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Phase 2 > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Name 3 types of skin cancer.

A
  1. BCC (75%) - in situ, grows slowly.
  2. SCC (20%) - can metastasise, grows rapidly.
  3. Melanoma (5%).
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2
Q

What is Keratoacanthoma?

A

A benign variant of SCC that arises in a hair follicle. It is unlikely to metastasise.
Presents as a dome shaped keratin plug

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3
Q

What is Bowen’s disease?

A

Bowen’s disease is also known as SCC in situ. It is characterised by red and scaly patches.mainly on lower leg

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4
Q

What is the treatment for bowens disease

A

Cautery
Cryotherapy
5-Fluouracil
Photodynamic phototherapy

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5
Q

What is Acitinic keratoses

A

Irregular crusty yellow white warty lesions on sun exposed areas that are premalignant

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6
Q

What is the treatment for actinic keratoses

A

Cautery
Cryotherapy
5-Fluouracil
Photodynamic phototherapy

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7
Q

Where is melanoma commonly found in men and women

A 
Men = back and chest 
Women = Lower legs
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8
Q

Give 5 early signs of melanoma.

A 
MAJOR
1. Enlargement. 
2. Colour change (almost always darkening). 
MINOR 
3. Irregular shape. 
4. Bleeding. 
5. Itching.
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9
Q

What is the ABCDE of melanoma?

A 
Asymmetrical.
Border irregularity. 
Colour variability. 
Diameter >5mm. 
Elevation irregularity.
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10
Q

Give 4 risk factors for melanoma.

A
  1. High density freckles.
  2. Red hair.
  3. > 100 moles.
  4. > 5 atypical moles.
  5. Family history.
  6. Sunlight - intense exposure in early years
  7. Increasing age
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11
Q

Give 4 differential diagnoses for melanoma.

A
  1. Melanocytic neavi.
  2. Seborrhoeic wart.
  3. Freckle.
  4. BCC.
  5. Pyogenic granuloma.
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12
Q

Give 3 factors that can be used to determine the prognosis of melanoma?

A
  1. Breslow’s thickness - the thinner (<1mm) the better.
  2. Younger = better prognosis.
  3. Female = better prognosis.
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13
Q

Describe the progression from melanocytic naevi (mole) to nodular melanoma.

A

Melanocytic naevi -> dysplastic melanocytic naevi -> in situ melanoma -> superficial spreading melanoma -> nodular melanoma.

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14
Q

What is the main cause of all skin cancer?

A

SUN EXPOSURE - UV light.

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15
Q

What is the treatment for malignant melanoma?

A

Surgical excision.
Lymphadenectomy
Adjuvant chemotherapy

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16
Q

Describe the characteristics of squamous cell carcinoma

A

Locally invasive malignant tumour of squamal keratinocytes that produce ulcerated lesions with hard, raised, everted edges
W

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17
Q

where is squamous cell carcinoma usually found

A

in sun exposed areas including the scalp, face, ears and lower leg

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18
Q

Describe the characteristics of basal cell carcinoma

A

Commonest malignant tumour

Tumour of the basal keratinocytes that produces pearly nodules with a rolled telangiectatic edge which may ulcerate

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19
Q

Where might basal cell carcinomas be found

A

Typically on the face in sun exposed areas

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20
Q

Describe the progression of SCC

A

solar/actinic keratosis to Bowens to SCC

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21
Q

Describe the treatment of SCC

A

Excision and radiotherapy to affected nods

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22
Q

Describe the treatment of BCC

A

Excision or cryo/radio for superficial BCC’s

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23
Q

What is psoriasis?

