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Pharmacology > Skin Disorders > Flashcards

Skin Disorders Flashcards

1
Q

What are skin functions? (not tested)

A
  • barrier
  • thermoregulation
  • vitamin D synthesis
  • sensory organ
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2
Q

Common Skin Disorders (not tested)

A

Acne: changes in circulating androgens stimulate sebaceous glands
Rosacea: chronic hyperaemia of facial skin
Eczema: a generic term referring to dry, itchy inflamed skin
Pruritus: itch
Urticaria: skin inflamm with raised wheals/bumps
Psoriasis: autoimmune, inflamm, hyperproliferation of keratinocytes
Warts: infection with HPV, small raised lesions

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3
Q

Glucocorticoids

what is it used to treat? (3)

MOA? (3 main)

A
  • psoriasis, eczema, pruritus

MOA:

  • turn on or off transc factors
  • inhibit release of inflamm mediators from mast cells
  • inhibit neutrophil activation, emigration
  • inhibit immune cell activation
  • *upregulate lipocortin expression (inhibits phospholipase A2), reducing formation of arachidonic acid-based inflamm mediators like prostaglandins and leukotrienes
  • *inhibition of DNA synthesis, mitosis, reduce prolif of epidermal cells
  • *vasoconstriction of skin (blanching rxn)
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4
Q

Glucocorticoids

AE (2)

A
  • steroid rebound: Worsening of inflammation at site of skin
    Downregulation of glucocorticoid receptor; circulating endogenous GC are no longer sufficient to maintain normal skin
    Taper the patient off of it
  • skin atrophy (thinning) due to inhibition of DNA synthesis and mitosis, thinning of stratum corneum (top)
  • spread of infection, systemic effects, steroid rosacea (reddening of facial skin), stretch marks
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5
Q

Glucocorticoids

How are they prepared?

A

Often formulated as fatty acid esters of the active drugs to promote absorption through the deep skin

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6
Q

Glucocorticoids

mild potency (1)

A

hydrocortisone

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7
Q

Glucocorticoids

moderate potency (4) (don’t need to know)

A

aclomethasone diproprionate, clobetasone butyrate, fludroxycortide, fluocortolone

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8
Q

Glucocorticoids

potent (7) (don’t need to know)

A

beclomethasone diproprionate, betamethasone, fluocinolone acetonide, flucocinonide, fluticasone, proprionate, mometasone fuorate, triamcinolone acetonide

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9
Q

Glucocorticoids

very potent (2)

A

clobetasol proprionate, diflucortolone valerate

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10
Q

Retinoids

derivatives of ___________ and metabolites of ______

Name 5

A

retinoic acid, vitamin A (retinol)

Tretinoin
Isotretinoin (accutane)
alitretinoin
tazarotene
bexarotene
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11
Q

Retinoids

What is vit A important? (2)

used to treat? (3)

dosage form?

A

healthy vision, cell differentiation

acne, eczema, psoriasis

topical, can be given orally for severe cases

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12
Q

Retinoids

MOA

A
  • agonists of retinoic acid receptor (RAR) and retinoid X receptor (RXR) which are trans factors that induce/repress gene transcription
  • reduce sebaceous gland activity and sebum production
  • have some anti-inflamm actions
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13
Q

Retinoids

AE (2)

A
  • *skin peeling
  • *teratogenic (women should be using suitable contraception)
  • dry flaky skin, stinging sensations, joint pain with oral admin
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14
Q

Retinoids

Bexarotene
Use?
MOA?

A
  • cutaneous T-cell lymphoma
  • 100x more potent for RXR than RAR

MOA:

  • blocks cell cycle progression
  • induces apoptosis and differentiation
  • inhibits angiogenesis and metastasis
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15
Q

Vit D Analogues

Name 3 primary analogues

used to treat? (1)

dosage form?

A

-mixture of several substances and plays role in calcium phosphate metabolism in bone formation

3 analogues:

  • calcitriol
  • calcipotriol
  • tacalcitol
  • used to treat psoriasis
  • topical, can be oral (sometimes combined w/ glucocorticoid therapy)

used when glucocorticoids are not that successful

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16
Q

Vit D Analogues

MOA?

