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MSK II Test 2 > Intro to Derm Pharm > Flashcards

Intro to Derm Pharm Flashcards

1
Q

What is the fxn of skin?

A
  • Protection
  • Thermal regulation
  • Immune responsiveness
  • Biochemical synthesis
  • Sensory detection
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2
Q

What does skin represent for pharm access? What are the variables determining response?

A
  • Complex series of diffusion barriers
  • Variables determining response:
  • Drug penetration
  • Concentration gradient
  • Dosing schedule
  • Vehicles and occlusion
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3
Q

What are the routes of drug absorption for skin?

A
  • Intact stratum corneum
  • Sweat ducts
  • Sebaceous follicles
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4
Q

What are the steps involved in percutaneous absorption?

A
  • Steps involved in percutaneous absorption:
  • Concentration gradient established
  • Partition coefficient
  • Diffusion coefficient
  • Rate of absorption:
  • J = Cveh · Km · D/x
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5
Q

What are the signs of chronic inflammation? Which are the appropriate vehicles?

A

Chronic inflammation with xerosis, scaling, lichenification:

creams and ointments

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6
Q

What are the signs of acute inflammation? What are the appropriate vehicles?

A

Acute inflammation with oozing, vesiculation, and crusting:

tinctures, wet dressings, and lotions

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7
Q

List different vehicles from drying to lubricating.

A

tinctures <

wet dressings <

lotions <

gels <

aerosols <

powders <

pastes <

creams <

ointments

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8
Q

What drugs are delivered transdermally? What are their indications?

A

fentanyl (Duragesic) - pain

lidocaine (Lidoderm) - neuralgia pain

Ethinyl estradiol/norelgestromin (Ortho-Evra) - contraceptive

nitroglycerine (Transderm Nitro) - Angina

scopolamine (Transderm-Scop) - motion sickness

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9
Q
  • A 10 yo male presents to the urgent care clinic with his father following a mountain bike accident. His knee and elbow have been scraped.
  • PE: mildly abraded areas over knee and elbow covered in dirt and rocks.
  • His father would like to know if Neosporin (bacitracin, neomycin, polymyxin B) would be effective?
  • What are the mechanisms of action of the individual components of Neosporin (bacitracin, neomycin, polymyxin B)?

A.Increases permeability of cell wall

B.Inhibits cell wall synthesis

C.Inhibits 30S ribosomal subunit

A

Bacitracin - Gram + (streptococci, pneumococci, staphylococci), anaerobic cocci (Peptostreptococcus), Neisseriae, Tetanus bacillis, Diptheria bacili

  • inhibits cell wall synthesis

Polymyxin B - Gram negative organsims (P. aeruginoas, E. coli, Enterobacter, Klebsiella)

  • increases permeability of cell wall

Neomycin - Gram negative organisms including E. coli, Enterobacter, Klebsiella, Proteus

  • aminoglycoside, inhibits 30s ribosome
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10
Q
  • A 5 yo female is brought to urgent care by her mother after returning from kindergarten with red sores around her mouth.
  • You suspect non-bullous impetigo and would like to suggest a topical antibiotic ointment.
  • Which two topical antimicrobials cover group A β-hemolytic streptococci and S. aureus (including MRSA)?

A.Mupirocin

B.Neomycin

C.Polymyxin B

D.Retapamulin

A

muciprocin - DOC for impetigo

retapamulin is good too

Group A beta hemolytic strep = Strep pyogenes

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11
Q

What is the treatment approach to non-bullous impetigo?

A
  • 5 yo female with non-bullous impetigo
  • General treatment approach:
  • Non-bullous impetigo – topical therapy with mupirocin or retapamulin for 5 days
  • More extensive forms of impetigo and bullous forms – oral antimicrobials for 7 days
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12
Q

What are hte benefits of topical therapy for non-bullous impetigo?

A
  • Benefits of topical therapy:
  • Fewer side effects
  • Lower risk of bacterial resistance
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13
Q

•Bacitracin-neomycin-polymyxin B has some activity against impetigo causing organisms – why can’t we use this combination?

A

d

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14
Q

What are the general requirements for topical AB in acne? What are the available options?

A
  • Avoid systemic exposure and achieve high follicular concentrations
  • Less effective than systemic administration of the same antibiotic
  • Available options:
  • Clindamycin
  • Erythromycin
  • Metronidazole
  • Sodium sulfacetamide
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15
Q

Are ABs used as monotherapy for acne?

A
  • Not used as monotherapy (bacterial resistance)!
  • Give with benzoyl peroxide or retinoids
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16
Q
  • A 35 yo male construction worker presents to his PCP with complaints of intense itching of both feet throughout the day.
  • PE: webs spaces white, macerated, cracked
  • Workup consistent with dermatophyte infection
  • What topical therapeutic options are available?
A

Topical Preps include:

azoles

ciclopirox olamine

allyamines

butenafine

tolnaftate

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17
Q

What is the MOA and uses for azoles? What are the drugs?

