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Revision Week > Dermatology > Flashcards

Dermatology Flashcards

1
Q

Starting with the most superficial, what are the layers of the epidermis?

A
  1. Keratin layer
  2. Granular layer
  3. Prickle cell layers
  4. Basal layer s
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2
Q

How would we recognise the sole of the foots or palm of hand on a biopsy?

A

Large keratin layer

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3
Q

What would psoriasis appear like on biopsy?

A

Epidermis is thickened and retiridges are longer. Keratin layer has dark dots (retained nuclei) showing skin is growing a lot quicker. Inflammatory infiltrate

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4
Q

What would acne appear like on biopsy?

A

Prominent sebaceous glands

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5
Q

What would a melanoma present like on biopsy?

A

Proliferation of melanocytes extending up through the epidermis

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6
Q

Describe the distribution and clinical features of psoriasis?

A

Symmetrical, favouring extensor surfaces

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7
Q

Morphology of psoriasis?

A

Erythematous, well defined scaly plaques

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8
Q

Treatments for psoriasis?

A

Emollients to reduce scaling. Steroids to reduce inflammation.
Vitamin D analogues to slow down rapid growth of epidermis.

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9
Q

What is the difference between bullous pemphigoid and bullous pemphigus?

A

Pemphigoid = ends in D because its a Deeper split. Roof of blister is thicker to remains in tact.

Pemphigus = ends in S because its a more Superficial split

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10
Q

What would you see on pathology and immunoflourence for bullous pemphigoid?

A

Sub-epidermal blister with linear band of IgG

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11
Q

What causes bullous pemphigoid?

A

Autoimmune - antibodies against the hemidesmosmes which attach epidermis to the dermis causing a sub-epidermal split

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12
Q

Treatment for bullous pemphigoid?

A

If localises, topical steroids (burst blisters but leave roof as natural dressing).
If extensive, oral tetracyclines due to anti-inflammatory effect or oral steroids.

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13
Q

Clinical presentation of bullous pemphigus?

A

Often see eroded blisters that have burst

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14
Q

Histology of bullous pemphigus?

A

blister within the epidermis rather than below, so roof is thinner and breaks more easily

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15
Q

Immunoflourencence of bullous pemphigus?

A

Chicken wire pattern, antibodies attacking desmosomes that hold keratinocytes together

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16
Q

Which structure of the skin is responsible for acne?

A

Pilosebaceous unit

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17
Q

Where are apocrine glands found?

A

Axilla

Pubic area

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18
Q

Typical sites affected by acne?

A

Upper back
Upper chest
Face

19
Q

Pathogenesis of acne?

A
  1. After puberty and androgen stimulation you get increased sebum production
  2. Pores are occluded by unshed keratin blocking sebum escaping
  3. Causing inflammation
  4. And bacterial growth
20
Q

How do you treat acne?

A

Reduce sebum production (retinoids topically or oral if severe).
Reduce inflammation/infection (topical benzoyl peroxide, oral antibiotics).

21
Q

What does a unilateral distribution suggest?

A

An external cause (eg. infection)

22
Q

What would a unilateral dermatomal distribution suggest

A

shingles (herpes zoster)

23
Q

Atopic eczema presentation?

A

Bilateral, symmetrical distribution. Favouring the flexor surfaces.
Poorly defined areas of involvement.
Fissures can be seen.

24
Q

Features of chronic eczema?

A

Linear thickening of skin called lichenification due to chronic scratching.

25
Q

Presentation of eczema herpeticum?

A

Multiple monomorphic eroded papules.

26
Q

Why is eczema herpeticum common in those with eczema?

A

Skin barrier is not working effectively so infection common.

27
Q

What does molluscum contagiosum look like?

A

Umbilicated papules that are skin coloured

28
Q

What is Type 4 hypersensitivity?

A

Delayed hypersensitivity.

Contact allergy.

29
Q

Typical features of a BCC?

A 
Pearly rolled edges.
Central ulcer .
Telangiectasia.
Slow growth.
History of sun exposure.
Doesn't heal.
30
Q

What is the time frame of an SCC?

A

Quicker growth - change in lesion over 2-3 months

31
Q

Management of BCC?

A

Excellent prognosis as locally invasive and doesn’t metastasise - cut it out

32
Q

Histology of BCC?

A

Proliferation of basaloid cells

33
Q

What does ABCD stand for?

A

Asymmetry
Border
Colour
Diameter

34
Q

What are the growth phases of a melanoma?

A
  1. Initial horizontal growth phase - they are in sity and can’t metastasise
  2. Vertical growth phase (measured in Breslow thickness) and gain ability to metastasise
35
Q

What can atypical moles lead on to?

A

Melanomas

36
Q

What can SCC’s arise from?

A

Actnic keratosis.

Bowen’s disease.

37
Q

What is actinic keratosis due to?

A

Keratinocyte dysplasia in the epidermis - partial thickness

38
Q

What is Bowen’s disease due to?

A

Full thickness dysplasia of the keratinocytes

39
Q

What is described as full thickness dysplasia of keratinocytes plus invasion?

A

SCC

40
Q

How would you know if an ulcer was venous?

A

Shallow
Irregular edge
Inverse champagne bottle appearance.
History of venous disease (varicose veins, DVT)

41
Q

How would you know if an ulcer was arterial?

A 
Pale leg.
Hard to feel pulses.
Punches out.
Deeper.
Can see underlying structure.
Tend to be distal and over bony prominences.
History of arterial disease (PVD, CVD, smoker).
History of claudication.
42
Q

How do you treat venous ulcers?

A

compression

43
Q

How do you treat arterial ulcers?

A

Vascular surgery. DONT COMPRESS

44
Q

What investigation determines if a patient is suitable for compression?

A

ABPI

Revision Week (13 decks)

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