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year 2 dermatology > Acute and Emergency Dermatology > Flashcards

Acute and Emergency Dermatology Flashcards

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Dermatology Board Prep flashcards
1
Q

describe the properties of skin as an organ?

A
  • The skin is the largest organ in the body
  • 10% of body mass of average person
  • Like any organ the skin can fail
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2
Q

A

A

sepsis

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3
Q

B

A

Hypo- and Hyper- thermia

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4
Q

C

A

Protein and fluid loss

Renal impairment

Peripheral vasodilation

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5
Q

what is Erythroderma?

A

Erythroderma is the term used to describe intense and usually widespread reddening of the skin due to inflammatory skin disease

A descriptive term rather than a diagnosis

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

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6
Q

what are the causes of erythroderma?

A

Psoriasis

Eczema

Drugs

Cutaneous Lymphoma

Hereditary disorders

Unknown

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7
Q

what are the principles of management for 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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8
Q

are drug reactions common or rare?

A

Common - 5% of inpatients

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9
Q

when do drug reacitons occur?

A

Can occur to any drug

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

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10
Q

what are examples of a mild and severe drug reactions?

A
  • Mild - Morbilliform exanthem
  • Severe - Erythroderma, Stevens Johnson Syndrome/Toxic epidermal necrolysis, DRESS
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11
Q

What is Stevens Johnson Syndrome/Toxic Epidermal Necrolysis?

A
  • 2 conditions which are thought to form part of the same spectrum
  • Rare:
  • 1-2/million/year (SJS)
  • 0.4-1.2/million/year (TEN)

(pictures showing Stevens Johnson Syndrome (SJS) & Toxic Epidermal necrolysis (TEN))

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12
Q

Stevens Johnson Syndrome/Toxic Epidermal Necrolysis can occur secondary to what drugs?

A

Antibiotics

Anticonvulsants

Allopurinol

NSAIDs

Can be delayed onset

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13
Q

In Stevens Johnson Syndrome/Toxic Epidermal Necrolysis what percentage of skin is usually affected?

A
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14
Q

what are the clinical features of SJS?

A
  • Fever, malaise, arthralgia (pain in a joint)
  • 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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15
Q

what are the clinical features of Toxic Epidermal Necrolysis?

A
  • Often presents with prodromal febrile illness
  • Ulceration of mucous membranes
  • Rash:
  • May start as macular, purpuric or blistering
  • Rapidly becomes confluent
  • Sloughing off of large areas of epidermis - ‘desquamation’ (skin peeling) > 30% BSA
  • Nikolsky’s sign may be positive
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16
Q

what is the management of SJS and Toxic Epidermal Necrolysis?

A
  • Identify and stop culprit drug as soon as possible
  • Supportive therapy

Not common so no high quality trials to see what works:

  • ?High dose steroids
  • ?IV immunoglobulins
  • ?Anti-TNF therapy
  • ?Ciclosporin
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17
Q

what is the prognosis of SJS and TEN and how is it determined?

A

Mortality up to 10% (SJS)/30% (TEN)

SCORTEN:

  • Age >40
  • Malignancy
  • Heart rate >120
  • Initial epidermal detachment >10%
  • Serum urea >10
  • Serum glucose >14
  • Serum bicarbonate <20
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18
Q

what are the long term complications of SJS and TEN?

A

Pigmentary skin changes

Scarring

Eye disease and blindness

Nail and hair loss

Joint contactures

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19
Q

what is Erythema Multiforme?

A

Hypersensitivity reaction usually triggered by infection - Most commonly HSV, then Mycoplasma pneumonia

SJS and TEN are drug related but this is viral related

20
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

SJS lesions are atypical target lesion but in this there is typical target lesions

21
Q

How do you treat Erythema Multiforme?

A
  • Self limiting and resolves over 2 weeks
  • Symptomatic and treat underlying cause
22
Q

How common is Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS), what is its prognosis and how long is its onset?

A
  • Incidence estimated between 1 in 1000-10,000
  • Mortality up to 10%
  • Onset 2-8 weeks after drug exposure

DRESS can be up to 2 months later from drug where as TEN tends to be quite soon after

DRESS and TNE are the 2 most severe type of drug reactions you do not want to miss

23
Q

what are the clinical features of DRESS?

