DERM Flashcards
(285 cards)
1
Q
Eruption
A
= rash
2
Q
Lesion
A
= any small area of skin disease
3
Q
Macule
A
= Flat (non-palpable) area of colour change <0.5cm
4
Q
Patch
A
Flat (non-palpable) area of colour change >0.5cm
5
Q
Papule
A
Raised (palpable) lesion <0.5cm (usually dome shaped)
6
Q
Nodule
A
Raised (palpable) lesion >0.5cm (usually dome shaped)
7
Q
Cyst
A
Fluctuant papule/nodule containing fluid/pus/keratin
8
Q
Plaque
A
Palpable, flat-topped lesion
9
Q
Vesicle
A
Fluid-filled lesion/papule <0.5cm
10
Q
Bulla
A
Fluid-filled lesion/papule >0.5cm
11
Q
Pustule
A
Pus-filled lesion
12
Q
Wheal/weal
A
Smooth, skin-coloured superficial swelling lasting <24 hours
Often surrounded by erythema
13
Q
Erosion
A
Partial break in skin: loss of epidermis only
14
Q
Ulcer
A
Complete break in skin: dermis included
15
Q
Fissure
A
Small, slit-like break in skin
16
Q
Excoriation
A
Erosion or ulcer due to scratching
17
Q
Lichenification
A
Thickening of skin and increased markings due to chronic scratching/rubbing
18
Q
Scale
A
Visible white loosening of outermost layer of skin
19
Q
Crust
A
Golden deposit on skin due to dried plasma
20
Q
What is psoriasis?
A
= chronic, relapsing inflammatory skin disorder (involving increased skin turnover and epidermal thickening).
21
Q
Who does psoriasis affect mostly?
A
- Bi-peak onset – early 20s and 50s
- Affects 2% of population
- M = F
22
Q
What other conditions is psoriasis linked with?
A
- Inflammatory – IBD, uveitis, coeliac, arthritis
- Obesity
- CVD
23
Q
Psoriasis - presentation
A
Red, scaly plaques on EXTENSOR surfaces and scalp
- Causes pain, itching, bleeding
- Significant psychological impact
Psoriatic Arthritis (in 10%)
24
Q
Psoriasis - Risk Factors
A
Genetics – FHx or HLA-CW6 gene
Environmental
- Strep throat infection
- Medications – BBs, antimalarials, lithium
- Stress, alcohol, smoking, trauma, sunlight
25
Psoriasis - principles of management
Depends on the severity and impact on the patient.
=> PASI
=> Dermatology Life Quality Index
Education – avoid lifestyle triggers (e.g. smoking, alcohol, stress)
Manage CV risk factors
1st line = topical
2nd line = phototherapy
3rd line = systemic Tx
Last line = biologics
26
Topical treatments for Psoriasis
- Emollients (e.g. E45)
- Corticosteroids +/- VitD analogues
- Keratolytics (e.g. 5% salicylic acid) for thick plaques
- Coal tar products for scalp
27
Phototherapy for Psoriasis
Requires 2o care referral
Exposure to UV light = immunosuppression to decrease symptoms from skin inflammation
2-3x per week for 15-30 episodes.
Base starting dose on skin type and gradually increase time of exposure.
UVB or PUVA
28
UVB vs PUVA phototherapy
Narrow band UVB = superficial (1st line, can be used if pregnant)
PUVA (UVA + Psoralen tablets) = deeper (not used if pregnant)
29
Side effects of phototherapy
Of UV – erythema/pruritis, cold sores, photoaging, SKIN CANCER
Of tablets – nausea, headaches
30
Dermatological indications for phototherapy
- Acne
- Psoriasis
- Vitiligo
- Lichen planus
31
Counselling for the patient before receiving phototherapy
* Only very short exposure (seconds to minutes)
* Dose carefully calculated for skin type
* Goggles to protect eyes and genitalia covered
32
Systemic Treatments for Psoriasis (and their side effects / monitoring)
Methotrexate
=> Teratogenic, hepatotoxic, BM suppression, GI upset/nausea
=> Monitor LFTs, FBC
Acitretin
=> Teratogenic, hepatotoxic, increases lipids, dry skin/hair thinning
=> Monitor LFTs, lipids
Ciclosporin
=> Nephrotoxic, increases BP, tingling peripheries
=> Monitor BP and U&Es
33
Topical steroid choices
MILD 1% hydrocortisone
=> any age, anywhere
```
MODERATE Eumovate (clobetasone)
=> any age, caution on face
```
```
POTENT Betnovate (betamethasone)
=> adults only, not used on face/genitals
```
V. POTENT Dermovate (clobetasol)
=> adults only, not used on face/genitals
34
Side effects of topical steroids
- Skin thinning
- Can trigger acne/rosacea
- Withdrawal can cause erythroderma
35
What is the most common type of leg ulcers?
Venous ulcers - Account for ~70% of ulcers
36
Pathophysiology of venous ulcers
* Valve incompetence and reflux
* Calf muscle dysfunction
Toxins accumulate => inflammation and necrosis of tissue.
37
Venous ulcers - risk factors
```
DVT,
varicose veins,
age,
pregnancy,
surgery
```
38
Venous ulcers - location
Generally located in the gaiter area (= below the knee and above the ankle)
39
Venous ulcers - Features
* Large and irregular
* Shallow with sloping edges
* Granulation tissue
40
Venous ulcers - Leg condition
* Lipodermatosclerosis
* Venous eczema
* Haemosiderin (red/brown colour)
* Atrophie Blanche (smooth, white sclerotic plaques)
* Heavy, aching, pruritis, oedema
41
GENERAL treatment for all ulcers
* Dressings +/- antibiotics +/- emollients
| * Debridement – surgery/dressings/larvae
42
Specific treatment for venous ulcers
MUST exclude arterial insufficiency before starting compression therapy (ABPI)
Elevation and compression
=> 1st line = 4-layer bandaging
=> Other = stockings
Skin graft / superficial venous surgery
43
Arterial ulcer - pathophysiology
Atheromatous changes cause compromised blood flow
Results in hypoxia and accumulation of toxins => inflammation and necrosis of tissue.
