Dermatology Flashcards

1
Q

What is basal cell carcinoma?

A

Most common type of cancer in the Western world
Related to exposure to sunlight
Clinically presents as a pearly white papulo-nodule or firm plaque

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2
Q

What is the aetiology of basal cell carcinoma?

A

Repetitive and frequent sun exposure, as ultraviolet radiation induces DNA damage in keratinocytes

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3
Q

What are the characteristics of basal cell carcinomas?

A

Slow-growth and local invasion
Initially a pearly, flesh-coloured papule with telangiectasia
May later ulcerate leaving a central ‘crater’

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4
Q

What sites are usually affected in basal cell carcinomas?

A

Sun-exposed sites, especially the head and neck account for the majority of lesions

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5
Q

What are the appropriate investigations for basal cell carcinoma?

A

Generally, if a BCC is suspected, a routine referral should be made on the 2WW
Biopsy for dermatohistopathology:
(diagnosis of a cancer is histological)

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6
Q

What are some of the management options for basal cell carcinoma?

A

Surgical removal
Curettage
Cryotherapy
Topical cream: imiquimod, fluorouracil
Radiotherapy

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7
Q

What is a burns injury?

A

A very common injury predominantly to skin and superficial tissues caused by heat from hot liquids, flame or contact with hot objects

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8
Q

How is the severity of burns injuries assessed?

A
  1. Burn size (% of total body surface area)
  2. Depth ( first to fourth degree)
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9
Q

What symptoms and signs would be seen on physical examination for a burns injury?

A

Erythema
Dry/ wet and painful
Dry and lacking of physical sensation (insensate)
Cellulitis
If face affected- clouded cornea

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10
Q

What are the risk factors for burn injuries?

A

Young children
Age > 60 years

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11
Q

What are the investigations for burn injuries?

A

A to E approach
Assess carbon monoxide (ABG) and fluid loss (ABG, urinary catheter)
Chest x-ray and ECG
Bloods
Wound biopsy and histology

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12
Q

What is the management of burns injuries?

A
  1. Initial first aid as above
  2. Review referral criteria to ensure can be managed in primary care
  3. Superficial epidermal: symptomatic relief - analgesia, emollients etc
  4. Superficial dermal: cleanse wound, leave blister intact, non-adherent dressing, avoid topical creams, review in 24 hours
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13
Q

What is the immediate first aid management in burns injuries?

A
  1. Airway, breathing, circulation
  2. Burns caused by heat:
    a. remove the person from the source
    b. within 20 minutes of the injury irrigate the burn with cool (not iced) water for between 10 and 30 minutes
    c. cover the burn using cling film, layered, rather than wrapped around a limb
  3. Electrical burns: switch off power supply and remove the person from the source
  4. Chemical burns:
    a. brush any powder off then irrigate with water
    b. attempts to neutralise the chemical are not recommended
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14
Q

How do you assess the extent of a burn injury?

A
  1. Wallace’s Rule of Nines:
    head + neck = 9%
    each arm = 9%
    each anterior part of leg = 9%, each posterior part of leg = 9%
    anterior chest = 9%, posterior chest = 9%
    anterior abdomen = 9%, posterior abdomen = 9%
  2. Lund and Browder chart: the most accurate method
    the palmar surface is roughly equivalent to 1% of total body surface area (TBSA). Not accurate for burns > 15% TBSA
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15
Q

How do you assess the depth of a burns injury?

A
  1. Superficial epidermal (first degree) = Red and painful, dry, no blisters
  2. Partial thickness (superficial dermal) (second degree) = Pale pink, painful, blistered. Slow capillary refill
  3. Partial thickness (deep dermal) (second degree) = Typically white but may have patches of non-blanching erythema. Reduced sensation, painful to deep pressure
  4. Full thickness (third degree) = White (‘waxy’)/brown (‘leathery’)/black in colour, no blisters, no pain
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16
Q

What is the criteria for referral to secondary care for a burns injury?

A

All deep dermal and full-thickness burns.
Superficial dermal burns of more than 3% TBSA in adults, or more than 2% TBSA in children
Superficial dermal burns involving the face, hands, feet, perineum, genitalia, or any flexure, or circumferential burns of the limbs, torso, or neck
Any inhalation injury
Any electrical or chemical burn injury
Suspicion of non-accidental injury

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17
Q

What is the pathophysiology of severe burns injuries?

A
  1. Local response with progressive tissue loss and release of inflammatory cytokines
  2. Systemically, there are cardiovascular effects resulting from fluid loss and sequestration of fluid into the third space
  3. There is a marked catabolic response
  4. Immunosupression is common with large burns and bacterial translocation from the gut lumen is a recognised event → Sepsis is a common cause of death following major burns.
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18
Q

What is the management of severe burn injuries?

A

The initial aim = stop the burning process and resuscitate the patient

  1. Airway:
    Smoke inhalation can result in airway oedema
    Early intubation should be considered e.g. if deep burns to the face or neck, blisters or oedema of the oropharynx, stridor etc
  2. IV fluids will be required for adults with burns greater than 15% (10% for children) of TBSA = Parkland formula, half of the fluid is administered in the first 8 hours
  3. Urinary catheter should be inserted and analgesia should be given
  4. Complex burns, burns involving the hand, perineum and face and burns >10% in adults and >5% in children should be transferred to a burns unit, circumferential burns affecting a limb or severe torso burns impeding respiration may require escharotomy to divide the burnt tissue (improve ventilation)
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19
Q

What is the prognosis of a burns injury?

A

Conservative management is appropriate for superficial burns and mixed superficial burns that will heal in 2 weeks
More complex burns may require excision and skin grafting

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20
Q

What is the fluid resuscitation formula used for burns injuries?

A

Parkland formula:
1. (Crystalloid only e.g. Hartman’s solution/Ringers’ lactate)
2. Total fluid requirement in 24 hours =
4 ml x (total burn surface area (%)) x (body weight (kg))
3. 50% given in first 8 hours, then 50% given in next 16 hours
4. Resuscitation endpoint:Urine output of 0.5-1.0 ml/kg/hour in adults (increase rate of fluid to achieve this)
Points to note: Starting point of resuscitation is time of injury, deduct fluids already given

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21
Q

What is the indication for fluid replacement in burns injuries?

A

Indication = >15% total body area burns in adults (>10% children)
The main aim of resuscitation is to prevent the burn deepening
Most fluid is lost 24h after injury
First 8-12h fluid shifts from intravascular to interstitial fluid compartments
Therefore circulatory volume can be compromised
However fluid resuscitation causes more fluid into the interstitial compartment especially colloid (therefore avoided in first 8-24h)

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22
Q

What is candidiasis of the skin?

A

When Candida colonises on the skin causing an infection
Also known as cutaneous candidiasis

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23
Q

What is the aetiology of candidiasis of the skin?

A

Candida is a yeast-like fungus = part of the normal commensal flora of the human gastrointestinal tract and the vagina
NOT part of the normal skin flora, but there may be transient colonization of fingers or body folds
Most common species = Candida albicans, responsible for over half of candidal skin infections
Usually asymptomatic but where mucosal barriers are disrupted or if the host’s defences are lowered, it can cause infections

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24
Q

What is the epidemiology of candidiasis of the skin?

A

Common
Being at extreme ages is a risk factor due to immature or weakened immunity

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25
Q

What are the risk factors for candidiasis of the skin?

A

Immunocompromised (HIV infection, chemotherapy, immunosuppressive drugs)
Cancer or malnutrition
Recent or concurrent use of drugs that promote candidal growth (broad-spectrum antibiotics and inhaled/oral corticosteroids)
Diseases in which the barrier function of the skin is disturbed (psoriasis and seborrhoeic eczema)
Endocrine disorders: DM and Cushing’s syndrome
Iron deficiency anaemia
High-oestrogen contraceptive pill or pregnancy
Poor hygiene

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26
Q

Where does candidiasis of the skin usually affect?

A

More likely to occur where skin rubs on skin (such as between skin folds in an obese person) and where heat and moisture lead to maceration and inflammation
-Armpits
-Groin
-Between the fingers
-Under the breasts

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27
Q

What are the features of candidiasis of the skin?

A

Rash-often causes redness and intense itching (armpits, groin, fingers/nails, under breasts)
Blisters and pustules
Scales may accumulate, producing a white-yellow, curd-like substance over the infected area
Satellite lesions
If web spaces (toes/fingers) involved = marked maceration with a thick, horny layer is usually prominent

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28
Q

What are the appropriate investigations for candidiasis of the skin?

A

Ix not necessary
But can exclude a differential diagnosis or an underlying condition (e.g. diabetes or anaemia) in people with widespread or recurrent infection
Standard bacteriology swabs for microscopy and culture may be required if:
1. Secondary bacterial infection is suspected
2. Immunocompromised
3. Diagnosis is uncertain

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29
Q

What is the management of candidiasis of the skin?

A
  1. Topical imidazole antifungal e.g. clotrimazole, econazole nitrate, ketoconazole, or miconazole
  2. Topical terbinafine is an alternative (not in refractory candidiasis)
  3. Topical application of nystatin is also effective for candidiasis but it is ineffective against dermatophytosis
  4. Refractory candidiasis requires systemic treatment generally with a triazole such as fluconazole (oral)
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30
Q

What is vaginal candidiasis?

A

Thrush
80% of cases of Candida albicans
Majority of women will have no predisposing factors, others may have DM, pregnancy, HIV, recent Abx or steroids
Features : ‘cottage cheese’, non-offensive discharge, vulvitis: superficial dyspareunia, dysuria
Ix: high vaginal swab for M+C not routinely needed unless >4 per year
Rx: oral fluconazole 150 mg as a single dose first-line, clotrimazole 500 mg intravaginal pessary as a single dose if oral therapy is contraindicated
(avoid oral in pregnancy)
Recurrent: check compliance, M+C, induction (oral fluconazole every 3 days for 3 doses) and maintenance (oral fluconazole weekly for 6 months)

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31
Q

What is Cellulitis?

