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Dermatology Crash Course > Acute and Emergency Dermatology > Flashcards

Acute and Emergency Dermatology Flashcards

1
Q

Name some functions of skin which may fail?

A

Barrier = Sepsis

Thermoregulation = Hyper or Hypothermia

Fluid/Electrolyte Balance = Loss of fluid, renal impairment, protein loss, vasodilation.

Can lead to Cardiac Failure.

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2
Q

What is Erythroderma?

A

Shows that skin failure has happened BUT IS NOT A DIAGNOSIS ITSELF - wouldnt diagnose someone with erythroderma.

Any inflamm condition which causes redness on >90% of the body = erythrodermic.

Very dangerous in elders.

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3
Q

What are the causes of Erythroderma?

A

Psoriasis

Eczema

Drugs

Cutaneous lymphoma

Hereditary disorders

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4
Q

What are the principles of management of Skin Failure/Erythroderma?

A

Admit to ICU/Burns Unit

Remove offending drugs

Maintain fluid balance

Good nutrition (losing lots of protein)

Ensure patient remains at suitable temperature (humidity and temp control)

Emollients - 50:50 liquid paraffin: white soft paraffin

Oral and eye care - to avoid long term effects

Anticipate and treat infection

Manage itch

Disease specific therapy; treat underlying cause (e.g - eczema, psoriasis, cutaneous lymphoma)

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5
Q

When do drug reactions resulting in skin symptoms often occur?

A

Commonly 1-2 weeks after drug - within 72 hours if re-challenged

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6
Q

What are the mild and severe forms of drug reactions?

A

Mild - morbilliform exanthem

Severe - Erythroderma, stevens johnson syndrome/toxic epidermal necrolysis, DRESS

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7
Q

What causes the onset of Stevens Johnson Syndrome and Toxic Epidermal Necrolysis?

A

Secondary to drugs -

–Antibiotics

–Anticonvulsants

–Allopurinol

–NSAIDs

Vital to recognise and treat - stop offending drugs.

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8
Q

What are the clinical features of SJS (Mild)?

A

Lost Epidermis and crusted erosions.

•Fever, malaise, arthralgia

•Rash

–Maculopapular, target lesions, blisters

–Erosions covering <10% of skin surface

•Mouth ulceration

–Greyish white membrane

–Haemorrhagic crusting

•Ulceration of other mucous membranes

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9
Q

Briefly describe TENS (Severe)?

A

Severe drug reaction with erythema/ulceration which covers >30% of body

Requires ITU setting, airway support, large haemorrhagic erosions, almost complete skin involvement

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10
Q

What is the clinical presentation of Toxic Epidermal Necrolysis?

A

Ulceration of mucous membranes

Rash:

–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 - rub finger across skin and it comes off

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11
Q

What is the management for TEN?

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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12
Q

What score is used to determine the prognosis of TEN?

A

SCORTEN

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

Score 5 or more = >90% mortality

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13
Q

What are the long term complications of TEN?

A

–Pigmentary skin changes

–Scarring

–Eye disease and blindness

–Nail and hair loss

–Joint contactures

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14
Q

What is erythema multiform?

A

Abrupt onset of 100s of lesions over 24 hours - hypersensitivty reaction usually triggered by infection (HSV and mycoplasma pneumonia)

Think of as diff condition, similar rash to SJS but its due to viral trigger NOT DRUGS. These patients do much better than SJS and TEN patients.

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15
Q

Where are the lesions located in erythema multiforme?

A

Go from distal to proximal

Start at the palms and the soles

Includes mucosal surfaces

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16
Q

What happens to the lesions over time?

A

They evolve over 72 hours - pink macules become elevated and may blister in the centre

Resolves over 2 weeks - dont treat

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17
Q

What does DRESS stand for?

A

Drug reaction with eosinophilia and systemic symptoms

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18
Q

What is the onset of DRESS?

A

2-8 weeks after drug exposure

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19
Q

What are the clinical featrures of DRESS?