A
  • Azoles – clotrimazole, miconazole
  • MOA: inhibits synthesis of ergosterol (inhibits lanosterol 14-α-demethylase)
  • Uses: tinea corporis (ring worm), tinea pedis (athlete’s foot), tinea cruris (jock itch), tinea versicolor, and cutaneous candidiasis, such as vaginal yeast infections, infections of the skin, diaper rash, and thrush (candidiasis of the oral mucosa and tongue, and sometimes the palate, gingivae, and floor of the mouth)
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18
Q

What is the MOA and uses for ciclopirox olamine?

A
  • MOA: inhibits uptake of precursors of macromolecule synthesis
  • Uses: topical dermatomycosis, candidiasis, tinea versicolor, mild-to-moderate onychomycosis
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19
Q

What are the MOA and uses for allylamines? What are the drugs?

A
  • Allylamines – terbinafine and naftifine
  • MOA: inhibits squalene epoxidase
  • Uses: tinea corporis, tinea cruris, and tinea pedis
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20
Q

What is the MOA and uses for tolnaftate?

A
  • MOA: unknown
  • Uses: tinea pedis, tinea cruris, and tinea corporis
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21
Q

What are some antifungal agents? How do they work?

A

Topical Preparations

  • Nystatin/amphotericin B
  • MOA: binds ergosterol in fungal cell membrane altering permeability
  • Nystatin limited to topical cutaneous and mucosal uses - Thrush
  • Amphotericin B broad antifungal spectrum but rarely used topically
  • Cumulative organ toxicity “ampho-terrible”
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22
Q

What are the types of oral preparationts of antifungal agents?

A

Oral Preparations

  • Azoles
  • Griseofulvin
  • Terbinafine
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23
Q

What are the uses and ADRs associated with oral azoles?

A
  • Azoles
  • Uses: vaginal, urinary, oropharyngeal, or esophageal candida infections
  • Systemic yeast infections more common: type 1 diabetes, leukemia, AIDS
  • Drug-drug interactions!
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24
Q

What is the MOA and uses for griseofulvin?

A
  • Griseofulvin
  • MOA: inhibits fungal cell mitosis at metaphase
  • Uses: dermatophyte infections but not Candida
  • Induces CYP enzymes
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25
Q

What is the metabolism and uses for terbinafine?

A
  • Terbinafine
  • High first pass metabolism; accumulates in skin, nails, fat
  • Uses: tinea corporis, tinea capitis, and onychomycosis
26
Q

What inhibits membrane function in fungus?

A

amphotericin B

27
Q

What inhibits ergosterol synthesis in fungi?

A

fluconazole

itraconazole

voriconazole

naftiline

terbinafine

28
Q

What inhibits nucleic acid synthesis in antifungal agents?

A

5-fluorocytosine

29
Q

What are the 4 examples of dermatophyte infections? What is used to treat each one?

A
  • Dermatophyte infections
  • Tinea capitis (scalp) – oral griseofulvin, terbinafine, itraconazole
  • Tinea pedis (feet) – topical antifungals
  • Tinea cruris (groin) – topical antifungals
  • Tinea corporis (body) – topical antifungals, oral antifungals
30
Q

What are the types of candida infections? What is used to fight each one?

A
  • Candida infections
  • Thrush (oropharyngeal candidiasis) – oral nystatin, clotrimazole troche, oral fluconazole
  • Esophageal candidiasis – systemic antifungals
  • Vulvovaginitis – topical antifungals, oral fluconazole
  • Invasive infection – systemic antifungals
31
Q
  • A 40 yo male seeks your recommendation regarding frequent cold sores.
  • He experiences about ten cold sores a year, exacerbated by “colds” or sun exposure.
  • What organism is causing these cold sores?

•

•He wants to know what treatment options are available to him.

A

HSV-1

Treat with topical acyclovir, penciclovir, or docosanol for modest benefit

  • apply within 1 hour of first sign or symptom, continue 4 days

Oral acyclovir, famciclovir, or valacyclovir for long term suppression

  • begin within 1 hour
32
Q

What is the MOA for antiviral agents (except docosanol)? What are the benefits?

A
  • Acyclovir, valacyclovir, penciclovir, famciclovir
  • MOA: converted to pharmacologically active triphosphate metabolites, inhibit DNA synthesis and viral replication
  • Topical – modest benefit for herpes labialis
  • Systemic –
  • Most effective in treating herpes labialis
  • Also used systemically for HSV and VZV infections
33
Q

What is the MOA and and benefits of using docosanol?