A

Inflammation of the skin and subcutaneous tissues, typically due to infection by Streptococcus pyogenes or Staphylcoccus aureus

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32
Q

What is cellulitis usually characterised by?

A

Erythema
Oedema
Warmth
Tenderness
Commonly occurs in an extremity

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33
Q

What are the features of cellulitis?

A

Commonly occurs on the shins
Erythema, pain, swelling
There may be some associated systemic upset such as fever

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34
Q

What are the risk factors for cellulitis?

A

Common
Skin break
Poor hygiene
Poor vascularisation of tissue (e.g. DM)

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35
Q

What are the appropriate investigations for cellulitis?

A

Diagnosis is clinical
No further investigations are required in primary care
Bloods and blood cultures may be requested if the patient is admitted and septicaemia is suspected
Consider taking a swab for microbiological testing only if the skin is broken and there is risk of infection by an uncommon pathogen

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36
Q

What is periorbital /orbital cellulitis?

A

Periorbital: Painful swollen red skin around eye/ swollen eyelids

Orbital cellulitis:
Painful or limited eye movements
*Visual impairment
Proptosis (protrusion of the eyeball)
Impaired acuity and eye movement
Test for relative afferent pupillary defect, visual acuity and colour vision
CT/ MRI = to assess posterior spread of infection
Refer to ophthalmology as an emergency → orbital decompression may be necessary

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37
Q

What classification is used to guide admission and management of cellulitis?

A

Eron Classification
I = no signs of systemic toxicity and the person has no uncontrolled co-morbidities

II = either systemically unwell or systemically well but with a co-morbidity (e.g. peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection

III = significant systemic upset such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable co-morbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromise

IV = sepsis syndrome or a severe life-threatening infection such as necrotising fasciitis

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38
Q

When do you admit for IV antibiotics in cellulitis?

A
  1. Eron Class III or Class IV cellulitis
  2. Severe or rapidly deteriorating cellulitis (e.g. extensive areas of skin)
  3. Is very young (under 1 year of age) or frail
  4. Is immunocompromised
  5. Has significant lymphoedema
  6. Has facial cellulitis (unless very mild) or periorbital cellulitis
    (Eron class II can also be given IV antibiotics in the community if available- otherwise oral)
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39
Q

What is the management of cellulitis?

A

First line = flucloxacillin for mild/moderate cellulitis (BNF)
Clarithromycin, erythromycin (in pregnancy) or doxycyline is recommended in patients allergic to penicillin

Severe cellulitis should be offered co-amoxiclav, cefuroxime, clindamycin or ceftriaxone (NICE)

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40
Q

What is Erysipelas?

A

More superficial, limited version of cellulitis
Localised skin infection caused by Streptococcus pyogenes

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41
Q

What is the management of Erysipelas?

A

Oral flucloxacillin

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42
Q

What is eczema?

A

An inflammatory skin reaction to endogenous or exogenous agents characterised by dry, pruritic skin with a chronic relapsing course

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43
Q

What are the different types of eczema?

A
  1. Atopic (Hx of atopy)
  2. Contact (immune sensitisation e.g. nickel)
  3. Discoid (coin shaped usually affecting limbs)
  4. Dyshidrotic
  5. Herpeticum (medical emergency)
  6. Seborrhoeic (chronic, affecting face, scalp, ears and flexures due to reaction of yeasts that colonise skin)
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44
Q

What is the epidemiology of eczema?

A

Occurs in around 15-20% of children and is becoming more common.
Typically presents before 2 years but clears in:
- around 50% of children by 5 years of age
- 75% of children by 10 years of age

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45
Q

What are the presenting symptoms of eczema?

A

Itching (can be severe), heat, tenderness, redness, weeping, crusting
Enquire into occupational exposures or irritants used at home (e.g. bleach)
FH/ PH of atopy (e.g. asthma, hay fever, rhinitis)

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46
Q

What are the features of acute eczema?

A
  1. Poorly demarcated erythematous oedematous dry scaling patches
  2. Atopic: Particularly affects face and flexures (inside elbow and knee)
  3. Papules, vesicles with exudation and crusting
  4. Excoriation marks
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47
Q

What are the features of chronic eczema?

A
  1. Thickened epidermis
  2. Skin lichenification
  3. Fissures
  4. Change in pigmentation
  5. Seborrhoeic: Yellow greasy scales on erythematous plaques, particularly in the nasolabial folds, eyebrows, scalp and presternal area
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48
Q

What is eczema herpeticum?

A

Severe primary infection of the skin by herpes simplex virus 1 or 2
It is more commonly seen in children with atopic eczema and often presents as a rapidly progressing painful rash

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49
Q

What are the features of eczema herpeticum?

A

Monomorphic punched-out erosions (circular, depressed, ulcerated lesions) usually 1–3 mm in diameter are typically seen

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50
Q

What is the management of eczema herpeticum?

A

Potentially life-threatening
Children should be admitted for IV aciclovir

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51
Q

What are the investigations for eczema?

