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*Dermatology > Acute and Emergency > Flashcards

Acute and Emergency Flashcards

1
Q

Skin function = mechanical barrier to infection; what happens when this fails?

A

Sepsis

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2
Q

Skin function = temperature regulation; what happens when this fails?

A

Hypo- and hyper- thermia

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3
Q

Skin function = fluid and electrolyte balance; what happens when this fails?

A
  • Protein and fluid loss
  • Renal impairment
  • Peripheral vasodilation
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4
Q

Erythroderma is a descriptive term rather than a diagnosis - what is it defined as?

A

‘Any inflammatory skin disease affecting >90% of total skin surface’

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5
Q

What are 6 possible causes of erythroderma?

A 
Psoriasis
Eczema
Drugs
Cutaneous lymphoma 
Hereditary disorders
Unknown
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6
Q

What are the principles of management in erythroderma (10))?

A
  • Appropriate setting (ITU/burns unit (>5%))
  • Remove offending drugs
  • Careful fluid balance
  • Good nutrition
  • Temp regulation
  • Emollients (paraffin = 50:50 Liquid: White soft)
  • Oral and eye care
  • Anticipate and treat infection
  • Manage itch
  • Disease specific therapy - treat underlying cause
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7
Q

When do drug reactions commonly occur?

A

1-2 weeks after drug

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8
Q

What is a mild drug reaction?

A

Morbilliform exanthem

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9
Q

What are some severe drug reactions?

A

Erythroderma
Steven Johnson Syndrome/Toxic epidermal necrolysis - worst
DRESS

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10
Q

What are Steven Johnson Syndrome and Toxic Epidermal Necrolysis thought of as?

A

2 conditions which form part of the same spectrum

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11
Q

What drugs can cause SJS/TEN?

A

Abx
Anticonvulsants
Allopurinol
NSAIDs

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12
Q

What are the surface of epidermal attachment boundaries between SJS and TEN?

A

SJS <10%
SJS-TEN overlap 10-30%
TEN 30%

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13
Q

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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14
Q

How does a patient with TEN often present?

A

With prodromal febrile illness
Ulceration of mucous membranes
Rash (sloughing off of large areas of epidermis - desquamation; Nikolsky’s sign may be positive)

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15
Q

What is used to score TEN patients?

A

SCORTEN

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16
Q

Try n name the components of SCORTEN

A 
Age>40
Malignancy 
Heart rate >120
Initial epidermal detachment >10%
Serum urea >10%
Serum glucose >14
Serum bicarbonate <20
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17
Q

What are some long term complications of TEN?

A

Pigmentary skin changes (due to loss of epidermis)
Scarring
Eye disease and blindness (opthalmology comes every day to ward to manage)
Nail and hair loss
Joint contractures

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18
Q

Management for SJS/TEN?

A

Identify and stop culprit drug ASAP

Supportive therapy

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19
Q

TEN does not occur v often so there is little research, but what are some well-tolerated options for drug treatment?

A

High dose steroids
IV immunoglobulins
Anti-TNF therapy (NOT in patients at high risk of infection)
Ciclosporin

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20
Q

What type of reaction is erythema multiforme?

A

Hypersensitivity (usually triggered by infection - most commonly HSV or mycoplasma pneumonia)

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21
Q

What is the presentation of erythema multiforme?

A

Abrupt onset of up to 100s of lesions over 24 hrs

22
Q

Where are the lesions located in erythema multiforme?

A

Distal to proximal
Palms and soles
Mucosal surfaces

23
Q

How do the lesions in erythema multiforme evolve over 2 hours?

A

Pink macules become elevated and may blister in centre (‘target’ lesions)

24
Q

How does erythema resolve?

