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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
Describe the pathology of psoriasis
Type IV hypersensitivity reaction to unidentified antigen leading to epidermal proliferation due to Th1 cell cytokine up regulation
26
What are the triggers for psoriasis
1. Group A streptococcal infection. 2. Lithium. 3. UV light. 4. Alcohol. 5. Stress. 6. Drugs (Li, Beta blockers, anti-malarials, ACEi and NSAIDs)
27
What are the signs of psoriasis
Symmetrical well defined red plaques with silvery scale Nail pitting and onycholysis Some develop seronegative arthritis
28
Where is psoriasis commonly found
On extensors (elbow, knees, trunk, palms and soles On flexures, axiallae, groins, Scalp, behind ears, navel an d sacrum
29
What are the 3 variants of psoriasis
Guttate Pustular Erythroderma and generalised pustular
30
Describe guttate psoriasis
Drop like salmon pink papule in a fine scale mainly on the trunk, upper arms and legs
31
In which individuals is guttate psoriasis most common
Occurs in children and young adults and is associated with streptococcus pharyngitis
32
Describe pustular psoriasis
Sterile pustules triggered by steroid withdrawal, drugs (li), topical psoriasis localised to the palms and soles
33
Describe the treatment for psoriasis.
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
34
Describe the UV phototherapy treatment for psoriasis
Use Psoralen which is a photosensitising agent followed by UVB
35
Describe the non-biological treatment for psoriasis
Methotrexate - inhibit folic acid metabolism and DNA replication = anti proliferative and anti inflammatory Ciclosporin Acretretin (Oral retinoid)
36
What are the biological treatments for psoriasis
Anti-TNF - Infliximab - Etanercept - Adalimumab
37
What are emollients used for?
They hydrate the skin and reduce itching.
38
What receptors do glucocorticoids target?
Cytoplasmic receptors.
39
How does hydrocortisone work?
Hydrocortisone targets cytoplasmic receptors. It leads to a reduction in pro-inflammatory cytokines and an increase in anti-inflammatories.
40
In what diseases would the use of hydrocortisone be indicated?
Eczema and contact dermatitis.
41
Give 3 potential side effects of glucocorticoids.
1. Skin thinning. 2. Oral candidiasis. 3. Acne. 4. Striae. 5. Bruising.
42
What receptors do vitamin A analogues target?
Nuclear retinoic acid receptors.
43
Name a Vitamin D analogue.
Calcipotriol.
44
How does calcipotriol work in the treatment of psoriasis?
Calcipotriol is a vitamin D analogue. It has anti-proliferative and anti-inflammatory effects.
45
In what diseases would the use of calcipotriol be indicated?
Psoriasis.
46
What receptors does tazarotene bind to?
Tazarotene is a Vitamin A analogue. It binds to nuclear retinoic acid receptors.
47
How does tazarotene work in the treatment of acne and psoriasis?
Tazarotene is a Vitamin A analogue. It binds to nuclear retinoic acid receptors and modifies gene expression and inhibits cell proliferation.
48
In what diseases would the use of tazarotene be indicated?
Psoriasis and acne.
49
Would you prescribe tazarotene to a pregnant lady?
NO! Tazarotene is highly teratogenic.
50
What class of drug is tacrolimus?
Calcineurin inhibitor.
51
Define eczema
A range of conditions where common pathologies is inflammation of the epidermis
52
Describe the presentation of eczema
Extreme itch = excoriation Poorly demarcated rash that has oozing papule and vesicles Chronic eczema presents with skin thickening and exaggeration of skin markings
53
Give 5 signs of eczema.
1. Superficial skin redness/inflammation. 2. Oozing. 3. Scaling. 4. Pruritus. 5. Flexors typically affected e.g. at elbows.
54
Describe the aetiology of eczema.
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
Describe the distribution and characteristics of infantile eczema.
Infantile eczema is generalised. The cheeks and foreheads are commonly affected. Scaly, dry and red patches.
56
Describe the distribution and characteristics of childhood eczema.
There is a shift from extensor surfaces being affected to flexural surfaces (knees and elbows) Lichenification.
57
Describe the distribution and characteristics of adult eczema.