44
Arterial ulcer - Risk Factors
Diabetes, HTN, arterial disease, high cholesterol, Raynaud's disease
Smoking
Trauma
45
Arterial ulcer - Location
Located on bony prominences (usually lateral malleolus and toes)
46
Arterial ulcer - Features
* Smaller and round
* “Punched out” borders
* Little granulation tissue and dry
* Very painful
47
Arterial ulcer - Leg condition
* 6Ps – pain, pulseless, pale, paraesthesia, paralysis, perishingly cold
* Claudication/ischaemic rest pain symptoms
* Cool, hairless, dry, shiny skin
48
Specific treatment for arterial ulcers
* Manage vascular risk factors – e.g. antiplatelets, stop smoking
* Surgical revascularisation
49
Neuropathic Ulcers - Pathophysiology
* Peripheral neuropathy => loss of protective sensation and trauma goes unnoticed
* Vascular disease => reduced wound healing
50
Neuropathic Ulcers - Risk factors
Diabetes,
Trauma,
Prolonged pressure
51
Neuropathic Ulcers - Location
Located on pressure areas
52
Neuropathic Ulcers - Features
* Small, round, deep
* “Punched out” borders
* Thick rim
* PAINLESS
53
Neuropathic Ulcers - Leg condition
* Surrounding callous
* Loss of sensation
* Dry, cracked skin
54
Specific treatment for neuropathic ulcers
* Optimise glycaemic control
* Treat co-existing arterial disease
* Good foot care
* Offload pressure
55
What is eczema?
= itchy skin condition, characterised by erythema, dry skin and scaling.
+/- vesicles and blisters (acute)
+/- fissures and lichenification (chronic)
56
Atopic Eczema - features
red, dry, scaly skin affecting FLEXURES
57
How common is atopic eczema?
Affects 20-30% of schoolkids, 5-10% of adults
Onset usually <2 years
58
Atopic Eczema - causes / risk factors
Genetics – PMHx/FHx of atopies
Environmental – irritants, allergens, illness/infection/stress, cold weather
59
Atopic Eczema - complications
= susceptible to infection
S. aureus/Strep – weeping pustules/crusting; fever/malaise
HSV (Eczema Herpeticum) – pain, fever, lethargy; clustered blisters and punched-out erosions
60
Management of Eczema
Patient education - avoiding triggers, how to apply treatments, signs of infection
1. First Line = TOPICAL emollients/steroids
2. Second Line = TOPICAL Calcineurin Inhibitors
3. Third Line = PHOTOTHERAPY / IMMUNOSUPPRESSANTS
4. Additional Treatments
=> Systemic ABX / acyclovir (infection)
=> Antihistamines
61
First line management for eczema
- Avoid irritants/allergens/triggers
- Emollients for dry skin – liberally, as often as needed.
- Topical steroids – for active areas; a “fingertip” portion 1-2x daily.
62
Second line management for eczema
Topical Calcineurin Inhibitors (e.g. Tacrolimus, Pimecrolimus)
=> Used if mod/severe eczema or if there are CIs to topical steroids
Usually initiated by specialists
63
Third line management for eczema
Phototherapy + emollients and topical steroids
Immunosuppressants (e.g. ciclosporin, methotrexate, azathioprine)
(Initiated by specialists)
64
Acne Vulgaris - Pathophysiology
1. Hyperkeratinisation of follicle = pore blockage
2. Increased sebum production (due to increased androgens at puberty)
3. Overgrowth of P. Acnes (a gram +ve commensal)
=> Releases pro-inflammatory mediators
=> Follicles rupture and contents leak into surrounding dermis
65
Acne Vulgaris - Risk factors
- Male
- Cosmetic/hair products
- Excess washing
- Progesterone-only OCP/steroids
- Hormonal changes / Endocrine disorders
66
Lesions of Acne
1. Non-Inflammatory:
- Closed comedones (whiteheads) – small papules that may burst
- Open comedones (blackheads) – flat or raised with impacted keratin
2. Inflammatory:
- Papules – burst comedones cause inflammation
- Pustules – papules containing pus
- Nodules – painful swellings lasting weeks-months
67
Sequelae of acne
1. Non-scarring:
- Hyper/hypo-pigmentation
- Eythematous macules
2. Scarring:
- “ICE-PICK” scars (atrophic) – collagen loss
- “KELOID” scars (hypertrophic) – increased collagen
68
Management of Acne
Depends on severity, psychological impact, response to previous Tx.
1. Topical retinoids/antibacterials/ABX = 1st line for mild/moderate
2. Systemic ABX = 2nd line or 1st line for severe
3. Oral Isotretinoin (Roaccutane) = severe or Tx resistant subtypes
4. Hormonal Tx = Tx resistant females/ cyclical flares/hirsutism
5. Tx for Scars
69
1st line for mild/moderate acne
= topical retinoids/antibacterials/ABX
Retinoids = unblock pores
Antibacterials – e.g. benzyl peroxide
Antibiotics – e.g. erythromycin/clindamycin
70
What is something to remember with all topical treatments for acne?
All may cause irritation/erythema and photosensitivity.
71
2nd line for mild/moderate acne
| 1st line for severe acne
Systemic ABX
| => Lymecycline/doxycycline
72
Treatment for severe or Tx-resistant acne
= Oral Isotretinoin (Roaccutane)
=> Retinoid, decreases sebum production
73
Side effects of Roaccutane
* Teratogenic
* Hepatitis – avoid alcohol (check LFTs)
* Photosensitivity and dry skin
* Muscle aches
* Mood changes
* Anaemia and thrombocytopaenia (check FBC)
* Increased TGs and cholesterol (check lipids)
74
Contraindications for Roaccutane
* Pregnancy
* Liver/renal disease
* Diabetes
* Peanut allergy
75
When is hormonal Tx used in acne?
= Tx resistant females/ cyclical flares/hirsutism
=> COCP Dianette
76
What are contraindications for the COCP dianette?
Pregnancy/lactation,
| PHx or FHx of VTE
77
Management of acne - Scar treatments
Microdermabrasion (removes dead skin) – superficial scars
Laser resurfacing – for atrophic scars
Punch biopsy/excision – for ice-pick scars
Intralesional steroids – for keloid scars
78
Severity of Psoriasis
=> PASI = Psoriasis Area and Severity Index.