A

Clinical diagnosis usually
Contact dermatitis = offer skin patch testing to suspected allergens (positive if allergen induces a red raised lesion after 48 hrs)
Swab for infected lesions (bacteria, fungi and viruses)

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52
Q

What is the management of eczema?

A

Avoid irritants
Simple emollients (large quantities, 10:1 ratio with a topical steroid if prescribed)
Topical steroids
Wet wrapping (large amounts of emollient applied under wet bandages)
In severe cases, oral ciclosporin may be used

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53
Q

What are the considerations of simple emollients in the management of eczema?

A
  1. Large quantities should be prescribed (e.g. 250g / week), roughly in a ratio of with topical steroids of 10:1
  2. Apply emollient first followed by waiting at least 30 minutes before applying the topical steroid
  3. Creams soak into the skin faster than ointments
  4. Emollients can become contaminated with bacteria - fingers should not be inserted into pots (many brands have pump dispensers)
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54
Q

What is the steroid ladder used in eczema management?

A

Help Every Busy Dermatologist
1. Hydrocortisone 0.5-2.5% (mild)
2. Eumovate: Clobetasone butyrate 0.05% (moderate)
3. Betnovate: Betamethasone valerate 0.1% (potent)
4. Dermovate: Clobetasol propionate 0.05% (very potent)

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55
Q

What is the fingertip rule used for topical steroids in eczema management?

A

1 finger tip unit (FTU) = 0.5 g
Sufficient to treat a skin area about twice that of the flat of an adult hand

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56
Q

What are epidermoid and pilar cysts (sebaceous cysts)?

A

Benign small bumps beneath the skin
Can appear anywhere on the skin, but are most common on the face, neck and trunk
Two of the most common types of cysts

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57
Q

What are the features of epidermoid and pilar cysts?

A

Small round bump under the skin
Have a central punctum
May contain small quantities of sebum

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58
Q

What is the difference between epidermoid and pilar cysts?

A

The cyst lining:
Epidermoid cyst = normal epidermis
Pilar cyst = outer root sheath of hair follicle

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59
Q

How is the diagnosis of an epidermoid or pilar cyst made?

A

Usually clinical
However, if suspicious the tissue can be excised and submitted for histology

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60
Q

What is the aetiology of epidermoid and pilar cysts?

A

Occluded pilosebaceous units

61
Q

What is the management of epidermoid and pilar cysts?

A

Most small uncomplicated epidermoid cysts will not require treatment
Most effective treatment: complete surgical excision with an intact cyst capsule

62
Q

What is Erythema multiforme?

A

An acute hypersensitivity reaction of the skin and mucous membranes, most commonly triggered by infections
Divided into major and minor

63
Q

What is the pathophysiology of erythema multiforme?

A
  1. Degeneration of basal epidermal cells and development of vesicles between the cells and the underlying basement membrane
  2. Lymphocytic infiltration
  3. Immune complex deposition is variable and non-specific
64
Q

What are the causes of erythema multiforme?

A
  1. Viruses = herpes simplex virus (the most common cause)
  2. Idiopathic
  3. Bacteria: Mycoplasma, Streptococcus
    4 Drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, OCP
  4. Connective tissue disease e.g. SLE
  5. Sarcoidosis
  6. Malignancy
65
Q

What is the epidemiology of erythema multiforme?

A

Any age group - mostly seen in children and young adults
M > F 2:1

66
Q

What are the features of erythema multiforme?

A

Non-specific prodromal symptoms
Target lesions: initially seen on the back of the hands / feet before spreading to the torso
Upper limbs are more commonly affected than the lower limbs
Pruritus is occasionally seen and is usually mild

67
Q

What are the characteristics of the target lesions seen in erythema multiforme?

A

3 zones (red rim, clearance zone, and central blister or erosion) on the distal extremities
Target (‘bull’s eye’) lesions with a rim of erythema surrounding a paler area
Often symmetrical
Affect upper limbs more including palms (can affect soles and extensor surfaces)

68
Q

What is erythema multiforme major?

A

The more severe form, erythema multiforme major is associated with mucosal involvement

69
Q

What is the management for erythema multiforme?

A

Identify cause e.g. HSV serology, PCR, CXR for mycoplasma pneumoniae, skin biopsy/ swab
Symptomatic treatment = antihistamines and topical steroids
Treat the underlying cause = e.g. antivirals, aciclovir for HSV
Self-limiting = 4-6 weeks

70
Q

What is Stevens-Johnson syndrome?

A

A severe systemic reaction affecting the skin and mucosa that is almost always caused by a drug reaction
(separate entity to erythema multiforme)

71
Q

What are the common causes of Stevens-Johnson syndrome?

A

Penicillin
Sulphonamides
Lamotrigine, carbamazepine, phenytoin
Allopurinol
NSAIDs
Oral contraceptive pill

72
Q

What are the features of Stevens-Johnson syndrome?

A

Rahs: typically maculopapular with target lesions
May develop into vesicles or bullae
Nikolsky sign is positive in erythematous areas - blisters and erosions appear when the skin is rubbed gently
Mucosal involvement
Systemic symptoms: fever, arthralgia

73
Q

What is the management for Stevens-Johnson syndrome?

