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Dermatology > Acute and emergency dermatology > Flashcards

Acute and emergency dermatology Flashcards

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Dermatology Board Prep flashcards
1
Q

What % of body mass of an average person is made up of skin?

A

10%

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2
Q

List some normal functions of skin

A 
–	Mechanical barrier to infection
–	Temperature regulation
–	Fluid and electrolyte balance
–	Vitamin D synthesis
–	Sensation
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3
Q

List some consequences of skin failure

A 
Sepsis
Hypo- and Hyper- thermia
Protein and fluid loss
Renal impairment
Peripheral vasodilation: can  lead to cardiac failure
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4
Q

Define erythroderma

A

A descriptive term rather than a diagnosis

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

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5
Q

What can cause erythroderma?

A 
–	Psoriasis
–	Eczema
–	Drugs
–	Cutaneous Lymphoma
–	Hereditary disorders
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6
Q

How do you manage erythroderma?

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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7
Q

What % of inpatients have drug reactions?

A

2-3%

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8
Q

When do drug reactions usually present on first exposure and second exposure?

A

Commonly 1-2 weeks after drug

Within 72 hours if re-challenged

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9
Q

What is an example of a mild drug reaction?

A

Morbilliform exanthem (rash that looks like measles)

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10
Q

Give some examples of dermatological presentations seen following severe drug reactions

A

Erythroderma
Stevens Johnson Syndrome/Toxic epidermal necrolysis
DRESS

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11
Q

What are some causative drugs to Stevens Johnson Syndrome (SJS) and Toxic Epidermal necrolysis (TEN) reactions?

A

– Antibiotics
– Anticonvulsants
– Allopurinol
– NSAIDs

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12
Q

How can SJS be differentiated from toxic epidermal necrolysis?

A

Prodrome - SJS more like flu, TEN more like fever

TBSA affected - SJS <10%, TEN >30%

Age - SJS more common in kids, TEN in adults

Onset time - SJS slower, TEN very rapid

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13
Q

Describe the clinical features of SJS

A

URI like prodrome: 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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14
Q

Describe the clinical features of toxic epidermal necrolysis

A

Often presents with prodromal febrile illness (fever)

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

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15
Q

Describe a positive Nikolskys sign

A

when slight rubbing of the skin results in exfoliation of the outermost layer.

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16
Q

How do you manage Stevens Johnson syndrome and Toxic epidermal necrolysis?

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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17
Q

Compare the mortality of SJS to toxic epidermal necrolysis

A

10% (SJS)

30% (TEN)

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18
Q

What is SCORTEN?

A

SCORTEN - a severity-of-illness scale with which the severity of certain bullous conditions can be systematically determined. It was originally developed for toxic epidermal necrolysis, but can be used with burn victims, sufferers of Stevens-Johnson Syndrome, cutaneous drug reactions, or exfoliative wounds.

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19
Q

What is the mortality risk associated with a SCORTEN score of 0-1?

A

> 3.2%

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20
Q

What is the mortality risk associated with a SCORTEN score of 2?

A

> 12.2%

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21
Q

What is the mortality risk associated with a SCORTEN score of 3?

A

35.3%

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22
Q

What is the mortality risk associated with a SCORTEN score of 4?

A

> 58.3%

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23
Q

What is the mortality risk associated with a SCORTEN score of 5 or more?

A

> 90%

24
Q

What are some long term complications seen in those who have had SJS or toxic epidermal necrolysis?

A 
o	Pigmentary skin changes
o	Scarring
o	Eye disease and blindness
o	Nail and hair loss
o	Joint contactures
25
Q

Describe erythema multiforme

A

Hypersensitivity reaction usually triggered by infection
Most commonly HSV, then Mycoplasma pneumonia
Abrupt onset of up to 100s of lesions over 24 hours
– Distal => proximal
– Palms and soles
– Mucosal surfaces (EM major)
– Evolve over 72 hours
Pink macules, become elevated and may blister in centre
• “Target” lesions
• Self limiting and resolves over 2 weeks
• Symptomatic and treat underlying cause

26
Q

How do you treat erythema multiform?

A

Self limiting and resolves over 2 weeks

Symptomatic and treat underlying cause (infection)

27
Q

What does DRESS stand for?

A

Drug Reaction with Eosinophilia and Systemic Symptoms

28
Q

Describe Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)

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

When does DRESS occur following drug exposure?

A

2-8 weeks after drug exposure

30
Q

How is DRESS treated?

