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Phase 4 > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is psoriasis?

A

Autoimmune, inflammatory and proliferative skin disease?

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2
Q

What is the epdemiology of psoriasis?

A

Two peaks: young adults, or 60s/70s.

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3
Q

What is the pathophysiology of psoriasis?

A

Abnormal T cell recruitment - cytokine mediated.

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4
Q

What are the sub-types of psoriasis?

A

Chronic plaque
Guttate
Generalised pustular
Palmo-plantar pustular

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5
Q

Which sites of the body are most likely to be affected by psoriasis?

A

Scalp
Face
Flexures
Genitalia

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6
Q

What is the management of psoriasis?

A 
Emollients
Vitamin D analogues (e.g. dovobet)
Topical tar preparations (e.g. exorex lotion)
Topical de-scaling agent
2nd line:
Phototherapy (UVB)
Ciclosporin
Methotrexate
Acitretin
3rd line:
Biological therapy
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7
Q

What are the complications of psoriasis?

A

Arthropathy

Spondyloarthropathy

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8
Q

Which systemic disease is psoriasis linked with?

A

Inflammatory bowel disease
Cardiovascular disease
Non-alcoholic fatty liver disease

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9
Q

What are the 2 main categories of skin cancer?

A

Cutaneous (malignant) melanoma

Non-melanoma

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10
Q

What are the risk factors for malignant melanoma?

A

Skin: type, multiple moles >2mm, atypical moles
UVA and UVB exposure (especially childhood)
Genetics
Increasing age

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11
Q

What is the clinical assessment of a mole?

A

Asymmetry - one half does not match the other half
Border - uneven borders
Colour - variety of colours like brown, tan, or black
Diameter - grows larger than the size of a pencil eraser
Evolution - change in size, shape, colour, elevation, another trait or new symptom

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12
Q

What are the types of cutaneous melanoma?

A 
Superficial spreading
Nodular
Lentigo maligna
Acral lentigrous
Desmoplastic
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13
Q

What is the staging score of a melanoma?

A 
Breslow depth:
<1.0 mm
1 - 2 mm
2-4 mm
>4mm
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14
Q

What is the management of a melanoma?

A 
Lymphatic examination
Wide local excision of biopsy site (1cm margin if <1mm thick, 1-2cm if 1-2mm thick)
If it has spread:
Adjuvant radiotherapy
Immunotherapy
BRAF and MINK inhibitors
Palliative care input
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15
Q

How is TNM classification of a melanoma carried out?

A

Sentinal node biopsy

Imaging (CT-head/CAP)

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16
Q

What is the follow up of a melanoma?

A

Stage 0: no follow up after initial treatment
Stage 1A: 2-4 reviews over 12 month period
Stage 1B-IIC: 3 monthly reviews for 3 years, 6 monthly reviews for 2 years
Stage III >: 3 monthly reviews for 5-10 years

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17
Q

What is a squamous cell carcinoma?

A

Epidermal tumour (arises from keratinising cells or epidermal appendages).

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18
Q

What does a squamous cells carcinoma look like?

A

Nodular keratinising or crusted tumour, that may ulcerate or an ulcer without evidence of keratinisation.

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19
Q

What are the risk factors for developing a squamous cell carcinoma?

A

Fair skin
UV/ionising radiation exposure
Immunosuppresion
HPV infection

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20
Q

What is the management of a squamous cell carcinoma?

A

Cryotherapy
Surgical excision
Radiotherapy
Chemotherapy

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21
Q

What are the risk factors for a basal cell carcinoma?

A

UV exposure
Fair skin
Age

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22
Q

What is the management of a basal cell carcinoma?

A 
Superficial:
Cryotherapy
Topical creams
Excision biopsy
Deeper:
Mohs micrographic surgery
Radiotherapy
Chemotherapy.
Sun protection
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23
Q

What is Bowen’s disease a precursor to?

A

Squamous cell carcinoma

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24
Q

What is actinic keratoses a precursor to?

A

Squamous cell carcinoma

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25
Q

Describe a keratoacanthoma.