A

By itself over 2 weeks; self-limiting

Symptomatic - treat underlying cause (often do viral throat swab)

25
What does DRESS stand for?
Drug Reaction with Eosinophilia and Systemic Symptoms
26
When is the onset of DRESS?
2-8 weeks after drug exposure
27
What are clinical features of DRESS?
Fevere and widespread rash Eosinophilia and deranged liver function Lymphadenopathy +/- other organ involvement
28
Management of DRESS?
Stop causative drug (e.g. abx, anticonvulsants) Symptomatic + supportive Systemic steroids (IV/oral) +/- immunosuppression or immunoglobulins
29
What is pemphigus?
Rare group of blistering autoimmune diseases that affect the skin and mucous membranes
30
What is the pathophysiology of pemphigus?
Antibodies targeted at desmosomes
31
Clinical features of pemphigus?
Flaccid blisters, rupture v easily (intact ones may not be seen) Common sites - face, axillae, groin Nikolskys may be +ve Commonly affects mucous membranes Ill defined erosions in mouth; can also affect eyes, nose, genitalia
32
Where are antibodies directed in pemphigoid?
Dermo-epidermal junction
33
How does pemphigoid present?
Intact epidermis forms roof of blister; blisters are usually tense and intact
34
Main differences between pemphigus and pemphigoid?
Pemphigus: uncommon, middle aged, blisters v fragile, mucous membranes affected, may be unwell, treat with systemic steroids Pemphigoid: common,elderly, blisters intact/tense, patients fairly well systemically, topical steroids may be sufficient
35
Common causes of erythrodermic psoriasis and pustular psoriasis?
Infection | Sudden withdrawal of oral steroids or potent topical steroid
36
Presentation of erythrodermic/pustular psoriasis?
Rapid development of generalised erythema, +/- clusters of pustules Fever, elevated WCC
37
What is the management for erythrodermic/pustular psoriasis?
Exclude underlying infection, bland emollient, avoid steroids Often require initiation of systemic therapy - retinoid/immunosuppressant
38
What causes eczema herpeticum?
Disseminated herpes virus infection on a background of poorly controlled eczema
39
What is the common presentation of eczema herpeticum?
Monomorphic blisters and 'punched out' erosions (painful, not itchy) Fever and lethargy Fever, lethargy (grumpy child, not wanting to move)
40
Treatment for eczema herpeticum?
Aciclovir (oral if well; admit and IV if v unwell) Mild topical steroid if required to treat eczema Treat secondary infection Opthalmology input if peri-ocular disease (in adults consider underlying immunocompromie - HIV viral screen etc)
41
What does staphylococcal scalded skin syndrome arise from? How does it work?
Initial Staph. infection | Staphylococcus produces a toxin which targets desmoglein 1
42
Who is SSSS common in?
Children (can occur in immunocompromised adults)
43
How does SSSS present?
Diffuse erythematous rash with skin tenderness; more prominent in flexures; blistering and desquamation follows Fever and irritability
44
How is SSSS managed?
Admission for IV abx initially and supportive care | Generally resolves over 5-7 days w treatment
45
2 key features of urticaria?
Weal, wheal or hive | Angioedema (deeper swelling of skin/mucous membranes)
46
Describe weals in urticaria?
Central swelling of variable size, surrounded by erythema Itchy, sometimes burning (histamine in dermis) Fleeting (duration 1-24hrs)
47
What are the 4 causes of acute urticaria? (<6 week history)
Idiopathic (50%) Infection, usually viral (40%) Drugs, IgE mediated (9%) Food, IgE mediated (1%)
48
What is the management for acute urticaria?
Oral antihistamine (taken continuously, up to 4x dose) Short course of oral steroid may be of benefit if clear cause and this is removed Avoid opiates and NSAIDs is poss (exacerbate it) Test for food allergy - skin prick; or bloods for specific IgE
49
What are the 3 causes of chronic urticaria? (<6 week history)
Autoimmune/idiopathic (60%) Physical (35%) (e.g. heat, cold, pressure) Vasculitic (5%) (rarely - type 1 hypersensitivity)
50
Management plan for chronic urticaria? (4 stages)
(initially identify triggers) 1. Standard does non-sedating H1 antihistamine 2. Higher dose up to 4x recomended or add second antihistamine 3. Consider 2nd line agent, anti-leukotriene, or if angiodema present - tranexamic acid 4. Consider immunomodulant (e.g. omalizumab, cyclosporin) (no evidence for oral steroids)
51
Omalizumab is a monoclonal antibody to what?
IgE
52
Conclusion point - principles of management of skin failures are the same regardless of cause... (4)
- good fluid and electrolyte balance - temp regulation - emollients - anticipate and treat infection

*Dermatology (11 decks)

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