A
  • Fever and widespread rash
  • Eosinophilia and deranged liver function
  • Lymphadenopathy
  • +/- other organ involvement
24
Q

what is the treatment of DRESS?

A
  • Stop causative drug
  • Symptomatic and supportive
  • Systemic steroids
  • +/- Immunosuppression or immunoglobulins
25
Q

photos showing blistering:

A

Blistering conditions can be due to many things but we are going to think about autoimmune conditions

26
Q

What is pemphigus?

A

Pemphigus is a rare skin disorder characterized by blistering of your skin and mucous membranes

27
Q

what are the clinical features of pemphigus?

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

28
Q

how is the pathology of pemphigus seen?

A
  • Immunofluorescence
  • Histopathology

Pictures:

Split in epidermis seen on the right photo

Left is key test for diagnosing blistering disorder

Left is strongly positive for IgG

29
Q

how adn where are blisters formed in pemphigoid?

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

This one is deeper

Where as last one was in-between the individual keratinocyte

This is type of blister seen on foot due to shoe

30
Q

what is the difference between Pemphigus vs Pemphigoid?

A

Both are autoimmune attacks

Pemphigoid tend to be well

Both immunosuppressants as treatment

pemphigus - cell to cell adhesion is impaired, affects individual keratinocytes

pemphigoid - deeper, affects between the dermis and epidermis

31
Q

what are the causes of Erythrodermic psoriais and Pustular Psoriasis?

A
  • Can occur without previous history of psoriasis
  • Common causes:
  • Infection
  • Sudden withdrawal of oral steroids or potent topical steroid
32
Q

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

A
  • Rapid development of generalised erythema, +/- clusters of pustules
  • Fever, elevated WCC
33
Q

what is the treatment of Erythrodermic psoriais and Pustular Psoriasis?

A
  • Exclude underlying infection (swab), bland emollient, avoid steroids
  • Often require initiation of systemic therapy
34
Q

what is Eczema Herpeticum? and its symptoms?

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

Lots of tiny vesicles – fluid collections

Very painful

35
Q

what is the treatment and management of Eczema Herpeticum?

A
  • Treatment dose Aciclovir
  • Mild topical steroid if required to treat eczema
  • Treat secondary infection
  • Ophthalmology input if peri-ocular disease - emergency
  • In adults consider underlying immunocompromise
36
Q

who is Staphylococcal Scalded Skin Syndrome common in? and what is the initial infection?

A
  • Common in children, can occur in immunocommpromised adults
  • Initial Staph. infection - May be subclinical

Infective complication

Confused with TEN

But here it is in children

37
Q

what are the clinical features of Staphylococcal Scalded Skin Syndrome?

A
  • Diffuse erythematous rash with skin tenderness
  • More prominent in flexures
  • Blistering and desquamation (skin peeling) follows - Staphylococcus produces toxin which targets Desmoglein 1
  • Fever and irritability
38
Q

What is the treatment of Staphylococcal Scalded Skin Syndrome?

A
  • Require admission for IV antibiotics initially and supportive care
  • Generally resolves over 5-7 days with treatment
39
Q

what is Urticaria?

A

Urticaria, also known as hives, is an outbreak of swollen, pale red bumps or plaques (wheals) on the skin that appear suddenly – either as a result of the body’s reaction to certain allergens, or for unknown reasons. Hives usually cause itching, but may also burn or sting

40
Q

what are other names for Urticaria?

A

Weal, wheal or Hive

41
Q

What does Urticaria cause?

A

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

itching, sometimes burning - Histamine release into dermis

fleeting nature, duration: 1- 24 hours

42
Q

what is Angioedema?

A

Deeper swelling of the skin or mucous membranes

43
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%
44
Q

What is the treatment of Acute Urticaria (< 6 week History)?

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)
45
Q

What are the causes of Chronic Urticaria (> 6 week history)?

A
  • Autoimmune/Idiopathic - 60%
  • Physical - 35%
  • Vasculitic - 5%
  • Rarely a Type 1 hypersensitivity reaction
46
Q

What is the management of Chronic Urticaria?

A

Limited role for oral steroids. No good evidence base

Omalizumab:

  • Monoclonal antibody to IgE, mechanism of action unknown
  • Recently licensed for use in chronic spontaneous urticaria
  • 300mg S/C ever 4 weeks
  • £6000 per year per patient

year 2 dermatology (11 decks)

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