A

Rapid growth

Central depression

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26
Q

What is pathophysiology of eczema?

A

Skin barrier breakdown:
- filaggrin gene mutations
- defective keratinocytes on outer epidermis
Immune dysregulations:
- secondary to enhanced antigen penetration through defective epidermal barrier

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27
Q

What are the key diagnostic features of eczema?

A

Itch
Onset <2 years old
Flexural sites affected
Personal or family history of atopy

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28
Q

What is the management of eczema?

A 
Regular emollients (creams/gels/ointments): applied downwards, in direction of hairgrowth.  Ointments less well tolerated, but no preservatives. 
Bath/shower using emollients (antiseptic/anti-pruritic properties) instead of soaps/gels
Avoid coarse clothes/extreme cold/triggers
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29
Q

What is the management of acute flares of eczema?

A

Moderate/potent topical steroid e.g. elocon (mometasone) cream - lowest appropriate potency for site/severity, apply steroid cream 30 mins before emollient
Antihistamine
Consider need for systemic antibiotic

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30
Q

Which immunomodulators can be used in eczema?

A 
Topical protopic (tacrolimus) and elidel (pimecrolimus). 
 - calcineurin inhibitors
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31
Q

When should immunomodulators be considered?

A

If skin atrophy, large surface area affected, skin around eyes affected

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32
Q

What are the second line treatments for eczema?

A 
Phototherapy
Immunosuppressants:
- oral steroids
- azathiprine
- ciclosporin
- alitretinoin
- monoclonal antibodies
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33
Q

What are the complications associated with eczema?

A

Secondary infections:

  • staph aureus
  • viral warts
  • molloscum
  • eczema herpeticum
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34
Q

Describe the presentation of eczema herpeticum?

A 
Clustered vesicles/punched out monommorphic erosions
Fever
Pain
Lethargy
Rapid progression
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35
Q

What is the management of eczema herpeticum.

A

PO aciclovir

Consider opthalmological assessment.

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36
Q

What is acne?

A

Inflammatory disease of pilosebaceous follicle.

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37
Q

What percentage of teenagers are affected by acne?

A

80%

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38
Q

What is the pathophysiology of acne?

A

Hormonally driven:

Flares at start of menstrual cycle/pregnancy

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39
Q

Which conditions are associated with acne?

A

PCOS

Endocrine disturbances

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40
Q

What are the modifiable risk factors for acne?

A

Drugs, especially anabolic steroids.

Cosmetics (oil-based)

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41
Q

What are the clinical findings in acne?

A 
Greasy skin (seborrhoea)
Non-inflamed lesions (comedones)
Inflammed lesions (papules/pustules/nodules)
Scarring
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42
Q

What is the first line management of acne?

A 
Cleanse no more than twice a day (soap and water)
Non greasy moisturiser, if skin dry
Topical anti-microbial
Topical retinoid
Systemic antibiotic
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43
Q

What is the second line management of acne?

A

Anti-androgens in females (typically Dianette)
Oral isotretinoin (Roaccutane)
High dose oral antibiotics
Short course of corticosteroids

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44
Q

What is the management of scarring due to acne?

A

Topical silicone gels
Topical steroids
Ablative and pulsed dye laser therapy
Intradermal collagen injections

45
Q

What is rosacea?

A

Chronic rash involving central face

46
Q

What is the typical onset of rosacea?

A

30-60 years old

47
Q

What aggravates rosacea?

A

Facial creams/oils

Topical steroids

48
Q

What is the first line management of rosacea?

A 
Avoid topical steroids
Avoid oil based moisturisers/make up
Sunscreen
Tetracycline antibiotics (6-12 week courses)
49
Q

What is the second line management of rosacea?

A

Topics - metronidazole gel or azelaic acid cream/lotion
NSAIDs
Isotretinoin (usually a lose dose long term to control acne)
Anti-flushing agents (clonidine, carvediolol)

50
Q

What is the scarring management in rosacea?