A

Stop causative drug
Symptomatic and supportive treatment
• Systemic steroids
• +/- Immunosuppression or immunoglobulins

31
Q

Describe pemphigus and where on the body it affects

A
  • 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
  • Commonly affects mucous membranes
  • Ill defined erosions in mouth
  • Can also affect eyes, nose and genital areas
32
Q

Describe pemphigoid

A
  • Antibodies directed at dermo-epidermal junction
  • Intact epidermis forms roof of blister
  • Blisters are usually tense and intact
33
Q

What are the differences between pemphigus and pemphigoid?

A

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

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

34
Q

How is pemphigus treated?

A

Treat with systemic steroids.
Dress erosions.
Supportive therapies

35
Q

How is pemphigoid treated?

A

Topical steroids may be sufficient if localised; systemic usually required if diffuse

36
Q

Describe Erythrodermic psoriasis and Pustular Psoriasis

A

Can occur without previous history of psoriasis
Common causes:
– Infection
– Sudden withdrawal of oral/potent topical steroid

Rapid development of generalised erythema (redness), +/- clusters of pustules
Fever, elevated WCC
• Exclude underlying infection, bland emollient, avoid steroids
• Often require initiation of systemic therapy

37
Q

How is Erythrodermic psoriasis and Pustular Psoriasis treated?

A
  • Exclude underlying infection, bland emollient, avoid steroids
  • Often require initiation of systemic therapy
38
Q

What causes Erythrodermic psoriasis and Pustular Psoriasis commonly?

A

– Infection

– Sudden withdrawal of oral/potent topical steroid

39
Q

Describe the clinical features of Eczema Herpeticum

A

Disseminated herpes virus infection on a background of poorly controlled eczema

Monomorphic blisters and “punched out” erosions
– Generally painful, not itchy

Fever and lethargy

40
Q

How is Eczema Herpeticum treated?

A
  • Treatment dose of Aciclovir
  • Mild topical steroid if required to treat eczema
  • Treat secondary infection
  • Ophthalmology input if peri-ocular disease
  • In adults consider underlying immunocompromise
41
Q

Who are commonly affected by Staphylococcal Scalded Skin Syndrome?

A

Common in children, can occur in immunocommpromised adults

42
Q

Describe Staphylococcal Scalded Skin Syndrome

A

Initial Staph. infection
– May be subclinical

Diffuse erythematous rash with skin tenderness

More prominent in flexures

Blistering and desquamation follows
– Staphylococcus produces toxin which targets Desmoglein 1

Fever and irritability

43
Q

How is Staphylococcal Scalded Skin Syndrome treated?

A

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

44
Q

Describe urticaria

A

Also known as a Weal or Hive:
– Central swelling of variable size, surrounded by erythema. Dermal oedema
– Itching, sometimes burning

Caused by histamine release into dermis
– Fleeting nature, duration: 1- 24 hours

45
Q

Whats the difference between acute and chronic urticaria?

A

Acute - <6 weeks

Chronic - >6 weeks

46
Q

What are some causes of acute urticaria?

A

o Idiopathic - 50%
o Infection, usually viral - 40%
o Drugs, IgE mediated - 9%
o Food, IgE mediated – 1%

47
Q

Whats the most common cause of chronic urticaria?

A

Idiopathic, 50%

48
Q

What % of urticaria is caused by infection (usually viral)?

A

40%

49
Q

What % of urticaria is caused by IgE mediated drug reactions?

A

9%

50
Q

What % of urticaria is caused by IgE mediated food reactions?

A

1%

51
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)

52
Q

What drugs need to be avoided in urticaria?

A

Opiates and NSAIDs - exacerbate urticaria

53
Q

What are some causes of chronic urticaria?

A

Autoimmune/Idiopathic - 60%

Physical trauma - 35%

Vasculitic - 5%

Rarely a Type 1 hypersensitivity reaction

54
Q

What is the most common cause of chronic urticaria?

A

AI/idiopathic

55
Q

How is chronic urticaria treated?

A

o 1st line- standard dose of non-sedating H1 antihistamine
o 2nd line – higher dose antihistamine (up to 4X recommended dose) or add in second antihistamine
o 3rd line – consider a second line agent, such as an anti-leukotriene or, if angioedema is present, use tranexamic acid
o 4th line – consider an immunomodulator e.g. omalizumab, ciclosporin

Also identify any triggers and educate on how to avoid it

56
Q

What are the basic principles of skin failure management?

A

– Good fluid and electrolyte balance
– Temperature regulation
– Emollients
– Anticipate and treat infection

Dermatology (12 decks)

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