A

Chronic inflammation in the dermis driven by T cells (Th1 and Th17) and cytokines leading to hyperproliferation of keratinocytes and abnormally rapid growth of the epidermis

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24
Q

Describe the epidemiology of psoriasis

A

Peaks in 20s and 50s
Sex F=M
Genetics = 30% have a FH

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25
Q

Describe the pathology of psoriasis

A

Type IV hypersensitivity reaction to unidentified antigen leading to epidermal proliferation due to Th1 cell cytokine up regulation

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26
Q

What are the triggers for psoriasis

A
  1. Group A streptococcal infection.
  2. Lithium.
  3. UV light.
  4. Alcohol.
  5. Stress.
  6. Drugs (Li, Beta blockers, anti-malarials, ACEi and NSAIDs)
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27
Q

What are the signs of psoriasis

A

Symmetrical well defined red plaques with silvery scale

Nail pitting and onycholysis

Some develop seronegative arthritis

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28
Q

Where is psoriasis commonly found

A

On extensors (elbow, knees, trunk, palms and soles

On flexures, axiallae, groins,

Scalp, behind ears, navel an d sacrum

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29
Q

What are the 3 variants of psoriasis

A

Guttate
Pustular
Erythroderma and generalised pustular

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30
Q

Describe guttate psoriasis

A

Drop like salmon pink papule in a fine scale mainly on the trunk, upper arms and legs

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31
Q

In which individuals is guttate psoriasis most common

A

Occurs in children and young adults and is associated with streptococcus pharyngitis

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32
Q

Describe pustular psoriasis

A

Sterile pustules triggered by steroid withdrawal, drugs (li), topical psoriasis localised to the palms and soles

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33
Q

Describe the treatment for psoriasis.

A
  1. Emollients and reassurance.
  2. Vitamin D and A analogues e.g. calcipotriol and tazarotene and steroids (Betmethasone or hydrocortisone) topical therapy
  3. Phototherapy
  4. Non biologicals
  5. Biologicals
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34
Q

Describe the UV phototherapy treatment for psoriasis

A

Use Psoralen which is a photosensitising agent followed by UVB

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35
Q

Describe the non-biological treatment for psoriasis

A

Methotrexate - inhibit folic acid metabolism and DNA replication = anti proliferative and anti inflammatory

Ciclosporin
Acretretin (Oral retinoid)

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36
Q

What are the biological treatments for psoriasis

A

Anti-TNF

  • Infliximab
  • Etanercept
  • Adalimumab
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37
Q

What are emollients used for?

A

They hydrate the skin and reduce itching.

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38
Q

What receptors do glucocorticoids target?

A

Cytoplasmic receptors.

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39
Q

How does hydrocortisone work?

A

Hydrocortisone targets cytoplasmic receptors. It leads to a reduction in pro-inflammatory cytokines and an increase in anti-inflammatories.

40
Q

In what diseases would the use of hydrocortisone be indicated?

A

Eczema and contact dermatitis.

41
Q

Give 3 potential side effects of glucocorticoids.

A
  1. Skin thinning.
  2. Oral candidiasis.
  3. Acne.
  4. Striae.
  5. Bruising.
42
Q

What receptors do vitamin A analogues target?

A

Nuclear retinoic acid receptors.

43
Q

Name a Vitamin D analogue.

A

Calcipotriol.

44
Q

How does calcipotriol work in the treatment of psoriasis?

A

Calcipotriol is a vitamin D analogue. It has anti-proliferative and anti-inflammatory effects.

45
Q

In what diseases would the use of calcipotriol be indicated?

A

Psoriasis.

46
Q

What receptors does tazarotene bind to?

A

Tazarotene is a Vitamin A analogue. It binds to nuclear retinoic acid receptors.

47
Q

How does tazarotene work in the treatment of acne and psoriasis?

A

Tazarotene is a Vitamin A analogue. It binds to nuclear retinoic acid receptors and modifies gene expression and inhibits cell proliferation.

48
Q

In what diseases would the use of tazarotene be indicated?

A

Psoriasis and acne.

49
Q

Would you prescribe tazarotene to a pregnant lady?

A

NO! Tazarotene is highly teratogenic.

50
Q

What class of drug is tacrolimus?

A

Calcineurin inhibitor.

