease/ steroid insufficiency?
1. Hyperpigmentation | 2. Acanthosis nigracans
257
What does the excessive production of cortisol in Cushings disease lead to?
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
Give 3 example cases of testosterone excess?
1. Polycystic Ovarian Syndrome 2. Testicular tumours 3. Testosterone drug therapy
259
What 2 skin problems does excess testosterone cause?
1. Acne | 2. Hirsutism
260
Give 2 example cases of progesterone excess?
1. Congenital adrenal hyperplasia | 2. Contraceptive treatment
261
What 2 skin problems does progesterone excess cause?
1. Acne | 2. Dermatitis
262
What 3 skin problems can indicate an internal malignancy?
1. Necrolytic migratory erythema 2. Erythema gyratum repens 3. Acanthosis nigricans
263
Describe Necrolytic migratory erythema (glucagonoma syndrome)?
- Rare disease | - Erythematous, scaly plaques on acral, intertriginous & periorificial areas
264
What is Necrolytic migratory erythema (glucagonoma syndrome) associated with?
Islet cell tumour of the pancreas
265
List 4 other signs of Necrolytic migratory erythema (glucagonoma syndrome)?
1. Hyperglycemia 2. Diarrhoea 3. Weight loss 4. Glossitis
266
How do you treat Necrolytic migratory erythema (glucagonoma syndrome)?
Removal of the tumour
267
Describe Erythema Gyratum Repens?
- Rare - Reddened concentric bands whorled woodgrain pattern - Severe pruritus & peripheral eosinophilia
268
What does Erythema Gyratum Repens have a strong association with?
Lung cancer
269
What does Erythema Gyratum Repens have a weak association with?
Breast, cervical, GI cancers
270
How do you treat Erythema Gyratum Repens?
Treatment of the underlying malignancy treats skin disease
271
Describe the appearance of Acanthosis nigricans?
Smooth, velvet-like, hyperkeratotic plaques in intertriginous areas (groin, axillae, neck)
272
What are the 3 types of Acanthosis nigricans?
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
What are 3 other skin problems that occasionally are associated with internal malignancy?
1. Erythema annulare 2. Sweet’s Syndrome 3. Sister Mary Joseph Nodule
274
What 3 nutritional deficiencies can lead to skin problems?
1. Vitamin B (B6, B12 & B3) 2. Zinc 3. Vitamin C
275
What is another form of Vitamin B6 & what can a deficiency in this result in?
- ANOTHER FORM: Pyridoxine | - DEFICIENCY RESULTS IN: Dermatitis
276
What is another form of Vitamin B12 & what can a deficiency in this result in?
- ANOTHER FORM: Cobalamin | - DEFICIENCY RESULTS IN: Angular chelitis
277
What is another form of Vitamin B3 & what can a deficiency in this result in?
- ANOTHER FORM: Niacin | - DEFICIENCY RESULTS IN: Pellagra
278
What is Pellagra?
- Disease characterised by diarrhoea, dermatitis & dementia - If left untreated= death - It occurs as a result of niacin (vitamin B-3) deficiency
279
Describe Acrodermatitis Enteropathica (Zinc deficiency)?
- Inherited or acquired condition | - Pustules, bullae, scaling (acral & perioral distribution)
280
Describe how Acrodermatitis Enteropathica (Zinc deficiency) is inherited?
Mutation in SLC39A, which encodes an intestinal zinc transporter
281
Describe Acrodermatitis Enteropathica (Zinc deficiency) in infants?
Can follow breast-feeding, when breast milk contains low levels of zinc
282
List 4 causes of Acrodermatitis Enteropathica (Zinc deficiency) in adults?
1. Alcoholism 2. Malabsorption states 3. Inflammatory bowel disease 4. Bowel surgery
283
What are the 2 differential diagnosis for Acrodermatitis Enteropathica (Zinc deficiency)?
1. Nutritional deficiencies | 2. Necrolytic migratory erythema
284
How do you treat Acrodermatitis Enteropathica (Zinc deficiency)?
Zinc supplementation
285
What does a vitamin D deficiency lead to?
Scurvy
286
List the 7 signs/symptoms of a vitamin D deficiency (scurvy)?
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
List 5 causes of Erythema nodosum?
1. Streptococcal infection 2. Pregnancy / Oral contraceptive 3. Sarcoidosis 4. Drug induced 5. Bacterial / Viral infection
288
Describe Erythema nodosum?
- Severe pain! - Inflammation of the subcutaneous fat, deep - Swells & gets tight - Common place is the shins
289
List 3 causes of Pyoderma gangrenosum?
1. Inflammatory Bowel Disease 2. Rheumatoid arthritis 3. Myeloma
290
Describe Pyoderma gangrenosum?
Rare skin condition that causes painful ulcers with a purple ring around it, usually affecting shins
291
Give 4 examples of dermatological hair & nail problems?
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
List the 10 types of skin drug reactions?
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
List 6 common drugs that cause acute rashes?
1. Antibiotics ie. penicillins, trimethoprim 2. NSAIDs 3. Chemotherapeutic agents 4. Psychotropic ie. chlorpromazine 5. Anti-epileptic ie. lamitrigine, carbamaz 6. Cardiac
294
Describe a Morbilliform rash?
