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Systems: Dermatology AB > Acute and Emergency Dermatology > Flashcards

Acute and Emergency Dermatology Flashcards

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Dermatology Board Prep flashcards
1
Q

What are the normal functions of the skin?

A
  • Mechanical barrier to infection
  • Temperature regulation
  • Fluid and electrolyte balance
  • Vitamin D synthesis
  • Sensation
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2
Q

What are the consequences of skin failure?

A
  • Sepsis
  • Hypo- and Hyper- thermia
  • Protein and fluid loss
  • Renal impairment
  • Peripheral vasodilation (Can occasionally lead to cardiac failure)
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3
Q

Erythroderma.

A
  • A descriptive term rather than a diagnosis

- “Any inflammatory skin disease affecting >90% of total skin surface”

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4
Q

What can cause erythroderma?

A
  • Psoriasis
  • Eczema
  • Drugs
  • Cutaneous Lymphoma
  • Hereditary disorders
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5
Q

What are the principles of management acute skin disease?

A
  • Appropriate setting - ?ITU or burns unit
  • Remove any offending drugs
  • Careful fluid balance
  • Good nutrition
  • Temperature regulation
  • Emollients – 50:50 Liquid Paraffin : White Soft Paraffin
  • Oral and eye care
  • Anticipate and treat infection
  • Manage itch
  • Disease specific therapy; treat underlying cause
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6
Q

How common are drug reactions?

A

Common

-2-3% of inpatients

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7
Q

What drugs can reactions occur with?

A

Any drug

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8
Q

When do drug reactions usually occur?

A
  • Commonly 1-2 weeks after drug

- Within 72 hours if re-challenged

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9
Q

Give an example of a mild drug reaction.

A

Morbilliform exanthem

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10
Q

Give examples of severe drugs reactions

A
  • Erythroderma
  • Stevens Johnson Syndrome
  • Toxic epidermal necrolysis
  • DRESS
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11
Q

What 2 conditions are thought to form part of the same spectrum and can occur as a result of sever drug reactions?

A
  • Stevens Johnson Syndrome

- Toxic Epidermal Necrolysis

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12
Q

What drugs normally cause SJS/TEN?

A
  • Antibiotics
  • Anticonvulsants
  • Allopurinol
  • NSAIDs
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13
Q

How rare are SJS/TEN?

A
  • 1-2/million/year (SJS)

- 0.4-1.2/million/year (TEN)

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14
Q

What is the difference between SJS and TEN?

A

-SJS affects <10% of body
TEN affects >30% of body
-Overlap between conditions 11-29%

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15
Q

What are the clinical features of SJS?

A
  • Fever, malaise, arthralgia
  • Rash
  • Mouth ulceration (Greyish white membrane, Haemorrhagic crusting)
  • Ulceration of other mucous membranes
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16
Q

Describe the rash present in SJS.

A
  • Maculopapular, target lesions, blisters

- Erosions covering <10% of skin surface

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17
Q

What does TEN often present with?

A

Prodromal febrile illness

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18
Q

Describe the rash in TEN.

A
  • May start as macular, purpuric or blistering
  • Rapidly becomes confluent
  • Sloughing off of large areas of epidermis – ‘desquamation’ > 30% BSA
  • Nikolsky’s sign may be positive
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19
Q

How should drug reactions be managed?

A
  • Identify and stop culprit drug as soon as possible
  • Supportive therapy
  • ?High dose steroids
  • ?IV immunoglobulins
  • ?Anti-TNF therapy
  • ?Ciclosporin
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20
Q

What system is used to identify prognosis of SJS/TEN?

A

SCORTEN

  • Age >40
  • Malignancy
  • Heart rate >120
  • Initial epidermal detachment >10%
  • Serum urea >10
  • Serum glucose >14
  • Serum bicarbonate <20
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21
Q

What is the mortality of SJS/TEN?

A
  • SJS up to 10%

- TEN up to 30%

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22
Q

What are the possible long term complications of SJS/TEN?

A
  • Pigmentary skin changes
  • Scarring
  • Eye disease and blindness
  • Nail and hair loss
  • Joint contactures
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23
Q

What is erythema multiforme?

A
  • Hypersensitivity reaction usually triggered by infection

- Most commonly HSV, then Mycoplasma pneumonia

24
Q

How does erythema multiforme present?

A
  • Abrupt onset of up to 100s of lesions over 24 hours
  • Distal to proximal
  • Palms and soles
  • Mucosal surfaces (EM major)
  • Evolve over 72 hours
  • Pink macules, become elevated and may blister in centre
  • “Target” lesions
25
Q

How should erythema multiforme be managed?

A
  • Self limiting and resolves over 2 weeks

- Symptomatic and treat underlying cause

26
Q

What does DRESS stand for?

A

Drug reaction with eosinophilia and systemic symptoms

27
Q

What is the incidence of DRESS?

