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PharmacologyII > Skin Pharmacology (Lect 9) > Flashcards

Skin Pharmacology (Lect 9) Flashcards

1
Q

Functions of skin

A
  • A barrier
  • Thermoregulation
  • Vitamin D synthesis
  • Sensory organ
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2
Q

Acne occurs due to

A
  • Changes in circulating androgens stimulate sebaceous glands
    (hair follicles become blocked with sebum and debris)
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3
Q

What is rosacea?

A

– Chronic hyperaemia of the facial skin
– Erythema spread across the nose, cheeks & forehead
– Erythema is due to vasodilation of blood vessels close to the
surface of the skin

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4
Q

What is eczema?

A

– A generic term referring to dry, itchy & inflamed skin
– Distributes usually on flexor surfaces (e.g. elbows, knees)
– Different types (e.g. atopic eczema, contact dermatitis, xerotic
eczema, etc.)

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5
Q

What is pruritus?

A

– Refers to itch
– Common with eczema, urticaria and psoriasis, and largely due
to release of inflammatory mediators from mast cells

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6
Q

What is Urticaria?

A

– Skin inflammation characterized by raised wheals/bumps
– Many causes (e.g. sun exposure, heat, cold, insect bites, food,
certain drugs, etc.)

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7
Q

What is Psoriasis?

A

– Autoimmune condition characterized by inflammation and
hyperproliferation of keratinocytes
– Life-long condition (can reappear and disappear)

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8
Q

What are warts?

A

– Infection with human papilloma virus
– Characterized by small raised lesions with an irregular shape
(hyperkeratinisation)

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9
Q

What are Glucocorticoids?

A
  • Transcription factors used to treat psoriasis, eczema, and pruritus
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10
Q

What is the MOA of glucocorticoids?

A

– Inhibit release of inflammatory mediators from mast cells
– Inhibit neutrophil activation and emigration
– Inhibit immune cell activation
– Upregulate lipocortin expression (inhibits phospholipase A2, reducing formation of arachidonic acid-based inflammatory mediators)
– Inhibition of DNA synthesis and mitosis, reducing proliferation of epidermal cells
– Topical application produces vasoconstriction of the skin (‘blanching’ reaction)

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11
Q

Adverse Effects of Glucocorticoids

A

– Steroid rebound
– Skin atrophy (skin thinning)

(NOT AS IMPORTANT)
– Systemic effects (not common with topical application)
– Spread of infection
– Steroid rosacea
– Production of stretch marks
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12
Q

Example of mildly potent glucocorticoid

A

hydrocortisone

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13
Q

Examples of moderately potent glucocorticoids

A
  • alclomethasone diproprionate
  • clobetasone butyrate
  • fludroxycortide,
  • fluocortolone
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14
Q

Examples of potent glucocorticoids

A
  • beclomethasone diproprionate
  • betamethasone
  • fluocinolone
  • acetonide
  • flucocinonide
  • fluticasone proprionate
  • mometasone fuorate
  • triamcinolone acetonide
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15
Q

Examples of VERY potent glucocorticoids

A
  • Clobetasol proprionate

- diflucortolone valerate

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16
Q

What are retinoids?

A
  • Are derivatives of retinoic acid (metabolites of vitamin
    A [retinol])

Used to treat
– Acne
– Eczema
– Psoriasis

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17
Q

Examples of retinoids

A 
– Tretinoin
– Isotretinoin (Accutane)
– Alitretinoin
– Tazarotene
– Bexarotene
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18
Q

MOA of retinoids

A

– Are agonists of the retinoic acid receptor
(RAR) and retinoid X receptor (RXR)

– Are transcription factors that induce/repress gene transcription

– Reduce sebaceous gland activity & sebum production

– Have some anti-inflammatory actions

19
Q

Adverse effects of retinoids

A

– Teratogenic (women should be using suitable contraception)
– Skin peeling

(NOT AS IMPORTANT)
– Dry/flaky skin
– Stinging/burning sensations
– Joint pain (oral administration)

20
Q

What is Bexarotene?

A

– A retinoid used to treat cutaneous T-cell lymphoma

– 100x more potent for RXR than RAR

21
Q

What is Bexarotene’s MOA?

A

– Blocks cell cycle progression
– Induces apoptosis and differentiation
– Inhibits angiogenesis and metastasis

22
Q

Primary Vitamin D analogues

A

– Calcitriol
– Calcipotriol
– Tacalcitol

23
Q

What are Vitamin D analogues used to treat ?