A
  • agonists of Vit D receptor (nuclear recport)
  • reduce proliferation and increase apoptosis of keratinocytes
  • inhibit T cell activation
17
Q

Vit D Analogues

AE (1)

A
  • skin irriation
  • calcium, bone metabolism problems - need to avoid
    oral/systemic admin
  • *hypercalcemia
  • GI pain
  • renal stones
18
Q

Keratolytics

Name 2 a-hydroxy acids
used to treat? (1)
dosage form?

A

a-hydroxy acids:

  • salicylic acid
  • glycolic acid
  • used to treat warts
  • topical, can be oral (sometimes combined w/ glucocorticoid therapy)
19
Q

Keratolytics

MOA?

A
  • keratolytics break down keratin in skin
  • by breaking down keratin, agents reduce thickness of stratum corneum:
  • solubilize protein components of desmosomes
  • activate endog. hydrolytic enzymes by lowering pH
  • diffuse into stratum corneum and increase water content making tissue easier to debride
20
Q

Keratolytics

AE

A
  • open wounds should not be treated with salicylic acid
  • local skin irritation (redness, itching)
  • salicylic acid toxicity (children at risk)
21
Q

Cryotherapy

MOA?
involves what substances?

A
  • removal of wart by freezing

involve liquid nitrogen, CO2, dimethyl ether

22
Q

Imiquimod

what is it?
what is it used for?
MOA?

A
  • an immune modifier used to treat anogenital warts

MOA

  • enhance both innate and acquired immune respones
  • binds toll-like receptors on B cells
  • increases release of inflamm mediators (TNFa and interleukins)
23
Q

Immunosuppressants

use (general)?
name 2

A
  • serious cases of eczema/psoriasis, glucocorticoid ineffective
  • ciclosporin
  • tacrolimus/pimecrolimus
24
Q

Immunosuppressants

Ciclosporin
how does it work?
what does it inhibit?

what is the normal immune response?

A
  • cylcic peptide that binds to cyclophilin and inhibits calcineurin which decrease IL-2 synthesis and prolif of T cells
  • will not affect current inflamm, but will prevent future ones

normal immune repsonse

  • increased intracellular Ca2+ activates calcineurin which dephosphorylates the nuclear factor of activated T cells (NFAT)
  • dephosphorylated NFAT turns on transc and propgates inflamm response (turn on transc of IL-2, leading to activation of T cells)
25
Q

Immunosuppressants

Ciclosporin
AE (3)

A
  • *nephrotoxicity (unrelated to calcineurin, unknown mech)
  • *hepatotoxicity
  • *hypertension
26
Q

Immunosuppressants

Tacrolimus/Pimecrolimus

how does it work?
AE? (2)

A
  • macrolide compounds (antibiotics) that also inhibit calcineurin to decrease IL-2 synthesis and prolif of T cells

AE

  • similar to ciclosporin
  • also hyperglycemia and alopecia (tacro only)
27
Q

Biologics for Psoriasis

name 5

A
  • infliximab
  • adalimumab
  • secukinmab
  • ixekizumab
  • ustekinumab
28
Q

Biologics for Psoriasis

Infliximab
Adalimumab
how do they work?

what does TNFa do?

A

Infliximab
- chimeric neutralizing antibody against tumor necrosis factor a (TNFa) same as for IBD/IBS

Adalimumab
-humanized monoclonal antibody against TNFa

both target membrane bound TNFa are given once every 2 weeks via sq injection

TNFa pro-inflamm cytokine

  • promotes release of other inflamm cytokines and interleukin (1/6/8)
  • promotes adhesion of leukocytes into target organs
29
Q

Biologics for Psoriasis

Newer antibodies for treatment, more expensive

Secukinumab - against which IL?
ixekizumab?
ustekinumab?

A

Secukinumab: monoclonal antibody agianst IL-17

ixekizumab: IL-17A
ustekinumab: IL-12, IL-23

IL are key mediators of inflamm, reduce inflamm

Pharmacology (12 decks)

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