A

Skin biopsy and bloods e.g. FBC, LFTs
Hospital admission for supportive treatment
Stop the causative drug (may have to stop all to identify drug)
Admit patient to ITU/ burns unit with dermatology and ophthalmology review
Pain management (avoid NSAIDs)
Fluid monitoring

74
Q

What is erythema nodosum?

A

Inflammation of subcutaneous fat
Presents as tender, erythematous, nodular lesions usually over the shins

75
Q

What are the causes of erythema nodosum?

A
  1. Infection = streptococci, TB, Brucellosis
  2. Systemic disease = Sarcoidosis, IBD, Behcet’s
  3. Malignancy/lymphoma
  4. Drugs = Penicillins, Sulphonamides, COCP
  5. Pregnancy
76
Q

What is the epidemiology of erythema nodosum?

A

Usually affects young female adults (3:1)

77
Q

What are the features of erythema nodosum?

A

Tender, erythematous, nodular lesions
Usually occurs over shins, may also occur elsewhere (e.g. forearms, thighs)
Fever and joint pain
Features of underlying cause

78
Q

What are the investigations for erythema nodosum?

A

Bloods e.g. FBC = high WCC
Anti-streptolysin O titre: elevated in streptococcal infection, ideally checked at first visit, and repeated 2 to 4 weeks later
Throat swab and culture
Serum ACE (raised in sarcoidosis)
Mantoux test: positive in TB
Skin biopsy
CXR:
-Bilateral hilar lymphadenopathy = sarcoidosis
-Unilateral hilar lymphadenopathy = TB, brucellosis

79
Q

What is the management of erythema nodosum?

A

Treatment is based on the underlying cause
Pain management e.g. NSAIDs, colchicine
Systemic corticosteroids if malignancy and sepsis have been excluded

80
Q

What is the prognosis of erythema nodosum?

A

Nodular lesions usually resolves within 6 weeks and heal without scarring
Important to recognise underlying cause
Relapses may occur in 1/3rd of cases (can become a chronic/ persistent disorder for months)

81
Q

What is erythroderma?

A

A term used when more than 95% of the skin is involved in a rash of any kind (usually due to an inflammatory skin disease)
Known as ‘red man syndrome’

82
Q

What are the causes of Erythroderma?

A

Eczema (especially atopic)
Psoriasis (especially after withdrawal of systemic steroids)
Drugs e.g. gold
Lymphomas, leukaemias
Idiopathic

83
Q

What is Erythrodermic psoriasis?

A

May result from progression of chronic disease to an exfoliative phase with plaques covering most of the body
Associated with mild systemic upset
More serious form is an acute deterioration:
- May be triggered by a variety of factors such as withdrawal of systemic steroids
- Patients need to be admitted to hospital for management

84
Q

What are the features of erythroderma?

A

Morbilliform (measles-like) eruption, dermatitis or plaque psoriasis which develops quite rapidly
Skin warmth
Itching/ excoriation marks → lichenification
Scaling
Ectropion/ blepharitis
Hair loss/ nail onycholysis (nail pitting)
Palmar karatoderma (thickening of palms)
Generalised dermatopathic lymphadenopathy

85
Q

What are the investigations for erythroderma?

A

Skin biopsy (if diagnosis is unclear)
Bloods including FBC, serum albumin (due to loss of protein), LDH (risk of malignancy), renal profile
Peripheral blood smear = sezary cells
Blood cultures and wound swabs

86
Q

What is the management for erythroderma?

A

Treat the underlying cause
Associated with skin failure from hypothermia and dehydration!
Temperature regulation
Stop all unnecessary medications
Emollients
Strict monitoring of fluid balance
Antihistamine if needed

87
Q

What are the complications of erythroderma?

A

Hypothermia
Electrolyte abnormalities and dehydration
High output heart failure
Secondary skin infection
Hypoalbuminaemia
Death

88
Q

What is Herpes Simplex Virus?

A

Common viral infection that presents with localised blistering from either HSV-1 or HSV-2

89
Q

What is the difference in type 1 and 2 of Herpes Simplex Virus?

A

HSV -1: mainly associated with oral and facial infections
HSV -2: mainly associated with genital and rectal infections
However there is considerable overlap

90
Q

What is the aetiology of Herpes Simplex Virus?

A

Alpha-herpes virus with double-stranded DNA (dsDNA)
Transmitted via close contact with an individual shedding the virus (e.g. kissing, sexual intercourse)

91
Q

What is the epidemiology of Herpes Simplex Virus?

A

90% adults seropositive for HSV1 by 30 years
35% adults >60s are seropositive for HSV2
Over 1/3 world population has recurrent HSV infections

92
Q

What are the features of a HSV infection?

A

Primary infection: may present with a severe gingivostomatitis (oral ulcers filled with yellow slough- make eating painful)
Cold sores
Painful genital ulceration
Can cause Erythema Multiforme (most common cause)

93
Q

What is the timeline for HSV-1 infection features?