Used to measure severity and extend of psoriasis
79
Non-cutaneous manifestations of Psoriasis
Psoriatic Arthritis (in 10%)
Cardiovascular risk factors and metabolic syndrome
80
Dermatology Life Quality Index
Used to identify the impact of a skin condition on the patient’s life
Guides treatment / monitor improvement
81
What is a problem with topical vit D analogues in management of psoriasis?
Skin irritation
Metabolic effects (limit use to 100 g per week)
82
How is methotrexate taken?
Taken once weekly
Folic acid on the OTHER days.
83
What is important to do before starting biologics?
screen for any sign of infection (esp. TB, HIV, Hep B&C)
84
What is erythroderma?
= a severe and potentially life-threatening inflammation of most of the body's skin surface
85
Causes of erythroderma
Psoriasis - withdrawal from steroids
Eczema
Drugs
Cutaneous T cell Lymphoma
86
Management of erythroderma
Admission to hospital
IV fluid, thermoregulation
Regular emollients
Consider moderate potency topical steroids
Prevent/treat any complications (e.g. infection)
87
How long do systemic ABX take to show improvement in acne?
Around 3 months
88
What is required for females to take Roaccutane (oral retinoid) for acne?
requires 2x contraception and monthly urinary pregnancy test
89
What is rosacea?
Who does it affect?
= a chronic inflammatory skin condition affecting the centre of the face
Can affect ANYONE
=> Peak onset age 30-60
=> more common with fair skin and Celtic/North European descent.
90
Pathogenesis of rosacea
thought to be multifactorial
| => genetics and environmental factors
91
Cutaneous features of rosacea
- Transient and persistent facial erythema
- Inflammatory papules and pustules ( but no comedones)
- Telangiectasia
- Rhinophyma
(Occasionally) Facial lymphoedema, burning/pain
92
neurogenic rosacea
Features of rosacea and also facial tenderness/ burning pain
93
Morbihan Disease
= chronic and persistent erythematous lymphoedema on the face
Sometimes occurs in rosacea
94
Telangiectasia in rosacea
Telangiectasia = persistent dilated capillaries/small blood vessels in the skin
In rosacea - present on facial skin, apart from nasal alar region.
95
Rhinophyma
Nasal skin is thickened and the sebaceous (oil) glands are enlarged.
Due to hyperplasia/fibrosis of the sebaceous glands of the face
More common in M > F
96
Ophthalmic complications of rosacea
Dryness
Conjunctivitis
Blepharitis – ophthalmology referral
Keratitis – ophthalmology referral
97
Rosacea - diagnosis
One diagnostic and 2 major criteria are needed for a diagnosis.
DIAGNOSTIC
1. Persistent centrofacial erythema, associated with periodic intensification by potential trigger factors
2. Phymatous changes
MAJOR (must occur in centrofacial distribution):
1. Flushing/transient centrofacial erythema
2. Inflammatory papules and pustules
3. Telangiectasia
4. Ocular rosacea (lid margin telangiectasia, blepharitis, keratitis/conjunctivitis/sclerokeratitis/anterior uveitis).
98
General management of rosacea
Assess the patient's psychosocial burden of disease and consider referral for psychological support where necessary.
Lifestyle advice:
- Avoid triggers, oil-based products, exfoliants
- Moisturise frequently
- NEVER apply topical steroid
- Sun protection
99
Tx for Papulopustular/Inflammatory Rosacea
Topical – metronidazole/ azelaic acid
Oral ABX – e.g. tetracyclines, metronidazole
Isotretinoin
100
Mx of Erythmatotelangiectatic Rosacea
Treat any inflammatory component first
Topical azelaic acid / metronidazole may also help erythema
Laser can be used for severe telangiectasia
101
When do drug eruptions usually occur?
Usually 8-21 days post-exposure
BUT can occur with drugs that have been used without issue for years.
102
Mechanism of Drug Eruptions
1. Allergy – e.g. ABX
2. Intrinsic Drug Action – e.g. tetracycline and photosensitivity
3. Non-specific – e.g. vasculitis
103
What are some common drugs causing rashes?
- Penicillins, sulphonamides
- Thiazide diuretics
- Gold, Penicillamine
- NSAIDs
- Allopurinol
- Anticonvulsants
104
General Management of a drug eruption
1. STOP DRUG
2. Supportive care (burns etc.)
3. Wound care
105
Features of Toxic Erythema
Drug reaction - ~7-10 days post-exposure
* Measle-like Rash
* Symmetrical erythematous macules & papules
* May merge into larger plaques
* +/- malaise, fever, pruritis
106
Complications of Toxic Erythema
can progress to erythroderma/TEN
107
Toxic erythema - management
1. Stop drug (resolves in a week)
| 2. Consider emollients and antihistamines
108
Urticaria - features, causes, complications, Mx
Occurs ~24 hours post-exposure.
Features:
- Wheals = raised, pale red, itchy plaques.
Causes:
- Drugs (salicylates, ACEIs)
- Infection
- Sun, exercise, stress
Complications = angioedema
Management = antihistamines
109
What is SJS/TEN?
= type 4 hypersensitivity reaction
Variants of severe skin reaction, with SJS being the less severe.
110
Who is affected by SJS/TEN?
Anyone on medication can develop SJS/TEN unpredictably.
It is more common in those with HIV
111
Features of SJS/TEN?
Usually a prodromal illness before the rash resembling an URTI or flu-like illness.
Abrupt onset of a tender/painful red skin rash
=> Starting on the trunk and extending rapidly over hours to days onto the face and limbs.
=> Symmetrical red macules and central blistering
=> 2+ mucosal sites involved (especially the mouth)
=> Severe eye involvement
Dermal necrolysis in TEN
112
How is severity/mortality measured in SJS/TEN?