A

Fever and widespread rash

Eosiniphilia and deranged liver function

Lymphadenopathy

Possible involvement of other organs

20
Q

What is the management for DRESS?

A

Stop causative drug

Treat symptoms

Systemic steroids

Possible immunosuppressants or immunoglobulins

21
Q

Describe Pemphigus?

A

Split more superficial than in Pemphigoid. Split is in epidermis.

  • Antibodies targeted at desmosomes
  • Skin – flaccid blisters, rupture very easily
  • Intact blisters may not be seen
  • Common sites – face, axillae, groins
  • Nikolsky’s sign may be +ve
22
Q

Describe Pemphigoid?

A
  • Antibodies directed at dermo-epidermal junction
  • Intact epidermis forms roof of blister
  • Blisters are usually tense and intact – have to pop them to get rid of
  • Usually older patients who get it
23
Q

Where are antibodies directed in Pemphigoid?

A

•Antibodies directed at dermo-epidermal junction

24
Q

What are the differences between Pemphigus and Pemphigoid?

A
25
Q

What are the causes of erythrodermic psoriasis and pustular psoriasis?

A

Infection

Sudden withdrawal of oral steroids or potent topical steroid

26
Q

What are the clinical features of Erythrodermic psoriais and Pustular Psoriasis?

A
  • Rapid development of generalised erythema, +/- clusters of pustules
  • Fever, elevated WCC
27
Q

What is the management of erythrodermic psoriasis and pustular psoriasis?

A

Exclude underlying infection, blsnd emollient and avoid steriods

Often requires initiation of systemic therapy

28
Q

What causes eczema herpeticum?

A

•Disseminated herpes virus infection on a background of poorly controlled eczema

29
Q

What are the clinical features of eczema herpeticum?

A

•Monomorphic blisters and “punched out” erosions

–Generally painful, not itchy

•Fever and lethargy

30
Q

What is the treatment for eczema herpeticum?

A

Treatment dose aciclovir

Mild topical steroid if required to treat eczema

Treat secondary infection

Ophthalmology input if peri-occular disease

In adults consider underlying immunocompromise

31
Q

What is staphylococcal scalded skin syndrome?

A

Initial staph infection, may be subclinical (common in children, but can occur in immunocompromised adults)

Diffuse erythematous rash with skin tenderness

Prominent in flexures

Blistering and desquamation follows

32
Q

What is the disease process of staphylococcal scalded skin syndrome?

A

Staphylococcus produces a toxin which targets desmoglein 1

33
Q

Despite the rash and the blistering, what other symptoms does the patient have?

A

Fever and irritability

34
Q

What is the treatment for staphylococcal scalded skin syndrome?

A

Admission for IV antibiotics initially and supportive care

Generally resolves over 507 days with treatment

35
Q

What is urticaria?

A

–Central swelling of variable size, surrounded by erythema. Dermal oedema

36
Q

What causes the itching / brining feeling of urticaria?

A

Histamine release into the dermis

37
Q

What is the disease progression of urticaria?

A

–fleeting nature, duration: 1- 24 hours

38
Q

What is angioedema?

A

–Deeper swelling of the skin or mucous membranes

39
Q

What are the causes of acute urticaria?

A

Idiopathic

Infection (viral)

Drugs, IgE mediated

Food. IgE mediated

40
Q

What is the treatment for acute urticaria?

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)
41
Q

What is the definition of chronic urticaria?

A

History of over 6 weeks

42
Q

What are the causes of chronic urticaria?

A

Autoimmune / idiopathic (60%)

Physical (35%)

Vasculitic (5%)

Rarely a type 1 hypersensitvity reaction

43
Q

What is the management of chronic urticaria?

A
44
Q

Describe % of detached epidermis in SJS vs TEN?

A

<10% = SJS

10-30% = Overlap grey area

>30% = TEN

45
Q

Name 2 derm presentations which involve blisters?

A

PEMPHIGUS

PEMPHIGOID

In blistering, at dermal epidermal junction, desmosomes and anchoring proteins are under AI attack, so split appears and epidermis lifts off.

Dermatology Crash Course (11 decks)

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