A

Primary infection = often asymptomatic
Recurrent infection/reactivation (herpes labialis/‘cold sore’) =
1. Prodrome (6 h) peri-oral tingling and burning
2. Vesicles appear (48 h duration), ulcerate and crust over
3. Complete healing in 8–10 days

94
Q

What are the appropriate investigations for HSV?

A

Usually a clinical diagnosis
Can be confirmed by culture or PCR of a viral swab
(HSV is not very informative as it is positive in most individuals)

95
Q

What is the management for HSV infection?

A

Mild, uncomplicated eruptions of HSV require no treatment
Gingivostomatitis: oral aciclovir, chlorhexidine mouthwash
Cold sores: topical aciclovir (not usual)
Genital herpes: oral aciclovir (if frequent exacerbations may benefit from longer term aciclovir)

96
Q

What is a lipoma?

A

A common, benign tumour of adipocytes

97
Q

What is the pathophysiology of lipomas?

A

Generally found in subcutaneous tissues
Rarely, they may also occur in deeper adipose tissues
Malignant transformation to liposarcoma is very rare

98
Q

What is the epidemiology of lipomas?

A

Approx 1% of the population have lipomas
Most common between ages 40-60 years (middle aged adults)

99
Q

What are the features of a lipoma?

A
  1. Smooth
  2. Mobile
  3. Painless
    (Small <5cm, soft ‘doughy’, superficial)
100
Q

How is the diagnosis of a Lipoma made?

A

Usually clinical
Based on the typical examination findings

101
Q

What is the management of a lipoma?

A

May be observed
If diagnosis uncertain, or compressing on surrounding structures then may be removed

102
Q

What is a liposarcoma?

A

A lipoma that has transformed a sarcomatous change:
1. Size >5cm
2. Increasing size
3. Pain
4. Deep anatomical location

103
Q

What is a melanoma?

A

A malignant tumour arising from melanocytes, the pigment-forming cells of the skin
It is the leading cause of death from skin disease

104
Q

What is the aetiology of Melanomas?

A

DNA damage in melanocytes caused by ultraviolet radiation results in neoplastic transformation
50 % arise in pre-existing naevi, 50 % in previously normal skin

105
Q

What are the four histopathological types of Melanoma?

A
  1. Superficial spreading (70%)
  2. Nodular (15%)
  3. Lentigo maligna (10%)
  4. Acral lentiginous (5%)
106
Q

What are the features of superficial spreading melanoma?

A

70% of cases
Typically arises from a pre-existing naevus, expands in radial fashion before vertical growth phase
Commonly on arms, legs, back and chest
Affects young people
A growing mole

107
Q

What are the features of a nodular melanoma?

A

Second most common melanoma
Occurs in sun exposed skin
Affects middle aged people
Arises de novo, most aggressive
Red/ black lump or lump which bleeds or oozes

108
Q

What are the features of lentigo maligna?

A

Less common
More common in elderly who have has chronically sun-exposed skin
Large flat lesions, follow an indolent growth course
Usually on the face

109
Q

What are the features of Acral lentiginous melanoma?

A

Least common form of melanoma
More common in people with darker skin pigmentation
Affects nails, palms or soles
Subungual pigmentation (Hutchinson’s sign) or on palms or feet

110
Q

What are the major and minor criteria for malignant melanoma?

A

Major (main) criteria:
1. Change in size
2. Change in shape
3. Change in colour
Secondary features (minor criteria):
1. Diameter >= 7mm
2. Inflammation
3. Oozing or bleeding
4. Altered sensation

111
Q

What is Molluscum contagiosum?

A

A common skin infection caused by molluscum contagiosum virus (MCV), a member of the Poxviridae family

112
Q

How is Molluscum contagiosum transmitted?

A

Occurs directly by close personal contact, or indirectly via fomites (contaminated surfaces) such as shared towels and flannels

113
Q

What is the epidemiology of molluscum contagiosum?

A

Majority of cases occur in children (often in children with atopic eczema), with the maximum incidence in preschool children aged 1-4 years

114
Q

What are the presenting symptoms of molluscum contagiosum?

A
  1. Characteristic pinkish or pearly white papules with a central umbilication, which are up to 5 mm in diameter
  2. Lesions appear in clusters in areas anywhere on the body (except the palms of the hands and the soles of the feet)
  3. In children: lesions are commonly seen on the trunk and in flexures, but anogenital lesions may also occur
  4. In adults, sexual contact may lead to lesions developing on the genitalia, pubis, thighs, and lower abdomen
  5. Rarely, lesions can occur on the oral mucosa and on the eyelids
115
Q

What is the management of molluscum contagiosum?

A
  1. Usually a self-limiting condition, with spontaneous resolution usually occurring within 18 months
  2. If lesions are troublesome or considered unsightly, use simple trauma or cryotherapy
  3. Referral in certain cases:
    a. HIV positive patients with extensive lesions
    b. Eyelid-margin or ocular lesions and associated red eye urgent = referral to an ophthalmologist
    c. Adults with anogenital lesions should be referred to genito-urinary medicine
116
Q

What is advice should be given to patients with molluscum contagiosum?