= SCORTEN
One point is scored for each of the seven criteria present at the time of admission
1. > 40 years
2. Urea >10 mmol/L
3. HCO3- <20 mmol/L
4. HR >120
5. Glucose >14mmol/L
6. >10% surface area
7. Presence of malignancy
113
SJS / TEN - complications
POTENTIALLY FATAL
- Sepsis
- Dehydration
- Electrolyte imbalance
- ARDS
- Shock and multiple organ failure
114
SJS / TEN - Management
1. STOP DRUG
| 2. ICU support (fluids, NG tube, analgesia)
115
Acanthrosis Nigricans
= Velvety, thickened, hyperpigmented skin
Affects skin folds (axilla, groin, neck)
Associations:
- Obesity, T2DM, Cushing’s, Addison’s, PCOS
- GI tract cancers
116
Pyoderma Gangrenosum - features
= auto-inflammatory chronic, recurrent ulceration.
Sudden onset:
- May start as a small pustule, red bump, or blood-blister, often misinterpreted as an insect bite.
- Very painful, ulcerated nodules
- Purple/blue border
- +/- fever and systemic illness
117
Pyoderma Gangrenosum - associations and differentials
ASSOCIATIONS
=> UC, Crohn’s, diverticulitis, vessel inflammation (Behcet’s)
=> Active hepatitis
=> Haematological malignancy
DIFFERENTIALS
Arterial/venous ulceration
118
Pyoderma Gangrenosum - Mx
= topical/PO steroids
119
What is dermatomyositis?
= rare, acquired muscle disease + RASH
120
Features of dermatomyositis
Violaceous rash on photoexposed areas
Helitrope rash on eyelids
Gottron’s papules on knuckles
121
Dermatomyositis - associations
MALIGNANCY (breast, cervix, ovaries, lungs, pancreas, GIT)
Autoimmune conditions
Drugs
122
Acquired Ichthyosis
= Fish-scale skin (dry)
Associations:
- Hodgkin’s Lymphoma (and other malignancies)
- Drugs – e.g. allopurinol
123
Erythema Multiforme
= inflammation of blood vessels
Red, “bulls-eye” lesions (usually on hands)
Associations:
- HSV infection (may follow cold sores)
- Drugs (penicillin, sulphonamides, allopurinol, phenytoin)
124
Erythema Nodosum - features
= inflammation of s.c. fat.
Bilateral red, tender subcutaneous nodules (3-20cm in diameter)
=> Usually lower legs
+/- fever, malaise, arthralgia
125
Erythema Nodosum - Associations
Associations:
- Infection – strep, TB
- Inflammatory disease – sarcoid, IBD, Behcet’s
- Drugs – sulphonamides, OCP
126
Dermatitis Herpetiformis
Chronic, recurrent pruritic rash.
=> Symmetrical
=> On extensor surfaces
Associations:
- Coeliac Disease
127
Cutaneous Vasculitis - features
= inflammation of skin blood vessels.
On legs/ankles/feet
Non-blanching, erythematous, purpuric rash
+/- pain, itching, burning
+/- fever, arthralgia
128
Cutaneous Vasculitis - investigations
Hx and examination
Skin biopsy
FBC and auto-Abs
U&E, BP, urine dip
129
Cutaneous Vasculitis - Triggers
- Infection – Meningococcus, strep, URTI, hep C
- Autoimmune – RA, Lupus, IBD
- Medications – ABX, NSAIDs, diuretics
- Haematological disorders/malignancies
130
Pre-tibial Myxoedema
= accumulation of excess glycosaminoglycans in the dermis and subcutis of the skin.
Most commonly seen on the shins (pretibial areas)
Characterised by swelling and waxy/ lumpiness of the lower legs.
Associations = Grave’s disease
131
What skin changes can occur in SLE?
```
Acute = malar (butterfly) rash
Subacute = discrete ring lesions => red & scaly
Chronic = discrete discoid lesions => thick & scarring
```
+/- photosensitivity, arthritis, Raynaud’s, renal disease
132
Diagnostic criteria for SLE
Malar skin rash
Antiphospholipid / ANA / Anti-DNA antibodies
Persistent thromocytopaenia
Persistent proteinuria
133
What skin changes can occur in diabetes?
Granuloma Annulare:
=> Small papules in annular configuration
Necrobiosis Lipodica:
=> Symmetrical plaques with telangiectasia +/- ulceration
Diabetic ulcer / gangrene / candidiasis
Acanthosis nigricans
Rubeosis & vitiligo
134
Benign pigmented lesions
1. Freckles
2. Congenital Melanocytic Naevi (Moles)
3. Acquired Melanocytic Naevi (Moles)
4. Atypical Melanocytic Naevi (Moles)
135
What is a mole?
A proliferation of melanocytes
Can be congenital or acquired (UV exposure, hormones, age)
136
Atypical Melanocytic Naevi - features and risk factors
Mole, which looks similar to melanoma
RFs – FHx, UV exposure, <30 years.
```
Features:
• 5+ mm
• Irregular border
• Variable pigmentation
• Asymmetrical
• Flat or raised
```
137
Atypical Melanocytic Naevi - management
1. Monitor for changes
2. Sun protection advice
3. Excision if suspicious
138
Features of malignant melanoma
* Asymmetrical
* Border = IRREGULAR
* Colour/pigmentation = VARIED
* Diameter >6 mm
* Evolution (ABCDE changes or bleeding/itching)
139
Risk factors for Melanoma
```
GENETIC
PHx or FHx melanoma
Pale skin / red hair
Many/large atypical naevi
Increasing age
```
```
ENVIRONMENTAL
Sun/UV exposure
Phototherapy
Tanning beds
Immunosuppression
```
140
Differentials of melanoma
Pigmented BCC
Seborrheic Keratosis
Atypical Mole
141
Melanoma - Ix
2WW referral to dermatology!!
1. History & Examination
2. Excision for biopsy – if suspected melanoma
3. Histopathology – Breslow Thickness = best prognostic factor.
142
Breslow Thickness
= the thickness of the tumour, measured from the granular layer of epidermis to the deepest point of invasion.
143
Melanoma - Mx
Breslow Thickness <1mm = WIDE LOCAL EXCISION (1cm margins)
Breslow Thickeness 1-4 mm = WIDE LOCAL EXCISION (1-3cm margins) + SENTIAL LN BIOPSY
=> +ve biopsy = total LN dissection + chemo/radiotherapy
=> -ve biopsy = monitor
Breslow Thickness >4mm = WIDE LOCAL EXCISION (3cm margins)
+/- LN Biopsy
144
What are signs of poor prognosis for melanoma?