51
Q

Define eczema

A

A range of conditions where common pathologies is inflammation of the epidermis

52
Q

Describe the presentation of eczema

A

Extreme itch = excoriation
Poorly demarcated rash that has oozing papule and vesicles
Chronic eczema presents with skin thickening and exaggeration of skin markings

53
Q

Give 5 signs of eczema.

A
  1. Superficial skin redness/inflammation.
  2. Oozing.
  3. Scaling.
  4. Pruritus.
  5. Flexors typically affected e.g. at elbows.
54
Q

Describe the aetiology of eczema.

A
  1. Genetic predisposition - loss of function mutations in filaggrin.
  2. Environmental triggers and irritants.
    - Detergent/soaps
    - Staph A infection
    - Extreme temp
    - Stress
    - Food - dairy
55
Q

Describe the distribution and characteristics of infantile eczema.

A

Infantile eczema is generalised. The cheeks and foreheads are commonly affected.
Scaly, dry and red patches.

56
Q

Describe the distribution and characteristics of childhood eczema.

A

There is a shift from extensor surfaces being affected to flexural surfaces (knees and elbows)
Lichenification.

57
Q

Describe the distribution and characteristics of adult eczema.

A

There is increasing dryness and lichenification.
S.aureus infections may be common.
Common on the hands

58
Q

Describe atopic eczema

A

TH2 driven inflammation causing IgE production

Most children grow out of it by 13 years old

Associated with asthma and hay fever

59
Q

Describe irritant contact dermatitis

A

Affects the finger webs and is triggered by soaps, detergents, oils, solvents, venous stasis

60
Q

Describe allergic contact dermatitis

A

Type IV hypersensitivity reaction

to common allergens including nickel, chromates (Leather) and lanolin

61
Q

Describe seborrhoeic dermatitis

A

Red, scaly rash which is inflammatory response to overgrowth of malassezia yeast

located on the scalp, eyebrows, cheeks

62
Q

What is the treatment for seborrhoeic dermatitis

A

Daktacort (Antifungal)

63
Q

Describe the treatment for eczema.

A
  1. Avoid irritants and allergens.
  2. Use emollients liberally and frequently.
  3. First line - hydrocortisone.
  4. Second line - tacrolimus (Calcineurin inhibitor), phototherapy, ciclosporin or azathioprine
  5. Third line - sedative anti-histamines.
64
Q

Describe the diagnostic criteria of eczema.

A

The patient must have had an itchy skin condition in the past 6 months and >3 or more of:

  • History of involvement of skin creases.
  • Personal history of asthma or hay-fever.
  • History of generally dry skin.
  • Visible flexural dermatitis.
65
Q

Give 5 causes of generalised pruritus but no rash.

A
  1. AGEING.
  2. Chronic renal failure.
  3. Cholestasis e.g. PBC.
  4. Iron deficiency.
  5. Lymphoma.
  6. Polycythaemia.
  7. Hypothyroid.
  8. Drugs.
66
Q

Give 3 causes of generalised pruritus with rash.

A
  1. Urticaria.
  2. Atopic eczema.
  3. Psoriasis.
  4. Scabies.
  5. Lichen planus.
67
Q

What investigations might you do in someone with pruritus?

A
  1. FBC.
  2. Ferritin levels.
  3. U+E.
  4. LFT’s.
  5. TFT’s.
68
Q

What cytokines are commonly targeted in the treatment of pruritus?

A

IL-4 and IL-13.

69
Q

Why do transdermal drugs need to be lipophilic?

A

They need to be lipophilic in order to get through the lipid rich stratum corneum.

70
Q

Give 2 essential properties of transdermal drugs.

A
  1. Lipophilic.

2. High affinity for their targets.

71
Q

Give 3 advantages of transdermal drug delivery.

A
  1. Avoids first pass effect, hardly metabolised.
  2. No pain.
  3. Controlled dosing.
72
Q

Name 3 drug induced dermatological reactions.