A
  1. Reassure people that molluscum contagiosum is a self-limiting condition: spontaneous resolution usually occurs within 18 months
  2. Explain that lesions are contagious, and it is sensible to avoid sharing towels, clothing, and baths with uninfected people (e.g. siblings)
  3. Encourage people not to scratch the lesions, if it is problematic, consider treatment to alleviate the itch
  4. Exclusion from school, gym, or swimming is not necessary
117
Q

What can develop around lesions from molluscum contagiosum?

A

Eczema or inflammation: treatment may be required if:
1. Itching is problematic; prescribe an emollient and a mild topical corticosteroid (e.g. hydrocortisone 1%)
2. The skin looks infected (e.g. oedema, crusting); prescribe a topical antibiotic (e.g. fusidic acid 2%)

118
Q

What is the management of malignant melanoma?

A
  1. Suspicious lesions should undergo excision biopsy
  2. The lesion should be removed in completely as incision biopsy can make subsequent histopathological assessment difficult
  3. Once the diagnosis is confirmed the pathology report should be reviewed to determine whether further re-excision of margins is required (Breslow thickness)
119
Q

What is the most important prognostic factor of malignant melanoma?

A

Breslow thickness

120
Q

What are the margins of excision related to Breslow thickness?

A

Lesions 0-1mm thick: 1cm
Lesions 1-2mm thick: 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick: 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick: 3cm

121
Q

What are the further treatments for malignant melanoma aside from excision biopsy?

A

Sentinel lymph node mapping, isolated limb perfusion and block dissection of regional lymph node groups

122
Q

What are Pressure Sores?

A
  1. Also known as pressure ulcers
  2. Localised injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure or of pressure in combination with shear
  3. Most commonly occur over bony prominences but can develop on any part of the body, including mucosal surfaces
123
Q

What are the four predisposing factors for pressure ulcers?

A

1 Malnourishment
2 Incontinence
3. Lack of mobility
4. Pain (leads to a reduction in mobility)

124
Q

What scoring system is used to screen patients at risk of pressure ulcers?

A

Waterlow score: factors including body mass index, nutritional status, skin type, mobility and continence

125
Q

What is the grading system for pressure ulcers?

A
  1. Grade 1:
    a. Non-blanchable erythema of intact skin
    b. Discolouration of the skin, warmth, oedema, induration or hardness may also be used as indicators, particularly on individuals with darker skin
  2. Grade 2:
    a. Partial thickness skin loss involving epidermis or dermis, or both
    b. The ulcer is superficial and presents clinically as an abrasion or blister
  3. Grade 3:
    a. Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia
  4. Grade 4:
    a. Extensive destruction, tissue necrosis, or damage to muscle, bone or
    supporting structures with or without full thickness skin loss
126
Q

What is the management of pressure sores?

A
  1. A moist wound environment encourages ulcer healing
  2. Hydrocolloid dressings and hydrogels may help facilitate this
  3. Avoid use of soap: avoid drying the wound
  4. Wound swabs should not be done routinely as the vast majority of pressure ulcers are colonised with bacteria
  5. Antibiotics: given on a clinical basis (e.g. evidence of surrounding cellulitis)
  6. Consider referral to the tissue viability nurse
  7. Surgical debridement may be beneficial for selected wounds
127
Q

What is psoriasis?

A
  1. A chronic inflammatory skin disease characterised by erythematous, circumscribed scaly papules, and plaques
  2. Generally presents with red, scaly patches on the skin, can increase risk of cardiovascular disease and arthritis
128
Q

What is the pathophysiology of psoriasis?

A
  1. Multifactorial and not yet fully understood
  2. Genetic:
    a. Associated HLA-B13, -B17
    b. Immunological: abnormal T cell activity stimulates keratinocyte proliferation
  3. Environmental:
    a. Recognised that psoriasis may be worsened (e.g. Skin trauma, stress)
    b. triggered (e.g. Streptococcal infection) or
    c. improved (e.g. Sunlight) by environmental factors
129
Q

What are the different subtypes of psoriasis?

A
  1. Plaque psoriasis:
    a. Most common sub-type
    b. Well-demarcated red, scaly patches affecting the extensor surfaces, sacrum and scalp
  2. Flexural psoriasis:
    a. in contrast to plaque psoriasis
    b. Skin is smooth
  3. Guttate psoriasis:
    a. Transient psoriatic rash frequently triggered by a streptococcal infection
    b. Multiple red, teardrop lesions appear on the body
  4. Pustular psoriasis: commonly occurs on the palms and soles
130
Q

What is the epidemiology of Psoriasis?

A
  1. Affects 1–2 % of the population
  2. Peak age of onset 􏰀 20 years
131
Q

What are the presenting symptoms of Psoriasis?

A
  1. Skin lesions on elbows, knees, extensor surfaces of limbs, scalp, and, less commonly, nails, ears, and umbilical region
  2. Itching or occasionally tender skin
  3. Auspitz phenomenon: pinpoint bleeding with removing scales
  4. Koebner phenomenon: Skin lesions may develop at the site of trauma/scars*
132
Q

What are some other features of psoriasis?