There is increasing dryness and lichenification. S.aureus infections may be common. Common on the hands
58
Describe atopic eczema
TH2 driven inflammation causing IgE production Most children grow out of it by 13 years old Associated with asthma and hay fever
59
Describe irritant contact dermatitis
Affects the finger webs and is triggered by soaps, detergents, oils, solvents, venous stasis
60
Describe allergic contact dermatitis
Type IV hypersensitivity reaction | to common allergens including nickel, chromates (Leather) and lanolin
61
Describe seborrhoeic dermatitis
Red, scaly rash which is inflammatory response to overgrowth of malassezia yeast located on the scalp, eyebrows, cheeks
62
What is the treatment for seborrhoeic dermatitis
Daktacort (Antifungal)
63
Describe the treatment for eczema.
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
Describe the diagnostic criteria of eczema.
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
Give 5 causes of generalised pruritus but no rash.
1. AGEING. 2. Chronic renal failure. 3. Cholestasis e.g. PBC. 4. Iron deficiency. 5. Lymphoma. 6. Polycythaemia. 7. Hypothyroid. 8. Drugs.
66
Give 3 causes of generalised pruritus with rash.
1. Urticaria. 2. Atopic eczema. 3. Psoriasis. 4. Scabies. 5. Lichen planus.
67
What investigations might you do in someone with pruritus?
1. FBC. 2. Ferritin levels. 3. U+E. 4. LFT's. 5. TFT's.
68
What cytokines are commonly targeted in the treatment of pruritus?
IL-4 and IL-13.
69
Why do transdermal drugs need to be lipophilic?
They need to be lipophilic in order to get through the lipid rich stratum corneum.
70
Give 2 essential properties of transdermal drugs.
1. Lipophilic. | 2. High affinity for their targets.
71
Give 3 advantages of transdermal drug delivery.
1. Avoids first pass effect, hardly metabolised. 2. No pain. 3. Controlled dosing.
72
Name 3 drug induced dermatological reactions.
1. Exanthematous reactions. 2. Urticaria. 3. Stephen Johnson syndrome.
73
Define impetigo
Contangious superficial rash caused by infection by staphylococcus aureus
74
What is the presentation of impetigo
Pustules that rupture and leave yellow, brown crusty plaques
75
Describe the epidemiology of impetigo
2-5yrs | On face
76
What is the treatment for impetigo
Mild = Topical Abx (Fusidic acid, mupirocin) More severe = flucoxacillin
77
Define cellulitis
Acute infection of the skin and soft tissues which mainly effects the lower extremities
78
What are the causes of cellulitis
B-haemolytic strep Staph aureus S.pyogenes
79
What is the presentation of cellulitis
1. Inflammation. 2. Swelling. 3. Redness. 4. Warmth. 5. Pain. 6. Unilateral. 7. Lymphadenopathy
80
What is the treatment for cellulitis
Penicillin and flucoxacillin
81
What are the two different types of acne
Acne vulgaris | Acne rosacea
82
Describe the pathology of acne vulgaris
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
What is the presentation of acne vulgaris
Inflammation of the pilosebaceus follicles Comedomes (Black/white) Papules, pustules, nodules and cysts
84
Where is acne vulgaris found
face, neck, upper chest and back
85
Describe the treatment for acne vulgaris
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
What is the presentation of acne rosacea
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
What is the treatment for acne rosacea
Avoid sun exposure Topical azelaic acid Oral doxycycline
88
Give 3 signs of Rosacea?
1. Flushing. 2. Erythema. 3. Papules and pustules. NO comedones!
89
How does Rosacea differ from Acne?
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
Briefly describe the pathophysiology of urticaria.
Mast cell and basophil activation, with resultant histamine release.
91
Give 2 clinical features of urticaria.
1. Wheals (hives) - superficial redness and swelling. Itching/burning. 2. Angio-oedema - more severe swelling. Painful.
92
Describe the sub-types of chronic urticaria.
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
What is the treatment for urticaria?
Anti-histamines and manage triggers.
94
What is necrotising fasciitis?
Deep spreading infection of all layers of the skin -> necrosis.
95
Give 3 risk factors for necrotising fasciitis.
1. IVDU. 2. Diabetes mellitus. 3. Homeless. 4. Recent surgery.
96
What bacteria can cause necrotising fasciitis?
1. Type 1: aerobic and anaerobic. | 2. Type 2: group A strep e.g. s.pyogenes.
97
What is the treatment for necrotising fasciitis?
1. Surgical debridement. | 2. Aggressive IV benzylpenicillin and clindamycin.

Phase 2 (16 decks)

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