```
Breslow Thickness (most important prognostic factor)
Ulceration
```
145
Sun protection advice
Sunscreen – at least SPF 30 (UVB protection) and high star rating (UVA protection), applied as per manufacturers advice.
Wear protective clothing in sunny weather
Direct sunlight:
=> Spend time in the shade between 11am and 3pm when it is sunny
=> Keep babies and young children out of direct sunlight
Avoid sunbeds
146
What risk factors are there for both BCC and SCC?
UV Exposure
Fair skin
Immunosuppression
Sites of inflammation/infection/wounds
147
What risk factors are there for SCC only (i.e. not necessarily BCC)?
Smoking
| Actinic keratosis / Bowen’s disease
148
What is the most common skin cancer?
Basal Cell Carcinoma
149
Where does BCC originate?
From basal cells of epidermis.
150
BCC - features
- Slow Growth (months/years)
- Locally invasive but decreased mets
- Generally asymptomatic
- Shiny or pearly nodule with a smooth surface (may have central depression or ulceration)
- Blood vessels cross the surface
151
BCC - Management
If elderly, may not treat.
- Simple Surgical Excision – margins 4mm
- Moh’s Micrographic Excision
- Curettage & Cautery – scrape & cauterise to stop bleed
- Cryotherapy – only if low-risk tumour
- Photodynamic Therapy (PDT) – only superficial BCC
152
What is Moh's Micrographic excision
Remove a layer of the lesion at a time & re-examine
153
Photodynamic therapy for skin lesions
photosensitiser + UV => phototoxic reaction destroys lesion
154
Where does SCC originate?
From keratinocytes.
155
SCC - features
- Rapid Growth (weeks/months)
- Highly metastatic
- Present as enlarging scaly or crusted lumps
- May ulcerate
- Often tender/painful
- Present on sun-exposed areas
156
Risk factors for metastasis of SCC
- >2cm or deep
- Poorly differentiated
- Lip/ear lesions
- Previous Tx failure
- Immunocompromised
157
SCC - management options
1. Simple surgical excision – margins 5mm
2. Moh’s Micrographic Excision
3. Radiotherapy – if extensive surgery not an option
158
SCC - 5-year survival
Non-metastatic – 75-90%
| Metastatic – 25%
159
Malignant non-pigmented skin lesions
BCC
| SCC
160
What is Bowen's Disease?
SCC in situ = epidermal dysplasia (considered SCC if penetrate basement membrane)
161
Bowen's Disease - features
Erythematous, scaly plaque/patch
162
Bowen's Disease - differentials
- Psoriasis
- Eczema
- Actinic Keratosis
- Superficial BCC
163
Bowen's Disease - Mx
- 5-flurouracil cream
- Cryotherapy
- Curette & cautery
- Photodynamic Therapy
164
Actinic Keratosis - features
Also “solar keratosis"
=> Results from long-term exposure to UV radiation
- Often appear as small dry, scaly or crusty patches of skin
- May be red, light or dark tan, white, pink, flesh-toned or a combination of colours and are sometimes raised
- Often easier to feel than see
- Common on sites often exposed to the sun
165
What are the risks/complications of actinic keratosis?
Can develop into SCC (~10% of AK)
166
Actinic Keratosis - Mx
excision / curettage / cryotherapy
167
When and where does Seborrhoeic Keratosis occur?
A common sign of skin aging (~90% of adults aged >60 years)
Can arise on any area of skin, with the exception of palms and soles and mucous membranes
168
Why is the name of seborrhoeic keratosis misleading?
not limited to a seborrhoeic distribution;
not produced by sebaceous glands;
not associated with sebum.
169
Seborrhoeic Keratosis - features
- Flat or raised papule or plaque
- 1 mm to several cm in diameter
- Skin coloured/ yellow/ grey/ light brown/ dark brown/ black or mixed colours
- Smooth, waxy or warty surface
- Solitary or grouped in certain areas, such as within the scalp, under the breasts, over the spine or in the groin
170
Is seborrhoeic keratosis malignant?
Not malignant or pre-malignant, but are sometimes hard to tell apart from malignant tumours.
(Very rarely, eruptive seborrhoeic keratoses may denote an underlying internal malignancy, most often gastric adenocarcinoma)
171
Seborrhoeic Keratosis - Mx
Can be left alone or removed – reasons for removal may be that it is unsightly, itchy, or catches on clothing.
- Cryotherapy for thinner lesions (repeated if necessary)
- Curettage and/or electrocautery
- Ablative laser surgery
- Shave biopsy
- Focal chemical peel with trichloracetic acid
172
What are the normal bacterial skin commensals?
- Staph. epidermidis
- Corynebacteria
- Micrococci
- Propriobacteria
173
What bacteria tend to cause skin infections?
Staphylococci
(Staph. Aureus = ALWAYS pathogenic)
Streptococci
(Strep. pyogenes (group A strep) = ALWAYS pathogenic.)
174
What skin infections do staphylococci cause?
Primary Infections:
- Folliculitis
- Cellulitis
- Impetigo
Secondary Infections:
- Cellulitis
- Wound/ulcer/eczema infection
Infections due to bacterial toxins:
- Bullous impetigo
- Staphylococcal Scalded Skin Syndrome
- Toxic Shock Syndrome
175
What skin infections do streptococci cause?