A

Docosanol - antiviral agent

  • Docosanol
  • MOA: inhibits fusion between the plasma membrane and the HSV envelope, thereby preventing viral entry and replication
  • When applied within 12 hours of the onset of prodromal symptoms, five times daily, median healing time was shortened by 18 hours compared with placebo in recurrent orolabial herpes
34
Q

What is the MOA, uses and ADRs for imiquimod?

A

Imiquimod - immunomodulator

  • MOA: may be related to stimulation of peripheral mononuclear cells to release interferon-α and macrophage stimulation to produce interleukins-1, -6, -8, and TNF-α
  • Uses: external genital and perianal warts in adults, actinic keratoses on the face and scalp, biopsy-proven primary basal cell carcinomas on the trunk, neck, and extremities (< 2 cm diameter)
  • ADRs: local inflammation, pruritus, erythema, superficial erosion
35
Q

What are the MOA, uses and ADRs of Tacrolimus?

A

Tacrolimus - immunomodulator

  • MOA: inhibit T-lymphocyte activation and prevent release of inflammatory cytokines and mediators from mast cells
  • Uses: treatment of atopic dermatitis and psoriasis but traditionally used to prevent heart, liver, and kidney allograft rejection due to potent immunosuppressive activity (oral forms)
  • Topical ADRs: transient erythema, burning, and pruritus
36
Q

•A 14 yo female presents to her physician’s office to ask about acne treatment.

She started experiencing acne last year. She has used benzoyl peroxide gel when the lesions “get really bad” but doesn’t think it works well for her.

What is the MOA for benzoyl peroxide?

A

releases free-radical oxygen which oxidizes bacterial proteins, activity against P. acnes too

37
Q

What other treatments, other than benzoyl peroxide, are available for acne?

A
  • Topical retinoids
  • Tretinoin (all-trans-retinoic acid) – also marketed as anti-aging
  • Adapalene – photo-chemically more stable, less irritating
  • Tazarotene – also approved for psoriasis, photoaging
38
Q

What is the MOA, ADRs, and CIs for topical retinoids?

A
  • MOA: may decrease cohesion between epidermal cells and increase epidermal cell turnover, expulsion of open comedones and the transformation of closed comedones into open
  • ADRs: erythema, mild peeling, and dryness; minimize sun exposure
  • CI: not recommended in pregnant women
39
Q

What is the MOA, PK, and ADRs for isotretinoin?

A
  • Isotretinoin (PO) - Accutane
  • MOA: reduces sebacerous gland size, reduces sebum production
  • PK: t1/2 10-20 hours; hepatic metabolism; highly protein bound (99-100%)
  • ADRs: resemble hypervitaminosis A (dryness and itching)

IMPORTANT CONTRAINDICATION = PREGNANCY IS A NO GO!!

40
Q

What are the different types of acne and the different treatment approaches for each?

A

•Comedonal (non-inflammatory) acne

  • Topical retinoid
  • Alternatives: azelaic acid, salicylic acid

•Mild papulopustular and mixed acne

•Topical retinoid AND topical antimicrobial (BPO alone or BPO +/- topical antibiotic)

•Moderate papulopustular and mixed acne

•Topical retinoid AND oral antibiotic AND topical BPO

•Moderate nodular acne

•Topical retinoid AND oral antibiotic AND topical BPO

•Severe nodular/conglobate acne

•Oral isotretinoin

41
Q

What are the different topical therapies for psoriasis?

A

emollients

keratolytics

topical glucocorticoids

coal tar

anthralin

calcipotriene

tazarotene

42
Q

What are the different uses of topical therapies for psoriasis?

A
  • Emollients – used as basic adjunct; reduces scaling, itching, and related discomfort
  • Keratolytics – reduce hyperkeratosis; enable other topical drugs to penetrate
  • Topical glucocorticoids – rapid response; control inflammation and itching; mainstay of topical treatment
  • Coal tar
  • Anthralin – used for widespread, refractory plaques
  • Calcipotriene – as effective as topical glucocorticoids but slower onset; no long-term glucocorticoid adverse effects
  • Tazarotene – extended response; maintenance therapy
43
Q

When is systemic therapy used for psoriasis? What are the agents used?

A

•Used for patients with > 5% body surface area involvement

Methotrexate, acitretin, and cyclosporine are used

44
Q

What is the MOA, uses and efficacy of methotrexate for psoriasis?

A
  • Methotrexate
  • MOA: inhibits dihydrofolate reductase (folic acid analog)
  • Used in combination with phototherapy or biological agents
  • Effective for both skin lesions and arthritis

Contraindicated with hepatitis or liver failure

45
Q

What is acitretin? How effective is it for psoriasis?

