Eczema, Psoriasis and Acne CUE CARDS Flashcards

1
Q

How do we assess disease severity in dermatology?

A

> Dermatology life quality index (DLQI)

> How much someone’s skin problem has affected them over the last week

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2
Q

What is Irritant Contact Dermatitis?

A

> Non T-cell mediated
Amount of Contact (cumulative): The longer the contact or the greater the concentration of the cause, the more it effects ( increased damage)
Painful

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3
Q

What is allergic contact dermatitis?

A

> T-cell mediated and/or Ig mediated response
Delayed or immediate
Exaggerated response to ‘non-toxic’ agent
Can be predictable if you know allergen
Often itchy

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4
Q

What is Atopic Dermatitis (Eczema)?

A

> Chronic inflammatory skin disease
Cutaneous Hyper-reactivity (susceptibility genes - Filaggrin Proteins, defective skin barrier function, immunologic responses)
Systemic disease (T-cell mediated)

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5
Q

What is a fingertip unit?

A

> One fingertip unit = 0.5g of cream or ointment = two hand (palm) surfaces

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6
Q

What does potency refer to in TCS?

A

> Potency is the formulation, not the drug itself (really about how effective it is)

> Hydrocortisone = Mild

> Betamethasone Valerate 0.02%, 0.05% = Moderate

> Betamethasone Valerate 0.1% = Potent

> Betamethasone Dipropionate 0.05% = Potent

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7
Q

What is the role of Betamethasone Dipropionate 0.05% OV?

A

> Very lipophilic base

> Delivers to skin more effectively and anchors it in the skin (almost none gets through skin)

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8
Q

Discuss the Effectiveness of a Mild TCS compared to Potent (e.g. HC and MM)

A

> Individualised

> Don’t know actual risk but have the same

> MM is more potent so can use for much shorter period of time but better effectiveness - skin inflammation under control quicker

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9
Q

What is Psoriasis?

A

> Thick/scaling erythematous skin: hyperproliferation of keratinocytes and hyperkaratosis, loss of keratinocyte differentiation, infiltration of lymphocytes, angiogenesis

> Cells take 3-5 days (vs 28-30 days) to reach cornified layer

> Primary T-lymphocyte based pathogenesis

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10
Q

What is the pathophysiology of acne?

A

> Increased sebum production secondary to increased androgen production

> Hypercorinification of the pilosebaceous duct - causing formation of keratin plugs

> Overgrowth of propionibacterium acnes (anaerobe)

> Resulting inflammation

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