Primary Infections:
- Erysipelas
- Necrotising Fasciitis
- Impetigo
Secondary Infections:
- Cellulitis
- Wound/ulcer/eczema infections:
Infections due to bacterial toxins:
- Scarlet Fever
Hypersensitivity Reactions (group A strep):
- Erythema Nodosum
- Vasculitis
176
Impetigo - cause and features
Stalphyococci/streptococci
Primary infection, affects young children
=> Golden crust +/- oozing blisters
CONTAGIOUS
177
Impetigo - Mx
- Soak crust with soap and water
- Topical antiseptic / ABX
- Systemic ABX if widespread
CONTAGIOUS – no school for 48 hours after starting oral ABX or until wounds are crusted (topical ABX)
178
Bullous Impetigo - features
Toxin reaction – specifically from Staph. aureus
2-3cm blisters (bullae)
Usually in areas with skin folds
179
Bullous Impetigo - Mx
Oral flucloxacillin
180
Bullous Impetigo - Complications
Can develop into a more severe and generalized form called staphylococcal scalded skin syndrome (SSSS)
RFs – Newborns/children (<5), immunocompromise, kidney failure
181
Folliculitis - features
Primary infection
Erythematous pustules around hair follicles
182
Folliculitis - Mx:
Screen and treat nasal carriage (mupirocin cream)
Topical or systemic ABX
183
Staphylococcal Scalded Skin Syndrome
Toxin reaction
Presentation:
- Erythema & sheets of peeling skin
- Malaise and fever
184
Why is Staphylococcal Scalded Skin Syndrome mostly seen in neonates and children <5 ?
Protective antibodies against staphylococcal exotoxins are usually acquired during childhood which makes SSSS much less common in older children and adults
185
Staphylococcal Scalded Skin Syndrome - Mx
ADMIT (emergency)
Supportive management (fluids & analgesia)
IV flucloxacillin/erythromycin
186
Toxic Shock Syndrome - features and associations
Toxin reaction
Presentation:
- Septic shock
- Days 1-3: widespread macular erythema
- Days 10-21 – desquamation, mucosal oedema & ulceration
Associations:
- Tampon use
- GI tract infection
187
Toxic Shock Syndrome - management
Supportive (fluids & analgesia)
IV flucloxacillin/erythromycin
188
What ABX are typically used for staphylococcal skin infections?
Topical ABX – fusidic acid, mupirocin
Oral ABX – flucloxacillin, clindamycin
189
What ABX are typically used for streptococcal skin infections?
Topical ABX – clindamycin
| Oral ABX – penicillin V (Phenoxymethylpenicillin)
190
Erysipelas - features
Primary infection
= a specific form of cellulitis caused by strep
Affects the upper layers of the skin
Presentation:
- Unilateral “beefy” red plaque
- PAINFUL
191
Erysipelas - Mx
Oral ABX – Penicillin V
192
Necrotising Fasciitis - cause
group A strep
+/- S. aureus
+/- others
193
Necrotising Fasciitis - presentation
Rapidly spreading erythema & necrosis
Systemic sepsis – high fever, intense pain, vomiting
194
Necrotising Fasciitis - Mx
```
Surgical debridement
IV ABX (vancomycin +/- gentamicin)
```
195
What is Cellulitis?
= infection of the deeper layers of skin and the underlying tissue
196
Erisypelas vs Cellulitis
Erysipelas affects the upper layers of skin and is specifically caused by streptococci
Cellulitis is an infection of the deeper layers of skin and the underlying tissue and can be strep or staph infection
197
Cellulitis - presentation
Gross oedema, erythema, heat
| PLUS pain
198
Cellulitis - Mx
Elevate affected limb
```
UNCOMPLICATED cellulitis (no signs of systemic illness or extensive infection)
=> oral ABX, analgesia, fluids
```
```
COMPLICATED cellulitis (severe / systemic upset / limb threatened)
=> admission, fluids, IV penicillin-based ABX
```
199
Scarlet Fever - cause and features
Toxin-mediated, follows strep throat infection.
Presentation:
- Widespread pink/read papules
- Preceding sore throat, fever, lymphadenopathy
- Strawberry tongue
200
When can a child with scarlet fever go back to school?
Can go back to school 24 hours after starting ABX
201
Scarlet fever - Mx
Oral penicillin
202
How do viral warts spread?
Via direct contact or indirect contact (e.g. swimming)
203
Management options for viral warts
1. Topical Paints – salicylic acid + lactic acid
=> 5 mins soak in warm water, apply Tx, nail file away dead skin
2. Cryotherapy – painful & may cause blisters
3. Curettage & cautery – need local anaesthetic
4. Formalin soaks / podophyllin – for RESISTANT warts
204
Types of viral wart
Common Warts (HPV 2):
- Elevated papules
- Dorsum of hands
- Common in children
Plane Warts (HPV 3):
- Flat-topped
- Face and back of hands
Plantar Warts (HPV 1, 2, 4, 57):
- May be uncomfortable to put pressure on
- Tend to be quite Tx resistant
Anogenital Warts (HPV 6 & 11):
- RF for cervical neoplasia in women
- Refer for STI screen
205
Chicken Pox - cause
= infection caused by varicella zoster virus
Usually an uncomplicated, self-limiting disease
=> More severe in adults
206
Chicken pox - presentation
Widespread rash
Itchy red papules progressing to vesicles on the stomach, back and face, and then spreading to other parts of the body.
Fever, headache, malaise
207
Chicken pox - complications
Pneumonia
Hepatitis
Encephalitis
Secondary bacterial infection of skin lesions caused by scratching
208
Chicken pox - Mx
Calamine lotion and oral antihistamines may relieve itching.
Only if immunocompromised – Oral/IV acyclovir
209
Shingles - cause
= herpes zoster
=> reactivation of dormant VZV (anyone who has had chickenpox may subsequently develop shingles)
210
Shingles - presentation
Dermatomal distribution of vesicles
DOES NOT CROSS MIDLINE
Preceding pain/tingling
211
Shingles - complications
Persisting pain, Scarring
Ramsay Hunt Syndrome
Ophthalmic Shingles
Deafness/dizziness
Encephalitis
212
Shingles - Mx
Oral acyclovir if:
- within 72 hours of onset
- mod/severe pain or mod/severe rash
- Immunocompromise
- Non-truncal involvement
Analgesia
If severely immunocompromised, consider admission.
213
What can HSV infection cause?
| What is the presentation and management of these?