- Looks like measles | - Macular lesions that are red & usually 2–10 mm in diameter but may be confluent in places
295
Describe a penicillin rash?
- Generalised redness - Urticaria - Swollen & puffy
296
Describe Urticaria / | Angiooedema?
- Deep dermal histamine release - If you scratch them it makes it worse - Mucosal surfaces affected ie. Lips
297
What 2 drugs can cause a Photo-toxic drug rash?
Quinine & bendroflumethiazide
298
What drugs commonly cause pustular rashes?
Antibiotics
299
Describe a Lichenoid rash?
- Purple, itchy rash & can be triggered off by drugs | - Tends to have a white network pattern on the top
300
List 3 triggers of vasculitis?
1. Infection 2. Drugs 3. Connective tissue disease ie RA
301
What should you check for with vasculitis?
Systemic vasculitis ie renal BP / Urinalysis
302
Describe vasculitis?
- Often localised & not rapidly progessive - Less unwell than in meningococcal rash - Inflammation of blood vessels ie. Small vessels in the skin
303
Describe drug induced psoriasiform rash?
- Psoriasis–like well demarcated pink erythema with scale | - Sudden onset, no FHx
304
What 2 drugs can cause drug induced psoriasiform rash?
1. Lithium | 2. Beta blockers
305
Describe a fixed drug rash?
Same area, same drug
306
What drug can cause a fixed drug rash?
Paracetamol
307
List 2 drug induced blistering disorders?
1. Steven Johnson Syndrome | 2. Toxic epidermal necrolysis
308
List 2 Immunobullous disease causing blistering?
1. Bullous pemphigoid | 2. Pemphigus vulgaris
309
Describe Steven Johnson Syndrome?
- Blistering around mouth, eyes & sometimes on the skin | - Haemorrhagic crusting in the lips
310
What is Toxic epidermal necrolysis (TEN)?
- Dermatological emergency - Majority drug induced - Disease spectrum - Most severe mucous membrane involvement - Stop suspect drug
311
In Toxic epidermal necrolysis (TEN) what is the condition if there is <10% of skin involved?
Steven Johnson Syndrome (SJS)
312
Describe the appearance of Toxic epidermal necrolysis (TEN)?
- Necrotic skin - Falling off - Looks like a 3rd degree burn - Extremely painful
313
Describe the management of Toxic epidermal necrolysis (TEN)?
- Analgesia - Fluid balance SCORTEN severity scale - Special mattress, sheets - Infection control / prophylaxis - Non adherent dressings - Urology, Gynae, Ophthalmology input
314
What is the prognosis for Toxic epidermal necrolysis (TEN)?
>50% mortality rate
315
Describe Staphlococcal scalded skin syndrome?
- Patient’s are not usually that unwell - Scaling - Temperature - No mucosal involvement
316
Describe Erythema multiforme?
- Self-limiting allergic reaction - HSV, EBV, occassionally drug - No or mild prodrome - Target lesions - Never --> TEN
317
What is the appearance of Erythema multiforme?
Dartboard appearance (3 rings together)
318
List 5 Immunobullous disorders (not triggered by drugs)?
1. Bullous pemphigoid 2. Mucous membrane pemphigoid 3. Paraneoplastic pemphigoid 4. Pemphigus 5. Dermatitis herpetiformis (coeliac disease)
319
Describe the difference between Bullous pemphigoid & Pemphigus vulgaris?
- 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
Describe the treatment of Immunobullous disorders?
- Oral steroids - Steroid sparing agents ie azathioprine - Burst any blisters - Dressings and infection control
321
What should you check for with Immunobullous disorders?
Oral / mucosal involvement
322
What should you consider doing for patients with Immunobullous disorders?
Screen for underlying malignancy
323
List the 3 treatments for Dermatitis herpetiformis (coeliac disease)?
1. Topical steroids 2. Gluten free diet 3. Oral dapsone
324
Describe the appearance of Dermatitis herpetiformis (coeliac disease)?
- Intensely itchy, even when only appearing as a mild rash | - Small blisters on extensor surfaces
325
Describe Urticaria?
- Itchy, wheals (hives) - Lesions last < 24 hours - Non-scarring
326
How long is acute & chronic Urticaria?
- Acute <6 weeks | - Chronic >6 weeks
327
What are the 2 types of Urticaria?
1. Immune-mediated: type 1 allergic IgE response | 2. Non-immune-mediated: direct mast cell degranulation eg opiates, antibiotics, contrast media, NSAIDs
328
List the 4 treatments for Urticaria?
1. Antihistamines 2. Steroids 3. Immunosuppression 4. Omiluzimab
329
List 5 causes of Acute Urticaria?
1. Viral infections 2. Medication- NSAIDS, Aspirin, ACE 3. Foods & food additives 4. Parasitic infections 5. Physical stimulants- cold, pressure, solar, cholinergic, aquagenic
330
What is Dermographism?
- Exaggerated wealing tendency when the skin is stroked | - Commonest form of physical urticaria
331
What is erythroderma?
Descriptive term for “Bright red”
332
List 4 causes of erythroderma?
1. Psoriasis 2. Eczema 3. Drug reaction 4. Cutaneous lymphoma
333
How do you treat erythroderma?
- Treat underlying skin disorder, supportive | - Fluid / temperature balance
334
Describe Pustular Psoriasis?
- 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