A
  • Acitretin
  • Systemic retinoic acid derivative
  • Not as effective as other systemic therapies
46
Q

What is the MOA, ADRs, and uses of cyclosporine?

A
  • Cyclosporine - for psoriasis
  • MOA: inhibits calcineurin, inhibits transcription of interleukin-1 and -2 receptors, blocks T-cell activation
  • ADRs: nephrotoxicity, hypertension, hepatotoxicity, gingival hyperplasia, and hirsutism
  • Used in extensive disease in patients who are unresponsive to other agents
47
Q

What are some biologic response modifiers that can be used for psoriasis?

MOA?

ADRs?

CIs?

A

Biologic Response Modifiers

  • Tumor necrosis factor inhibitors (etanercept, infliximab, adalimumab)
  • MOA: prevents TNF mediated immune responses
  • ADRs: risk of serious life-threatening infections (sepsis, pneumonia), exacerbation of congestive heart failure, and cause demyelinating disease in predisposed patients
  • What infectious disease must be ruled out before initiating therapy with TNF inhibitors? TB
48
Q

How can corticosteroids be administered? When is systemic therapy used? Topical application?

A
  • Topical Corticosteroids
  • Immunosuppressive and anti-inflammatory
  • Local (topical & intralesional) or systemic (IM, IV, PO)
  • Systemic therapy reserved for severe dermatological illness (allergic contact dermatitis to plants, life-threatening vesiculobullous dermatoses)
  • Corticosteroids are minimally absorbed following application to normal skin
49
Q

What is the relative variation of percutaneous corticosteroid absorption?

A

plantar arch - 0.14% absorbed

palm - 0.83%

forearm - 1.0%

scalp - 3.5%

forehead - 6.0%

genitalia - 42%

50
Q

How are topical corticosteroids grouped?

A

•Grouped into classes based on potency or approximate relative efficacy

51
Q

What are low to medium efficacy topical corticosteroids? What are they used for?

A

lowest - hydrocortisone 0.25-2.5%

low - betamethasone valerate 0.01%

intermediate - hydrocortisone valerate 0.1%

•Low to medium efficacy produce remission in disorders responsive to corticosteroids: seborrheic dermatitis, psoriasis of genitalia and face

52
Q

What are the high efficacy corticosteroids? What are they used for, and what are the ADRs?

A

high - betamethasone dipropionate 0.05%

highest - clobetasol propionate 0.05%

  • High efficacy preparations useful in disorder less responsive to corticosteroids: psoriasis of palms and soles, sarcoidosis
  • ADRs: suppression of pituitary-adrenal axis
  • Atrophy, steroid rosacea, steroid acne, allergic contact dermatitis
53
Q

What do keratolytic agents do? What is an example of one?

A
  • Keratolytic: peeling agent causing softening/dissolution or peeling of stratum corneum
  • Salicylic acid
54
Q

What are the uses and ADRs of salicylic acid?

A

salicylic acid - keratolytic agents

  • Uses: acne, seborrheic dermatitis, psoriasis, hyperkeratosis (corns, plantar warts, calluses); in combination with antifungal sodium thiosulfate for tinea versicolor
  • Salicylate toxicity can occur (nausea, vomiting, dizziness, loss of hearing, tinnitus, lethargy, diarrhea, psychic disturbances)
55
Q

What are some antipruritic agents? What are they used for?

A
  • Corticosteroids, local anesthetics
  • Topical therapy useful in localized pruritus
  • Systemic therapy generally used for generalized pruritus
  • Antihistamines
56
Q

What are some first and some second generation antihistamines? What are the ADRs?

A
  • First generation H1-receptor antagonists
  • Diphenhydramine, promethazine
  • Some anticholinergic activity, sedating, useful in nocturnal pruritus
  • Second generation H1-receptor antagonists
  • Cetirizine, loratadine, desloratadine, fexofenadine
  • Do no cross blood-brain barrier, lack anticholinergic side effects, non-sedating
57
Q

What are trichogenic agents? What are some drugs?

A
  • Trichogen: agent that promotes hair growth
  • Minoxidil
  • Finasteride
58
Q

What is the MOA and effects of minoxidil?

A

Minoxidil - trichogen

  • MOA: unknown
  • Originally developed as an antihypertensive (PO dosing)
  • Percutaneous absorption minimal but systemic effects on BP should be monitored in those with cardiac disease
59
Q

What is the MOA, ADRs and CIs of finasteride?

A
  • Finasteride
  • MOA: competitive and selective inhibitor of steroid 5α-reductase; blocks the conversion of testosterone to dihydrotestosterone (DHT)
  • ADRs: decreased libido, ejaculation disorders, erectile dysfunction
  • Pregnant women should not handle drug
60
Q
A

MSK II Test 2 (7 decks)

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