1. Cold Sores (HSV 1):
- 30-50% recur
- Pain, tingling, vesicular eruption
- Mx = topical acyclovir
2. Genital Herpes (HSV 2):
- 95% recur
- Pain, tingling, dysuria
- Mx = oral acyclovir
214
Molluscum Contagiosum - cause and features
Caused by Molluscipox virus (MCV)
Presentation:
- Small, umbilicated papules (mainly trunk)
- Erythema, pus, crusting
Common in infants/children = contagious
215
Molluscum Contagiosum - Mx
Mx = self-limiting (if not, cryotherapy/topical podophyllin)
216
Hand, foot & mouth disease - cause and presentation
Caused by Coxsackie Virus
Presentation:
=> Erythematous vesicles on hands, soles of feet, mouth
Common in infants/young children
217
Hand, foot & mouth disease - Mx
self-limiting (5-7 days)
218
Pityriasis Rosea - cause
Unknown cause
| ?herpes virus
219
Pityriasis Rosea - presentation
Initially – herald patch (oval erythematous plaque + scaling)
5-15 days later – generalised, smaller, well-defined erythematous macules (CHRISTMAS TREE DISTRIBUTION)
220
Pityriasis Rosea - Mx
if symptomatic/itchy => topical steroids or UVB
221
What are dermatophytes?
fungi that require keratin for growth.
Cause tinea / ringworm (most common fungal infections).
222
Wood's UV lamp
= a light that uses long wave ultraviolet light
When an area of scalp that is infected with tinea is viewed under a Wood's light, the fungus may glow.
223
What are the genera of fungi in the dermatophyte group?
Microsporum,
Trichophyton,
Epidermophyton
224
Dermatophyte infection - Ix
Skin scrapings, Hair pluckings, Nail clippings => microscopy & culture
Or view under wood's lamp
225
Dermatophyte infection - Tx
Topical Anti-fungals for LOCALISED INFECTION
=> Miconazole, ketonazole, terbinafine, nystatin
Systemic anti-fungals for WIDESPREAD INFECTION or HAIR/SCALP/NAILS or IMMUNOCOMPROMISED
=> Terbinafine, itraconazole, griseofulvin (for <12 years)
226
Candida
A yeast that causes the fungal infection thrush (can affect genitalia, periungual, oral).
227
Candidiasis - features
Erythema extending from body folds (unclear border)
Small satellite lesions +/- pustules at edges of eruption.
228
Candidiasis - risk factors
Extremes of age
| Immunocompromise
229
Candidiasis - Mx
1. Topical Azoles – clotrimazole
2. Systemic Azoles – fluconazole
3. Nystatin / amphotericin B
230
What are the fungal skin commensals?
Malassezia (formerly known as Pityrosporum)
231
What infections can be caused by Malassezia/Pityrosporum?
1. Pityriasis Versicolor
| 2. Seborrhoeic Dermatitis
232
Pityriasis Versicolor - features and treatment
Features:
- Finely scaled, yellow/brown macules on trunk
- Hypo/hyperpigmented
Treatment:
- Topical antifungal – miconazole
- Selenium sulphide shampoo
- Systemic itraconazole if immunocompromised.
233
Seborrhoeic Dermatitis - features and Tx
Affects scalp, eyebrows, paranasal/periorbital areas.
Features:
- Yellow/white flaking
- +/- erythematous, itchy, GREASY/WET-looking skin
- +/- patchy hair loss.
Treatment:
- Topical azoles
- Low potency steroids (rapid, short-term Tx)
234
Tinea Corporis
Affects body
Erythematous ANNULAR SCALY PLAQUE
Central clearing
Very itchy
235
Tinea Cruris
Affect genitals
Well-demarcated, erythematous plaque
Very itchy
236
Tinea Manum
Affects hands
Scaling that spreads proximally
Asymmetrical involvement
237
Tinea Unguium (onchomycosis)
Very common => often with atheletes foot
Hyperkeratosis of nail
White discolouration
Loss of nail plate and lifting from bed (oncholysis)
238
Athlete's foot
= Tinea Pedis
White maceration between toes
RFs – communal floors, occlusive shoes, wet feet.
239
Moccasin foot
= severe form of Tinea Pedis / Athlete's foot
Erythema, scaling, pustules, widespread
240
Tinea Capitis
Affects scalp
More common in afro-Caribbean’s & children
Patchy hair loss
Scales, erythema, pustules
241
Kerion
= complication of tinea capitis
Boggy, painful swelling (honey-coloured)
+ alopecia/lymphadenopathy
(Occurs due to epidermal invasion & inflammatory response)
242
Skin infestations
= parasites living on the host's skin
Scabies
Head lice
243
Scabies - cause and features
Caused by the sarcoptes scabies mite.
Features:
- Itchy papules (worse at night)
- Burrows/small tracts
- Usually symmetrical
Common sites – Finger webs, Axillae, Breasts, Scalp, Ankles, Feet
244
Scabies - RFs
1. Close contact – dorms, wards, care homes
2. Extremes of age or immunocompromise
=> risk of “crusted scabies” = severe form
245
Scabies - management
1. Permethrin / Malathion creams (insecticides)
- Apply to whole body for 12 hours
- Repeat in 1 week
- TREAT ALL CLOSE CONTACTS AT SAME TIME
2. Wash all bedding/clothing.
246
Head lice - features
Live on hair, feed on blood, spread via close contact.
Features:
- Persistent itching of scalp
- Redness & excoriated papules
247
Head lice - Mx
1. Fine comb & conditioner REGULARLY = most important
| 2. (Malathion/ Permethrin) = not very effective
248
What is important to remember in a dermatology history?
Identify site, onset, character, exacerbating/relieving factors, associated Sx, time course.
Any treatments tried already?
Any previous episodes similar to this?
Contact Hx with infectious diseases (e.g. chickenpox)
PMHx (especially skin cancer)
DHx, Allergies
FHx of skin conditions or cancers
Travel Hx
Sun exposure (including sunbed use)
Occupation
Recent changes (in diet, washing powder, etc.)
249
Inspection of an eruption
=> DCM
D – Distribution
• Where is it?
• E.g. flexures/extensors, sun exposed/covered
C – Configuration
• Shape or outline of rash
• Symmetrical/asymmetrical
• Any articular patter? e.g. diffuse, linear, grouped or scattered
```
M – Morphology
• The form and structure of the rash
• E.g. papules, plaques, etc.
• Weeping, crusting, bleeding, excoriations
• Odour
```
250
Inspection of a pigmented lesion
=> ABCDE
```
A – Asymmetry
B – Border
C – Colour
D – Diameter
E – Elevation / evolution
```
251
Inspection of a non-pigmented lesion
```
Site and Side
Shape (macule, papule, plaque, nodule, cyst, etc.)