A

Pulsed light or laser therapy for telangiectasia

Carabon dioxide laser for rhinophyma

51
Q

What is a blister?

A

A fluid filled lesion:
vesicle <5mm
bullae >5mm

52
Q

What causes acute onset blisters?

A

Burn
Trauma
Allergic
Infection

53
Q

What causes chronic blisters?

A

Autoimmune
Inflammatory
Metabolic
Genetic

54
Q

What is the investigations and management of blistering skin conditions?

A

A-E management
Bloods: inflammatory markers, coeliac serology, autoantibody screen
Blood cultures
Swabs (bacterial/viral)
Porphyrin testing (urine, stool, blood)
Skin biopsy (intact blister and normal skin): pathology and direct immunofluorescence

55
Q

What are the commonest aetiologies of blisters?

A

Infective:

  • impetigo
  • herpes simplex
  • herpes zoster

Autoimmune:

  • bullous pemphigoid
  • pemphigoid vulgaris

Physical:

  • bites
  • burns
  • trauma
  • inflammatory
56
Q

What is impetigo?

A

Acute bacterial skin infection with s. aureus

57
Q

What does impetigo look like?

A

Pustules and honey coloured erosions

58
Q

What is the pathophysiology of impetigo?

A

Bullae develops due to staph toxins, which target desmosomes

59
Q

Who is most at risk of impetigo?

A

School-children

Immunosuppressed

60
Q

What are the complications of impetigo?

A 
Cellulitis
Rheumatic fever
Staphylococcal scalded skin syndrome
Toxic shock syndrome
Post strep glomerulonephritis
61
Q

What is the treatment of impetigo?

A

Anti-septics

Antibiotics

62
Q

What are the two subtypes of herpes simplex?

A

HSV-1: oral/facial

HSV-2: PV/PR

63
Q

What does herpex simplex look like?

A

Painful vesicles, ulcers, redness and swelling with fever and lymphadenopathy

64
Q

How can a diagnosis of herpex simplex be confirmed?

A

PCR viral swab

65
Q

What are the complications of herpes simplex?

A

Eczema herpeticum
Erythema multiforme
Meningitis

66
Q

What is the treatment of herpes simplex?

A

Supportive

Oral/IV antivirals

67
Q

What does herpes zoster (shingles) look like?

A

Localised, blistering, painful rash.

68
Q

What is the distribution of herpes zoster?

A

Dermatomal

69
Q

Who gets herpes zoster?

A

Adults

Immunosuppressed

70
Q

What are the typical areas to get herpes zoster?

A

Chest
Neck
Forehead
Lumbar/sacral

71
Q

What are the complications of herpes zoster?

A

Eye
Facial nerve palsy
Encephalitis
Post-herpetic neuralgia

72
Q

What is the treatment of herpes simplex?

A

Antivirals
Capsaicin cream
Analgesia

73
Q

What is the pathophysiology of bullous pemphigoid?

A

Autoantibodies form against antigens between epidermis and dermis

74
Q

Who gets bullous pemphigoid?

A

Elderly

75
Q

What does bullous pemphigoid look like?

A

Tense blisters

Erythema

76
Q

Where on the body is bullous pemphigoid found?

A

Trunk

Limbs

77
Q

What is the treatment for bullous pemphigoid?

A

Wounds dressings
Topical steroids
Nicotinamide
Immunosuppressants (methotrexate)

78
Q

What are the triggers for bullous pemphigoid?

A

Spironolactone
Neuroleptics
UVB

79
Q

What is the pathophysiology of pemphigus vulagaris?

A

Autoantibodies against epidermal antigens (intra-epidermal split)

80
Q

Who is most likely to get pemphigus vulgaris?

A

Middle-aged people

81
Q

What does pemphigus vulgaris look like?

A

Flaccid

Erosions/crusts

82
Q

What is the treatment of pemphigus vulgaris?

A

High dose oral steroids
Immunosuppressants (methotrexate)
Plasmapheresis
IV-immunoglobulins

83
Q

What are the triggers for pemphigus vulagaris?