A
  1. Exanthematous reactions.
  2. Urticaria.
  3. Stephen Johnson syndrome.
73
Q

Define impetigo

A

Contangious superficial rash caused by infection by staphylococcus aureus

74
Q

What is the presentation of impetigo

A

Pustules that rupture and leave yellow, brown crusty plaques

75
Q

Describe the epidemiology of impetigo

A

2-5yrs

On face

76
Q

What is the treatment for impetigo

A

Mild = Topical Abx (Fusidic acid, mupirocin)

More severe = flucoxacillin

77
Q

Define cellulitis

A

Acute infection of the skin and soft tissues which mainly effects the lower extremities

78
Q

What are the causes of cellulitis

A

B-haemolytic strep
Staph aureus
S.pyogenes

79
Q

What is the presentation of cellulitis

A
  1. Inflammation.
  2. Swelling.
  3. Redness.
  4. Warmth.
  5. Pain.
  6. Unilateral.
  7. Lymphadenopathy
80
Q

What is the treatment for cellulitis

A

Penicillin and flucoxacillin

81
Q

What are the two different types of acne

A

Acne vulgaris

Acne rosacea

82
Q

Describe the pathology of acne vulgaris

A

Narrow hir follicles become plugged with hair, sebum and keratinocytes causing comedomes (White/blackhead) which allows the propinobacterium acne to proliferate leading to inflammation

83
Q

What is the presentation of acne vulgaris

A

Inflammation of the pilosebaceus follicles
Comedomes (Black/white)
Papules, pustules, nodules and cysts

84
Q

Where is acne vulgaris found

A

face, neck, upper chest and back

85
Q

Describe the treatment for acne vulgaris

A

Treatment is important to avoid scarring and psychological distress:

  • Regular washing with acne soaps to remove grease.
  • Benzoyl peroxide and topical clindamycin.
  • 2nd line - topical retinoids e.g. tazarotene.
  • 3rd line - low dose oral antibiotics e.g. doxycycline.
  • Hormone treatment can also be used.
86
Q

What is the presentation of acne rosacea

A

Chronic flushing precipitated by alcohol or spicy foods
Fixed erythema of the nose, chin, cheeks, forehead
Telangiectasia, papules, pustules
Rhinophyma = swelling and soft tissue overgrowth of nose in males

87
Q

What is the treatment for acne rosacea

A

Avoid sun exposure
Topical azelaic acid
Oral doxycycline

88
Q

Give 3 signs of Rosacea?

A
  1. Flushing.
  2. Erythema.
  3. Papules and pustules.
    NO comedones!
89
Q

How does Rosacea differ from Acne?

A

Rosacea tends to affect older people and isn’t associated with comedone formation.
Acne affects adolescents and often the presenting feature is open and closed comedones.

90
Q

Briefly describe the pathophysiology of urticaria.

A

Mast cell and basophil activation, with resultant histamine release.

91
Q

Give 2 clinical features of urticaria.

A
  1. Wheals (hives) - superficial redness and swelling. Itching/burning.
  2. Angio-oedema - more severe swelling. Painful.
92
Q

Describe the sub-types of chronic urticaria.

A

Chronic - recurrent or continous signs:

  1. Chronic spontaneous: idiopathic or associated with infection.
  2. Chronic inducible: physical (triggered by temperature or pressure) OR contact (triggered by allergens).
93
Q

What is the treatment for urticaria?

A

Anti-histamines and manage triggers.

94
Q

What is necrotising fasciitis?

A

Deep spreading infection of all layers of the skin -> necrosis.

95
Q

Give 3 risk factors for necrotising fasciitis.

A
  1. IVDU.
  2. Diabetes mellitus.
  3. Homeless.
  4. Recent surgery.
96
Q

What bacteria can cause necrotising fasciitis?

A
  1. Type 1: aerobic and anaerobic.

2. Type 2: group A strep e.g. s.pyogenes.

97
Q

What is the treatment for necrotising fasciitis?

A
  1. Surgical debridement.

2. Aggressive IV benzylpenicillin and clindamycin.

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