A
  • Incidence estimated between 1 in 1000-10,000

- Mortality up to 10%

28
Q

How does DRESS present?

A
  • Onset 2-8 weeks after drug exposure
  • Fever and widespread rash
  • Eosinophilia and deranged liver function
  • Lymphadenopathy
  • +/- other organ involvement
29
Q

How is DRESS treated?

A
  • Stop causative drug
  • Symptomatic and supportive
  • Systemic steroids
  • +/- Immunosuppression or immunoglobulins
30
Q

What causes pemphigus?

A

Antibodies targeted at desmosomes

31
Q

How does pemphigus present?

A
  • Skin – flaccid blisters, rupture very easily

- Intact blisters may not be seen

32
Q

What are the common sites of pemphigus?

A
  • Face
  • Axillae
  • Groins
33
Q

What sign be positive in pemphigus?

A

Nikolsky’s sign may be +ve

34
Q

What is commonly affected in pemphigus?

A
  • Commonly affects mucous membranes
  • Ill defined erosions in mouth
  • Can also affect eyes, nose and genital areas
35
Q

What causes pemphigoid?

A

Antibodies directed at dermo-epidermal junction

36
Q

How does pemphigoid present?

A
  • Intact epidermis forms roof of blister

- Blisters are usually tense and intact

37
Q

Summarise pemphigus

A
  • Uncommon
  • Middle aged patients
  • Blisters very fragile – may not be seen intact
  • Mucous membranes usually affected
  • Patients may be very unwell if extensive
  • Treat with systemic steroids. Dress erosions. Supportive therapies
38
Q

Summarise pemphigoid

A
  • Common
  • Elderly patients
  • Blisters often intact and tense
  • Even if extensive, patients are fairly well systemically
  • Topical steroids may be sufficient if localised; systemic usually required if diffuse
39
Q

What are common causes of erythrodermic and pustular psoriasis?

A
  • Infection

- Sudden withdrawal of oral steroids or potent topical steroid

40
Q

How do erythrodermin and pustular psoriasis present?

A
  • Rapid development of generalised erythema, +/- clusters of pustules
  • Fever, elevated WCC
41
Q

How is erythrodermic and pustular psoriasis treated?

A
  • Exclude underlying infection, bland emollient, avoid steroids
  • Often require initiation of systemic therapy
42
Q

What is eczema herpeticum?

A

Disseminated herpes virus infection on a background of poorly controlled eczema

43
Q

How does eczema herpeticum present?

A
  • Monomorphic blisters and “punched out” erosions
  • Generally painful, not itchy
  • Fever and lethargy
44
Q

How is eczema herpeticum treated?

A
  • Treatment dose Aciclovir
  • Mild topical steroid if required to treat eczema
  • Treat secondary infection
  • Ophthalmology input if peri-ocular disease
  • In adults consider underlying immunocompromise
45
Q

Who is staphylococcal scalded skin syndrome common in?

A

Common in children, can occur in immunocommpromised adults

46
Q

How does SSSS present?

A
  • Diffuse erythematous rash with skin tenderness
  • More prominent in flexures
  • Blistering and desquamation follows
  • Fever and irritability
47
Q

How is SSSS treated?

A

Require admission for IV antibiotics initially and supportive care
Generally resolves over 5-7 days with treatment

48
Q

What may SSSS follow?

A

Initial staph infection as Staphylococcus produces toxin which targets Desmoglein 1

49
Q

What is urticarial?

A

Weal or hive

50
Q

How does urticarial present?

A
  • Central swelling of variable size, surrounded by erythema. Dermal oedema
  • Itching, sometimes burning
51
Q

How long does urticarial usually last?

A

Fleeting nature, duration: 1- 24 hours

52
Q

What is angioedema?

A

Deeper swelling of the skin or mucous membranes

53
Q

What causes urticarial?

A

Histamine released into dermis

54
Q

What are the causes of acute urticaria (<6 week history)?

A
  • Idiopathic (50%)
  • Infection, usually viral (40%)
  • Drugs, IgE mediated (9%)
  • Food, IgE mediated (1%)
55
Q

How is acute urticaria treated?

A
  • Oral antihistamine (Taken continuously, Up to 4 x dose)
  • Short course of oral steroid may be of benefit if clear cause and this is removed
  • Avoid opiates and NSAIDs if possible (exacerbate urticaria)
56
Q

What are the causes of chronical urticaria (>6 week history)?

A
  • Autoimmune/Idiopathic (60%)
  • Physical (35%)
  • Vasculitic (5%)
  • Rarely a Type 1 hypersensitivity reaction
57
Q

How is chronic urticaria managed?

A
  • Limited role for oral steroids. No good evidence base.
  • Step up anti-histamine approach
  • Consider anti-leukitrine
  • Consider immunomodulant such as omalizumab (Monoclonal antibody to IgE, mechanism of action unknown)

Systems: Dermatology AB (11 decks)

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