A

Drugs (ACEi)

Paraneoplastic (lymphoma)

84
Q

What is dermatitis herpetiforms?

A

Extremely itchy rash.

Intact vesicles

85
Q

What is dermatitis herpetiforms exacerbated by?

A

Gluten

86
Q

What should investigations look for in suspected dermatitis herpetiforms?

A

IgA anti-endomysial antibody

TTG auto-antibodies

87
Q

What is the treatment for dermatitis herpetiforms?

A

Dapsone (itching will subside in 48-72 hours)

Gluten-free diet

88
Q

What are the commonest examples of blistering and acute skin failure?

A

Eczema herpeticum
Staphylococcal scalded skin syndrome
Severe mucocutaneous adverse reactions

89
Q

Give 5 examples of severe mucocutaneous adverse reactions.

A
  1. Anaphylaxis/angio-oedema
  2. Red man syndrome
  3. Steven-Johnston syndrome
  4. Toxic epidermal necrolysis
  5. D.R.E.S.S.
90
Q

Who is most at risk of staphylococcal scalded skin syndrome?

A

Infants/children
Elderly
Immunosuppressed

91
Q

What is the pathophysiology of staphylococcal scalded skin syndrome?

A

Staph release epidermolytic toxins, cleaves the skin high in epidermis

92
Q

What is seen on examination in staphylococcal scalded skin syndrome?

A

Erythroderma (flexures/periorbital), superficial blisters (differentiates from TEN)

93
Q

What is the treatment of staphylococcal scalded skin syndrome?

A

Flucloxacillin

94
Q

What are the clinical features of severe mucocutaneous adverse reactions?

A 
Airway swelling
Wheeze/stridor/dyspnoea
Hypotension
Pyrexia (<40C)
Distress/pain
Mucocutaneous - erythroderma +/- scale, swelling, urticaria, erosions, lymphadenopathy
Vasculitis: purpura
95
Q

What is found on investigation of severe mucocutaneous adverse reactions?

A

Eosinophilia
Lymphocytosis
LFTs deranged

96
Q

What is the general management of severe mucocutaneous adverse reactions?

A

Withdraw offending drug
Urgent skin biopsy
Supportive management

97
Q

What is the clinical presentation of red man syndrome?

A 
Erythema
Fushing
Itch
Angio-oedema
Dyspnoea
Chest pain
Hypotension
98
Q

What is the pathophysiology of red man syndrome?

A

Anaphylactoid (not IgE-mediated) reaction

Histamine release from mast cells/basophils

99
Q

What are typical offending drugs of red man syndrome?

A

Ciprofloxacin
Rifampicin
Teicoplanin

100
Q

When does red man syndrome tend to occur?

A

Several weeks after offending drug started

Can occur acutely (post-vancomycin infusion)

101
Q

What is stevens-johnson syndrome?

A

Painful, erythematous ‘drug rash’ with mucosal involvement

102
Q

What is found on examination of stevens-johnson syndrome?

A

Tender ‘erythema-multiforme’ like rash. Severe mucosal blistering and erosions
May also involve respiratory/GI tract.

103
Q

When does stevens-johnson syndrome or severe epidermal necrosis occcur?

A

2-3 weeks after drug started

104
Q

Which drugs can cause stevens-johnson syndrome or severe epidermal necrosis?

A

Allopurinol
NSAIDs
AEDs
Penicillins/cephalosporins

105
Q

What is the diagnostic criteria for D.R.E.S.S. (drug rash, eosinophilia, systemic symptoms)

A 
Acute drug rash (variable)
Pyrexia >38
Lymphadenopathy
Eosinophilia +/- lymphocytosis
Systemic involvement (hepatitis, nephritis, pneumonitis, pericarditis, arthritis)
106
Q

When does D.R.E.S.S develop?

A

1-2 months after drug started.

107
Q

Which drugs tend to cause D.R.E.S.S.?

A

Dapsone
AEDs
Allopurinol
Calcium-channel blockers

108
Q

What is the mortality rate in D.R.E.S.S.?

A

10%

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