Size
Symmetry
Surface
Surrounding Skin
Colour
```
252
What is important to palpate for in examination of a skin eruption/lesion?
Tenderness
Surface texture
Scaling
Elevation
Skin thickness
=> Any atrophy (tissue loss)?
=> Wrinkling or dimpling (loss of fat)?
Firmness
=> Solid or fluctuant?
Tethering
Blanching (if necessary)
Temperature
253
How can you differentiate between erythema and purpura?
Erythema - blanches with light pressure
Purpura - non-blanching
254
Flat vs palpable purpura
Flat purpura suggests leakage without inflammation
Palpable purpura suggests associated inflammation (likely to be caused by a small-vessel cutaneous vasculitis)
255
Why is it important to compare temperature of skin abnormality to normal skin?
Inflamed skin is hot
Poorly perfused skin is cold
256
Where are flexures?
Inside of elbows
Front of neck
Back of knees
Under buttocks
257
How would you counsel a patient about emollients?
Moisturiser - creates a barrier on the skin to prevent water loss
Apply liberally to the skin, following direction of hair growth
Use MINIMUM twice a day - no limit to how much you can use them
Use even when you have no flare-ups
Re-apply after bathing/showering
Most contain paraffin which is EXTREMELY FLAMMABLE => avoid contact with open flames/cigarettes
258
Important things to remember about use of ointments as a topical formulation
Best option for dry skin
BUT - more greasy and less cosmetically acceptable for the patient
259
How much topical steroid should be applied?
Finger-tip units are a useful way to explain to a patient how much topical steroid should be applied.
260
How would you counsel a patient for applying topical steroid?
Used more sparingly (not liberally like the emollient).
Try to leave 30-60 minutes between applying any emollients and the steroid
Side effects are usually with prolonged/ regular/ inappropriate use and are rare with topical use.
=> skin thinning
=> with potent/very potent steroids, sometimes adrenal suppression and Cushing's
261
How long are topical steroids used for?
Once or Twice daily for maximum 14 days
| 5 days on the face
262
Maintenance topical steroids
Initiated by specialist
use of topical steroids twice weekly as a preventative measure for patients who suffer frequently from flare ups
263
Methotrexate - important drug interactions
Trimethoprim / co-trimoxazole - FATAL IMMUNIOSUPPRESSION
NSAIDs - increases risk of toxicity
Penicillins / ABX - increased risk of toxicity
Can increase the risk of nephrotoxicity if given alongside nephrotoxic drugs
264
Nikolsky's sign
Positive when slight rubbing / mild lateral pressure of the skin results in separation of the epidermis
almost always present in SJS/ TEN and SSSS
265
How would you differentiate Spider naevi from telangiectasia?
When pressure is applied to blanch the area, spider naevi refill from the centre and telangiectasia refills from the edges.
266
Erythema Nodosum - Mx
Treat underlying cause
Analgesia and follow-up
Usually resolves within 6 weeks and lesions heal without scarring
267
How long do children with Molluscum contagiosum need to stay off school for?
Not required to stay off school
Contagious but the chances of passing it on during normal school activities are low.
Advice should be given to limit spread amongst family members e.g. no sharing towels.
268
What can trigger/exacerbate rosacea?
Sunlight,
Pregnancy,
Certain drugs and food
269
Koebner phenomenon
= the appearance of new skin lesions of a pre-existing dermatosis on areas of cutaneous injury in otherwise healthy skin.
270
Hutchinson's Sign
a rash on the tip, side, or root of the nose in a patient with shingles
Representing the dermatome of the nasociliary nerve
=> prognostic factor for subsequent eye inflammation and permanent corneal denervation.
271
Guttate psoriasis
= a form of acute psoriasis described as a shower of small, pink-red, scaly ‘raindrops’ that has fallen over the body.
Typically develops 1–2 weeks after a streptococcal URTI, and some viral URTIs
272
Lichen Planus - presentation
planus = Ps
=> purple, pruritic, papular, polygonal rash on flexor surfaces.
Oral involvement common
273
Cutaneous manifestations of SLE
Photosensitive 'butterfly' rash
Discoid lupus (coin-shaped lesions)
Alopecia
Livedo reticularis (net-like rash)
274
What is Vitiligo?
Autoimmune condition which results in the loss of melanocytes and consequent depigmentation of the skin
Features:
- well-demarcated patches of depigmented skin
- peripheries tend to be most affected
- trauma may precipitate new lesions (Koebner phenomenon)
275
Types of BCC
1. Nodular BCC
2. Superficial BCC – shallow plaques, pink to almost skin coloured, that slowly expand over many years.
3. Sclerosing BCC – can look like a small white scar on the skin (can expand to a very large size before it is clinically obvious as a skin cancer)
4. Pigmented BCC – occurs in darker skinned individuals.
276
Skin Type I
Pale white skin, blue/green eyes, blond/red hair
Always burns, does not tan
277
Skin Type II
Fair skin, blue eyes
Burns easily, tans poorly
278
Skin Type III
Darker white skin
Tans after initial burn
279
Skin Type IV
Light brown skin
Burns minimally, tans easily
280
Skin Type V
Brown skin
Rarely burns, tans darkly easily
281
Skin Type VI
Dark brown or black skin
Never burns, always tans darkly
282
Alopecia Atreata
Presumed to be an autoimmune condition
Features:
- - Localised, well demarcated patches of hair loss.
- - At the edge of the hair loss, there may be small, broken 'exclamation mark' hairs
Hair will regrow in 50% of patients by 1 year, and in 80-90% eventually.
283
Pompholyx eczema
Characterised as an itchy vesicular rash over the palms and soles of feet and is associated with sweating.
Heat often exacerbates the rash.
284
Dermatofibroma
A solitary firm papule/nodule that dimples when pinched.
Tend to occur following injury
285
Lichen Planus - Mx
POTENT topical steroids are the mainstay of treatment
Benzydamine mouthwash or spray is recommended for oral lichen planus
Extensive lichen planus may require oral steroids or immunosuppression