A
  1. Nail signs: pitting, onycholysis (nail separates from the bed)
  2. Arthritis
133
Q

What are the investigations for psoriasis?

A
  1. Clinical diagnosis
  2. Skin biopsy: when diagnosis is in doubt
  3. Guttate psoriasis: Anti-streptolysin-O titre, throat swab
  4. Joint involvement: Rheumatoid factor (negative), radiographs (distal interphalangeal joints)
134
Q

What are the nail changes in psoriasis and what is it associated with?

A
  1. Associated with psoriatic arthropathy
  2. pPitting
  3. Onycholysis (separation of the nail from the nail bed)
  4. Subungual hyperkeratosis
  5. Loss of the nail
135
Q

What are the exacerbating factors for psoriasis?

A
  1. Trauma
  2. Alcohol
  3. Drugs: beta blockers, lithium, antimalarials (chloroquine and hydroxychloroquine), NSAIDs, ACE inhibitors, infliximab
  4. Withdrawal of systemic steroids
  5. For guttate psoriasis: Streptococcal infection may trigger
136
Q

What is guttate psoriasis?

A
  1. More common in children and adolescents
  2. It may be precipitated by a streptococcal infection 2-4 weeks prior to the lesions appearing
  3. Tear drop papules on the trunk and limbs
  4. Acute onset over days
137
Q

What is the management of guttate psoriasis?

A
  1. Most cases resolve spontaneously within 2-3 months
  2. No firm evidence to support the use of antibiotics to eradicate streptococcal infection
  3. Topical agents as per psoriasis
  4. UVB phototherapy
  5. Tonsillectomy may be necessary with recurrent episodes
138
Q

What is the management of chronic plaque psoriasis?

A
  1. Regular emollients may help to reduce scale loss and reduce pruritus
  2. First-line: NICE recommend a potent corticosteroid applied once daily plus vitamin D analogue applied once daily
    a. Should be applied separately, one in the morning and the other in the evening
    b. For up to 4 weeks as initial treatment
  3. Second-line: if no improvement after 8 weeks then offer: a vitamin D analogue twice daily
  4. Third-line: if no improvement after 8-12 weeks then offer either:
    a. Potent corticosteroid applied twice daily for up to 4 weeks, or
    b. Coal tar preparation applied once or twice daily
139
Q

What is the secondary care management for chronic plaque psoriasis?

A
  1. Phototherapy:
    a. Now the treatment of choice
    b. If possible given three times a week
    c. Risk of SCC
  2. Systemic therapy
    a. Oral methotrexate is first line (especially if there is arthropathy)
    b. Others: ciclosporin, biologics e.g. infliximab, etanercept
140
Q

What advice is given regarding topical corticosteroids in the management of psoriasis?

A
  1. May lead to skin atrophy, striae and rebound symptoms
  2. The scalp, face and flexures are particularly prone to steroid atrophy: so should not be used for more than 1-2 weeks/month
  3. NICE recommend that we aim for a 4-week break before starting another course of topical corticosteroids
  4. Also recommend using potent corticosteroids for no longer than 8 weeks at a time
141
Q

What is Syphilis?

A
  1. A sexually transmitted infection caused by the spirochaete Treponema pallidum
  2. Infection is characterised by primary, secondary and tertiary stages
  3. The incubation period is between 9-90 days
142
Q

What are the primary features of Syphilis?

A
  1. Chancre - painless ulcer at the site of sexual contact
  2. Local non-tender lymphadenopathy
  3. Often not seen in women (the lesion may be on the cervix)
143
Q

What are the secondary features of Syphilis?

A
  1. Occurs 6-10 weeks after primary infection
  2. Systemic symptoms: fevers, lymphadenopathy
  3. Rash on trunk, palms and soles
  4. Buccal ‘snail track’ ulcers (30%)
  5. Condylomata lata (painless, warty lesions on the genitalia )
144
Q

What are the tertiary features of Syphilis?

A
  1. Gummas (granulomatous lesions of the skin and bones)
  2. Ascending aortic aneurysms
  3. General paralysis of the insane
  4. Tabes dorsalis: slow degeneration of the nerve cells in the dorsal column
    Argyll-Robertson pupil
145
Q

How is Syphilis diagnosed?

A
  1. Usually based on clinical features, serology and microscopic examination of infected tissue
  2. Serology can be divided into:
    a. Non-treponemal tests (not specific for syphilis)
    b. Treponemal-specific tests
146
Q

What is the first line management of Syphilis?

A

Intramuscular benzathine penicillin (doxycycline as an alternative)

147
Q

What is Lymphogranuloma venereum (LGV)?

A
  1. Caused by Chlamydia trachomatis serovars
  2. Risk factors include:
    a. Men who have sex with men
    b. Majority of patients who present in developed countries have HIV
148
Q

What are the stages of Lymphogranuloma venereum (LGV)?

A
  1. Stage 1: small painless pustule which later forms an ulcer
  2. Stage 2: painful inguinal lymphadenopathy, may occasionally form fistulating buboes
  3. Stage 3: proctocolitis (inflammation of rectum and colon)
149
Q

What is the management of LGV?

A

Doxycycline