A

– Psoriasis

– Vitamin D is a mixture of several substances and plays an essential role in calcium/phosphate metabolism and in bone formation

24
Q

What is the MOA for Vitamin D analogues?

A

– Are agonists of the Vitamin D receptor (nuclear receptor)
– Reduce proliferation and increase apoptosis of keratinocytes
– Inhibit T cell activation

25
Q

Adverse Effects of Vitamin D analogues

A

– Systemic (oral) administration
▪ Hypercalcemia
▪ GI pain
▪ Renal stones

(NOT AS IMPORTANT)
– Skin irritation (topical administration)
– Avoid in people with problems related to calcium or bone
metabolism

26
Q

What are Keratolytics and what are they used to treat?

A

– Keratolytics break down keratin in the skin

– Used to treat warts

27
Q

Examples of keratolytics

A

• α-hydroxy acids
– Salicylic acid
– Glycolic acid

28
Q

MOA of Keratolytics

A

– By breaking down keratin, these agents reduce thickness of the stratum corneum

  • Solubilize the protein components of desmosomes
  • Activate endogenous hydrolytic enzymes within the stratum corneum
  • Diffuse into the stratum corneum and increase water content making the tissue easier to physically debride
29
Q

Adverse Effects of Keratolytics

A

– Local skin irritation (redness, itching)

– Salicylic acid toxicity (children at increased risk for systemic toxicity)

30
Q

Mechanism of action of Cryotherapy

A

– Removal of the wart by freezing

– Can involve liquid nitrogen, carbon dioxide, or dimethyl ether

31
Q

What is Imiquimod?

A

An immune modifier used to treat anogenital warts

32
Q

What is the MOA of Imiquimod?

A

– Enhances both the innate and acquired immune response
▪ Binds toll-like receptors on B cells
▪ Increases release of inflammatory mediators (e.g. TNFα and interleukins)

33
Q

Adverse effects of Imiquimod

A

– Local skin reactions (e.g. burning, itching, swelling)
– Long-term skin reactions (e.g. pigmentation changes)
– Systemic reactions (fatigue, diarrhea, flu-like symptoms, headache)

34
Q

What can immunosuppressants be used for?

A

For more serious cases of eczema or

psoriasis (or if glucocorticoids prove ineffective)

35
Q

What is ciclosporin and what is its MOA?

A

– An immunosuppressant

MOA:
– Cyclic peptide that binds to cyclophilin and inhibits calcineurin, which decrease IL-2 synthesis and the proliferation of T cells

36
Q

Adverse Effects of Ciclosporin

A 
(MAIN)
– Nephrotoxicity (not related to
calcineurin inhibition)
–  Hepatotoxicity
–  Hypertension
(LESS SERIOUS)
– anorexia
– lethargy
– hirsutism
– tremor
– Paresthesia (tingling, prickling sensations in hands and toes)
– GI disturbances
37
Q

What are Tacrolimus/Pimecrolimus and what are their MOA?

A

– (Immunosuppressant like ciclosporin) Macrolide compounds that also inhibit calcineurin to decrease IL-2 synthesis and the proliferation of T cells

38
Q

Adverse Effects of Tacrolimus/Pimecrolimus

A

– Similar adverse effects to ciclosporin, but also
• hyperglycemia
• alopecia (tacrolimus only)

(MAIN)
– Nephrotoxicity (not related to
calcineurin inhibition)
–  Hepatotoxicity
–  Hypertension
(LESS SERIOUS)
– anorexia
– lethargy
– hirsutism
– tremor
– Paresthesia (tingling, prickling sensations in hands and toes)
– GI disturbances
39
Q

What is Infliximab?

A

– A biologic for psoriasis
– Chimeric neutralizing antibody against tumor necrosis factor α (TNFα)
– Reduces inflammation by neutralizing activity of TNFα (which is a pro-inflammatory cytokine)

40
Q

What is Adalimumab?

A

– A biologic for psoriasis
– Humanized monoclonal antibody against TNFα
– Reduces inflammation by neutralizing activity of TNFα (which is a pro-inflammatory cytokine)

41
Q

Secukinumab is a

A

monoclonal antibody against IL-17 (newer antibody for treatment of psoriasis)

42
Q

Ixekizumab is a

A

monoclonal antibody against homodimers of IL-

17A (newer antibody for treatment of psoriasis)

43
Q

Ustekinumab is a

A

monoclonal antibody against IL-12 and IL-23 (newer antibody for treatment of psoriasis)

44
Q

Interleukin are key mediators of

A

INFLAMMATION

PharmacologyII (12 decks)

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