Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

*Dermatology > Acute and Emergency > Flashcards

Acute and Emergency Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
1
Q

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

A

Sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Hypo- and hyper- thermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A
  • Protein and fluid loss
  • Renal impairment
  • Peripheral vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are 6 possible causes of erythroderma?

A 
Psoriasis
Eczema
Drugs
Cutaneous lymphoma 
Hereditary disorders
Unknown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When do drug reactions commonly occur?

A

1-2 weeks after drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a mild drug reaction?

A

Morbilliform exanthem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some severe drug reactions?

A

Erythroderma
Steven Johnson Syndrome/Toxic epidermal necrolysis - worst
DRESS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

2 conditions which form part of the same spectrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What drugs can cause SJS/TEN?

A

Abx
Anticonvulsants
Allopurinol
NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical features of SJS?

A

Fever, malaise, arthralgia
Rash
Mouth ulceration (greyish white membrane, haemorrhagic crusting)
Ulceration of other mucous membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is used to score TEN patients?

A

SCORTEN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Management for SJS/TEN?

A

Identify and stop culprit drug ASAP

Supportive therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What type of reaction is erythema multiforme?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

What does DRESS stand for?

A

Drug Reaction with Eosinophilia and Systemic Symptoms

26
Q

When is the onset of DRESS?

A

2-8 weeks after drug exposure

27
Q

What are clinical features of DRESS?

A

Fevere and widespread rash
Eosinophilia and deranged liver function
Lymphadenopathy
+/- other organ involvement

28
Q

Management of DRESS?

A

Stop causative drug (e.g. abx, anticonvulsants)
Symptomatic + supportive
Systemic steroids (IV/oral)
+/- immunosuppression or immunoglobulins

29
Q

What is pemphigus?

A

Rare group of blistering autoimmune diseases that affect the skin and mucous membranes

30
Q

What is the pathophysiology of pemphigus?

A

Antibodies targeted at desmosomes

31
Q

Clinical features of pemphigus?

A

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
Q

Where are antibodies directed in pemphigoid?

A

Dermo-epidermal junction

33
Q

How does pemphigoid present?

A

Intact epidermis forms roof of blister; blisters are usually tense and intact

34
Q

Main differences between pemphigus and pemphigoid?

A

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
Q

Common causes of erythrodermic psoriasis and pustular psoriasis?

A

Infection

Sudden withdrawal of oral steroids or potent topical steroid

36
Q

Presentation of erythrodermic/pustular psoriasis?

A

Rapid development of generalised erythema, +/- clusters of pustules
Fever, elevated WCC

37
Q

What is the management for erythrodermic/pustular psoriasis?

A

Exclude underlying infection, bland emollient, avoid steroids
Often require initiation of systemic therapy - retinoid/immunosuppressant

38
Q

What causes eczema herpeticum?

A

Disseminated herpes virus infection on a background of poorly controlled eczema

39
Q

What is the common presentation of eczema herpeticum?

A

Monomorphic blisters and ‘punched out’ erosions (painful, not itchy)
Fever and lethargy
Fever, lethargy (grumpy child, not wanting to move)

40
Q

Treatment for eczema herpeticum?

A

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
Q

What does staphylococcal scalded skin syndrome arise from? How does it work?

A

Initial Staph. infection

Staphylococcus produces a toxin which targets desmoglein 1

42
Q

Who is SSSS common in?

A

Children (can occur in immunocompromised adults)

43
Q

How does SSSS present?

A

Diffuse erythematous rash with skin tenderness; more prominent in flexures; blistering and desquamation follows
Fever and irritability

44
Q

How is SSSS managed?

A

Admission for IV abx initially and supportive care

Generally resolves over 5-7 days w treatment

45
Q

2 key features of urticaria?

A

Weal, wheal or hive

Angioedema (deeper swelling of skin/mucous membranes)

46
Q

Describe weals in urticaria?

A

Central swelling of variable size, surrounded by erythema
Itchy, sometimes burning (histamine in dermis)
Fleeting (duration 1-24hrs)

47
Q

What are the 4 causes of acute urticaria? (<6 week history)

A

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

48
Q

What is the management for acute urticaria?

A

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
Q

What are the 3 causes of chronic urticaria? (<6 week history)

A

Autoimmune/idiopathic (60%)
Physical (35%) (e.g. heat, cold, pressure)
Vasculitic (5%)
(rarely - type 1 hypersensitivity)

50
Q

Management plan for chronic urticaria? (4 stages)

A

(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
Q

Omalizumab is a monoclonal antibody to what?

A

IgE

52
Q

Conclusion point - principles of management of skin failures are the same regardless of cause… (4)

A
  • good fluid and electrolyte balance
  • temp regulation
  • emollients
  • anticipate and treat infection

*Dermatology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions