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MSK II Exam I > Drugs- Dermatologic Pharm (Kinder) > Flashcards

Drugs- Dermatologic Pharm (Kinder) Flashcards

1
Q

what are the major variables determining pharm response of skin

A

drug penetrance

concentration gradient

dosing schedule

vehicles and occlusion
-occlusion is trapping of a liquid within cavities on the skin, which can be extremely effective in maximizing drug efficacy

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2
Q

what are the three routes that molecules can penetrate the skin

A

through intact stratum corneum

sweat ducts

sebaceous follicles

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3
Q

what is the rate of absorption

A

J = Cveh * Km * D/x

i) Where J is the rate of absorption, Cveh is the concentration of drug in vehicle, Km is the partition coefficient, D is the diffusion coefficient, and x is the thickness of the stratum corneum (Piacquadio and Kligman, 1998).
ii) The rate of absorption is directly related to the concentration of drug, the partition coefficient, and the diffusion coefficient and inversely related to the thickness of the stratum corneum.

corneum is the rate limiting step

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4
Q

what is the partition coefficient

A

release of drug from the vehicle

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5
Q

what is the diffusion coefficient

A

drug diffusion across the layers of the skin reaching its site of action

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6
Q

what are the preferable characteristics of topical drugs

A

low molecular mass

adequate solubility in oil/lipids and water

high lipid:water partition coefficient

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7
Q

in order of their ability to retard evaporation from the surface of skin, name some dermatological vehicles

A

tinctures < wet dressings < lotions < gels < aerosols < powders < pastes < creams < ointments

wet - pulls excess moisture from the skin

acne preps
-if the pt has oily skin, using a wet dressing are good for oily skin
dry skin- use cream or ointment to prevent evaporation

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8
Q

i) Acute inflammation with oozing, vesiculation, and crusting is best treated with what?

A

drying preparations such as tinctures, wet dressings, and lotions.

picks up excess moisture from the skin

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9
Q

ii) Chronic inflammation with xerosis, scaling, and lichenification is best treated with what ?

A

more lubricating preparations such as creams and ointments.

prevents excess evaporation

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10
Q

where is drug penetrance of skin higher

A

face

intertriginous areas

perineum

axilla, grow

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11
Q

how does water content of the stratum corneum affect absorption

A

i) Absorption of pharmaceutical agents is increased as the water content of the stratum corneum is increased (i.e., the more hydrated the skin the more drug absorption will occur).
iii) Methods of hydration include occlusion with an impermeable film, application of lipophilic occlusive vehicles such as ointments, and soaking dry skin before occlusion.

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12
Q

how does age affect absorption of drugs via skin

A

i) Due to the fact that children have a greater surface area to mass ratio than adults, a given amount of topical drug will result in a greater systemic dose in children.
ii) Research studies have shown that term infants possess a stratum corneum with barrier properties comparable with adults; however, preterm infants have markedly impaired barrier function.

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13
Q

MOA of bacitracin and gramicidin

A

i) MOA: inhibits cell wall synthesis (bacitracin); binds phospholipids and increases permeability of cell wall (gramicidin).

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14
Q

spectrum of bacitracin and gramicidin

A

ii) Spectrum: gram-positive organisms (streptococci, pneumococci, staphylococci) and most anaerobic cocci, neisseriae, tetanus bacilli, and diphtheria bacilli.

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15
Q

MOA mupirocin (pseudomnonic acid A)

A

i) MOA: inhibits protein synthesis (binds to bacterial isoleucyl-tRNA synthetase).

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16
Q

spectrum of Mupirocin

A

ii) Spectrum: most gram-positive aerobic bacteria, including methicillin-resistant S. aureus (MRSA).
iii) Effective treatment for impetigo caused by S. aureus and group A β-hemolytic streptococci.

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17
Q

Polymyxin B sulfate MOA

A

i) MOA: binds phospholipids and increases permeability of cell wall membrane.
iii) Among main ingredients in Neosporin (with bacitracin and neomycin).

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18
Q

Polymyxin B sulfate spectrum

A

ii) Spectrum: gram-negative organisms including P. aeruginosa, E. coli, Enterobacter, Klebsiella.

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19
Q

high levels of polymyxin B sulfate can cause what?

A

neurotoxicity and nephrotoxicity

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20
Q

MOA neomycin and gentamicin

A

i) MOA: irreversibly binds 30S subunit and inhibits protein synthesis.

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21
Q

Spectrum of Neomycin and Gentamicin

A

gram-negative organisms including E. coli, Enterobacter, Klebsiella, Proteus, P. aeruginosa (gentamicin), staphylococci (gentamicin), group A β-hemolytic streptococci (gentamicin).

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22
Q

if a pt has renal failure and is taking neomycin and gentamicin , what might happen

A

renal failure may cause nephrotoxicity, neurotoxicity, ototoxicity if serum levels become detectable (rare).

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23
Q

Clindamycin
Erythromycin
Metronidazole

A

used as topical antibiotics in treatment of acne

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24
Q

MOA and spectrum of Clindamycin

A

ii) Clindamycin
(1) MOA: inhibits protein synthesis by reversibly binding to 50S ribosomal subunit.

(2) Activity against Propionibacterium acnes thought to be beneficial effect in acne treatment.

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25
Q

MOA of erythromycin

A

iii) Erythromycin

(1) MOA: inhibits protein synthesis by reversibly binding to 50S ribosomal subunit.

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26
Q

what complications might occur with the use of topical erythromycin for acne

A

(2) Complications include development of antibiotic resistant staphylococci; if this occurs, discontinue topical treatment and begin systemic antibiotic therapy.

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27
Q

Metronidazole

MOA and spectrum

A

(1) MOA: interacts with DNA resulting in strand breakage; anti-inflammatory effects.
(2) Effective in the treatment of acne rosacea.

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28
Q

in what pt’s is metronidazole contraindicated

A

(3) Not recommended during pregnancy or nursing due to carcinogenic nature.

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29
Q

Topical antifungal:

azole MOA

A

(1) MOA: inhibits synthesis of ergosterol (an essential component of the fungal cell membrane) by inhibiting fungal cytochrome P450 activity (lanosterol 14-α-demethylase).

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30
Q

what are the uses of azoles

A

(2) Used for 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).
(3) Clotrimazole and miconazole are the prototype azoles used for Candidiasis infections that can be treated topically (topical formulations not suitable for oral, vaginal, or ocular use).

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31
Q

Ciclopierox olamine

A

topical antifungal

(1) Broad-spectrum antimycotic agent.
(2) MOA: inhibits the uptake of precursors of macromolecular synthesis disrupting synthesis of DNA, RNA, and protein.

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32
Q

uses for ciclopirox olamine

A

(3) Used to treat topical dermatomycosis, candidiasis, and tinea versicolor and mild to moderate onychomycosis of fingernails and toenails at higher topical concentrations (poor efficacy with overall cure rate approximately 12%).

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33
Q

allylamines (terbinafine and naftifine) MOA and uses

A

topical antifungal

(1) MOA: inhibits squalene epoxidase, a key enzyme in ergosterol biosynthesis.
(2) Effective for topical treatment of tinea corporis, tinea cruris, and tinea pedis.

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34
Q

Butenafine

A

(1) Similar to allylamines in MOA and use.

topical antifungal

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35
Q

Tolnaftate
MOA and uses

what is this ineffective against ?

A

Topical antifungal

(1) Effective in the treatment of most cutaneous mycoses but is ineffective against candida.
(2) MOA: exact antifungal MOA unknown.
(3) Used for tinea pedis, tinea cruris, and tinea corporis.

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36
Q

Nystatin and amphotericin B

MOA

A

(1) MOA: binds to ergosterol in fungal cell membrane and alters membrane permeability, leading to the loss of potassium and other cell constituents (ineffective against dermatophytes).
(2) Nystatin is limited to topical cutaneous and mucosal uses (poor oral bioavailability), which includes its use as an oral suspension for the treatment of oral candidiasis (thrush).
(3) Amphotericin B has a broader antifungal spectrum and is used intravenously (lesser applications topically; may cause yellowing of the skin if used in a cream vehicle).

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37
Q

ADR’s of amphotericin B

A

topical antifungal

(4) Amphotericin B causes infusion related toxicity (fever, shills, muscle spasms, vomiting, headache, and hypotension) and cumulative organ toxicity (kidney in almost all patients, liver, anemia), which has given this drug the nickname ‘ampho-terrible’

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38
Q

what are the oral antifungal agents

A

azoles

  • fluconazole
  • itraconazole

Griseofulvin

Terbinafine

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39
Q

what are the uses of oral azoles and what are the drug drug interactions

A

(1) Applicable in cases of vaginal, urinary, oropharyngeal or esophageal candida infections, onychomycosis.
(2) Systemic yeast infections are more common in immune compromised patients, such as those with type 1 diabetes, leukemia, or AIDS.

(4) Involved in numerous drug-drug interactions by decreasing rate of drug metabolism (e.g., results in increased INR in patients receiving warfarin and co-administration with statins increases risk of rhabdomyolysis).

40
Q

what are the topical antivirals used?

A

acyclovir

penciclovir

docosanol (Abreva)

41
Q

MOA of acyclovir and penciclovir

A

(1) Randomized trials of patients with sporadic recurrences of HSV-1 infection showed that antiviral therapy with topical creams or ointments are of modest benefit.
(2) Synthetic guanine analogs; inhibitory activity against members of herpesvirus family (HSV1 & 2)
(3) MOA: converted to pharmacologically active triphosphate metabolites, inhibit viral DNA synthesis and viral replication

topically used for recurrent orolabial HSV infections (immunocompetent)

42
Q

Docosanol MOA

A

(1) MOA: inhibits fusion between the plasma membrane and the HSV envelope, thereby preventing viral entry and replication.

can shorten duration of orolabial herpes

43
Q

Imiquimod

MOA

uses

A

Immunomodulator

i) Approved for the treatment of 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.
ii) MOA: may be related to stimulation of peripheral mononuclear cells to release interferon-α and macrophage stimulation to produce interleukins-1, -6, -8, and tumor necrosis factor-α (TNF-α).

44
Q

Tacrolimus and Pimecrolimus MOA

A

immunomodulators

iii) MOA: inhibit T-lymphocyte activation and prevent release of inflammatory cytokines and mediators from mast cells.

45
Q

uses of Tacrolimus

A

i) Macrolide immunosuppressant beneficial in treatment of atopic dermatitis as a second-line agent.

46
Q

what are the ADR’s of tacrolimus and which patients do you NOT use this drug

A

iv) Common topical adverse effects include transient erythema, burning, and pruritus (systemic adverse effects are hypertension, nephrotoxicity, neurotoxicity, GI symptoms, hyperglycemia, hyperlipidemia).

do not use in immunocompromised patients or children < 2 years.

47
Q

Exposure to what is responsible for most of the erythema and sunburn associated with sun exposure and tanning

A

a) Exposure to UVB rays responsible for most of the erythema and sunburn associated with sun exposure and tanning.

b) Chronic exposure to UVB rays (280-320 nm) induces aging of the skin and photocarcinogenesis.
c) Long-wave UVA rays (320-400 nm) associated with skin cancer and aging.

48
Q

what three classes of chemicals are most often used in sunscreens

A

i) p-aminobenzoic acid (PABA)
ii) Benzophenones (oxybenzone, dioxybenzone, sulisobenzone)
iii) Dibenzoylmethanes (Parasol, Eusolex)

49
Q

how long is sunscreen effective period.

A

2 hours

i) Sunscreens should be uniformly applied approximately 15-30 minutes before sun exposure.
ii) The American Academy of Dermatology recommends a sunscreen of SPF 30 or higher be used in most circumstances.
iii) Most adults need one ounce of sunscreen. Reapply every 2 hours.

50
Q

Tretinoin (all trans retinoic acid)

(Acid form of Vitamin A)

MOA

A

(a) MOA: exact mechanism in the treatment of acne unknown; may decrease cohesion between epidermal cells and increase epidermal cell turnover, thought to result in the expulsion of open comedones and the transformation of closed comedones into those that are open (also marketed as an anti-wrinkle cream).

51
Q

what are Adapalene and Tazarotene

A

retinoic acid derivatives

52
Q

Adapalene

uses

A

retinoic acid derivative

(a) Photo-chemically more stable and less irritating than tretinoin.
(b) Used to treat mild to moderate acne vulgaris.

53
Q

tazarotene uses

A

retinoic acid derivative

(a) Approved for psoriasis, photoaging, acne

54
Q

in what pt’s are topical retinoids NOT recommended

A

pregnant women

55
Q

Adverse effects of tretinoin

A

(c) Common adverse events include erythema, mild peeling, and dryness; patients advised to avoid or minimize sun exposure (patients may experience photosensitivity reactions because of enhanced reactivity to UV radiation, increases their risk for severe sunburn).
(d) Initial therapy may aggravate acne but continual treatment increases the likelihood of optimal clinical improvement.

56
Q

(1) Isotretinoin
what is this?
MOA

uses

A

oral acne preparation

(b) MOA: reduces sebaceous gland size and reduces sebum production.
(a) Use restricted to the treatment of unmanageable severe cystic acne, disorders of keratinization, psoriasis, and cutaneous and extracutaneous malignant neoplasms.

57
Q

Adverse effects of isotretinoin

A

(a) Use restricted to the treatment of unmanageable severe cystic acne, disorders of keratinization, psoriasis, and cutaneous and extracutaneous malignant neoplasms.
(f) Severe side effects include headache, corneal opacities, pseudotumor cerebri, inflammatory bowel disease, anorexia, alopecia, muscle and joint pains, suicide risk.

58
Q

in what pt’s is isotretinoin contraindicated

A

pregnancy

(g) Teratogen; serum pregnancy test MUST be obtained within 2 weeks before starting therapy.

59
Q

MOA of Benzoyl peroxide

A

i) MOA: releases free-radical oxygen which oxidizes bacterial proteins in the sebaceous follicles decreasing the number of anaerobic bacteria and decreasing irritating-type free fatty acids.
ii) Prodrug converted to benzoic acid within the epidermis and dermis.

used for P. acnes

60
Q 
Acitretin 
Tazarotene
Calcipotriene
cyclosporine
TNF inhibitors
A

Drugs for psoriasis

61
Q

acitretin

A

i) Retinoic acid derivative given orally for the treatment of severe psoriasis, especially pustular form

62
Q

contraindications of acitretin

A

v) Contraindicated in any women who are pregnant or may become pregnant during treatment or at any time for at least 3 years after treatment (patient must commit to using two effective forms of birth control starting 1 month prior to treatment and for 3 years after discontinuation); similar restrictions for blood donation.
iv) Combination with ethanol can form etretinate, a highly teratogenic compound that may be found in plasma and subcutaneous fat for up to 3 years.

63
Q

b) Tazarotene

A

i) Topical retinoid prodrug used in the treatment of psoriasis, acne, photoaging.
ii) Active metabolite binds to retinoic acid receptors; may affect expression of genes that modulate cell differentiation, proliferation, and inflammation.

64
Q

Calcipotriene

A

i) Synthetic vitamin D3 analog that regulates skin cell production and proliferation.

ii) Used alone or in fixed combination with betamethasone dipropionate for the topical treatment of plaque-type psoriasis. Combination more effective than either agent used alone.
iii) Adverse effects include burning, itching, mild irritation, dryness, erythema; avoid contact with face and eyes.

65
Q

cyclosporine

MOA

A

i) MOA: inhibits calcineurin (phosphatase that enhances cytokine transcription) and thereby inhibits transcription of interleukin-1 and -2 receptors; blocks T-cell activation (immunosuppressant agent).
ii) PO dosing approved for treatment of psoriasis, rheumatoid arthritis, and liver, heart, kidney, and bone marrow transplants.

66
Q

what are the side effects of cyclosporine

A

iii) Side effects include significant nephrotoxicity, hypertension, hepatotoxicity, gingival hyperplasia, and hirsutism.

67
Q

Etanercept
infliximab
adalimumab

A

Biologic response modifiers

TNF inhibitors

68
Q

Etanercept MOA

A

(a) Dimeric fusion protein of the extracellular ligand-binding portion of the human tumor necrosis factor (TNF) receptor linked to the Fc portion of human IgG1.
(b) MOA: binds to TNF α and β and prevents TNF-mediated immune response.

treat psoriasis

69
Q

infliximab MOA

A

(a) Chimeric IgG1 monoclonal antibody.
(b) MOA: binds to soluble and transmembrane forms of TNF-α and inhibits TNF receptor activation.

psoriasis treatment

70
Q

adalimumab MOA

A

(a) Recombinant IgG1 monoclonal antibody
(b) MOA: binds to TNF-α and inhibits TNF receptor activation.

psoriasis treatment

71
Q

ADR;s of TNF alpha inhibitors

A

(4) TNF-α inhibitors can cause serious life-threatening infections (e.g., sepsis, pneumonia), exacerbate congestive heart failure, and cause demyelinating disease in predisposed patients.
(5) Evaluate for tuberculosis risk factors and latent disease prior to initiating therapy.
(6) There is a possible association between the use of TNF blockers and the development of lymphoma and other cancers.

72
Q

what are the adverse effects of topical corticosteroids

A

(1) Suppression of the pituitary-adrenal axis, Cushing’s syndrome and other systemic effects with long-term use.
(2) Atrophy, steroid rosacea, perioral dermatitis, steroid acne, increased intraocular pressure, allergic contact dermatitis.

73
Q

what are some examples of common topical corticosteroids

A

hydrocortisone (among the lowest efficacy), (methyl)prednisolone, dexamethasone, betamethasone, mometasone, triamcinolone, and clobetasol propionate (among the highest efficacy).

74
Q

what is a keratolytic agent

A

a) A keratolytic agent is a peeling agent that causes softening/dissolution or peeling of the stratum corneum of the epidermis.

75
Q

salicylic acid

A

keratolytic agent

i) Approved for treatment of acne, seborrheic dermatitis, psoriasis, hyperkeratosis (corns, plantar warts, calluses); in combination with antifungal sodium thiosulfate for tinea versicolor.
ii) Can be destructive to tissues at concentrations greater than 6% (keratolytic at 3-6%).

76
Q

what are the adverse effects of salicylic acid and in what pt’s must you use caution

A

iii) Salicylate toxicity can occur (nausea, vomiting, dizziness, loss of hearing, tinnitus, lethargy, diarrhea, psychic disturbances).
iv) Use care in patients with diabetes or peripheral vascular disease.

77
Q

MOA of Fluorouracil

A

keratolytic agent

i) Fluorinated pyrimidine antimetabolite resembling uracil used in the topical treatment of multiple actinic keratosis.
ii) MOA: inhibits thymidylate synthetase and interferes with DNA synthesis (effects most pronounced on rapidly proliferating cells).
iii) Adverse topical effects include pain, pruritus, burning, residual post-inflammatory hyperpigmentation; avoid excessive exposure to sun during treatment.

78
Q

first generation antihistamines as antipruitic agents

examples?
uses?

A

iv) First generation H1-receptor antagonists
(1) Examples include diphenhydramine and promethazine
(2) Have some anticholinergic activity and are sedating, making them useful for the control of nocturnal pruritus.

79
Q

2nd generation antihistamines as antipruitic agents

examples
uses

A

v) Second generation H1-receptor antagonists
(1) Lack anticholinergic side effects, do not cross blood-brain barrier, and are nonsedating.

(2) Examples include cetirizine, loratadine, desloratadine, fexofenadine hydrochloride.
(3) Second generation blockers are metabolized by CYP3A4 and CYP2D6 and should not be co-administered with medications that inhibit these enzymes (e.g., imidazole antifungals, macrolide antibiotics).
i) H¬1-receptor antagonists are useful in the treatment of pruritus.

80
Q

what is a trichogen

A

an agent that promotes the growth of hair

81
Q

minoxidil (rogaine)

A

used for androgenic alopecia
MOA not known

iii) Response rate better for vertex balding than frontal balding.
iv) Treatment must be continued or any drug-induced hair growth will be lost.
v) Percutaneous absorption is minimal but systemic effects on blood pressure should be monitored in patients with cardiac disease.

82
Q

finasteride MOA

A

i) Used for treatment of androgenic alopecia and benign prostatic hypertrophy.
ii) MOA: competitive and selective inhibitor of steroid 5α-reductase; blocks the conversion of testosterone to dihydrotestosterone (DHT).
iv) Treatment must be continued to sustain benefit.

83
Q

what are the predictable adverse effects of finasteride

A

iii) Predictable adverse effects: decreased libido, ejaculation disorders, erectile dysfunction.
v) Pregnant women should not be exposed to drug, either by use (not approved for use in women) or handling, due to risk of hypospadias in male fetus.

84
Q

Which two topical antimicrobials cover group A β-hemolytic streptococci and S. aureus (including MRSA)?

A

retapamulin

mupirocin

85
Q

general treatment approach for non-bullous impetigo

A

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

why can’t we used bacitracin-neomycin-polymyxin B?
-not as effective
can cause contact dermatitis

86
Q

increased sebum production in acne creates a lipid rich micro-aerobic environment favorable to what organism

A

gram positive rod –> propionbacterium acne

87
Q

what are the options for treatment of dermatophyte infections ?

A

Tinea capitis (scalp) – oral griseofulvin, terbinafine, itraconazole

Tinea pedis (feet) – topical antifungals

Tinea cruris (groin) – topical antifungals

Tinea corporis (body) – topical antifungals, oral antifungals

88
Q

what are the treatment options for candida

A

Thrush (oropharyngeal candidiasis) – oral nystatin, clotrimazole troche, oral fluconazole
Esophageal candidiasis – systemic antifungals
Vulvovaginitis – topical antifungals, oral fluconazole
Invasive infection – systemic antifungals

89
Q

mild acne?

A

few lesions, little or no inflammation

90
Q

moderate acne

A

many lesions

signficiant inflammation

91
Q

severe acne

A

numerous lesions

extreme inflammation, signficant scarring

92
Q

treatment for comedonal (non-inflammatory acne)

A

topical retinoid

93
Q

mild papulopustural and mixed acne treatment

A

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

94
Q

treatment for moderate papulopustular and mixed acne or moderate nodular acne?

A

topical retinoid AND oral antibiotic AND topical BPO

95
Q

treatment for Severe nodular/conglobate acne

A

Oral isotretinoin

96
Q

in the treatment of mild/moderate psoriasis, what are the first line agents

A

emollients - reduce scaling, itching

keratolytics - reduce hyperkeratosis

topical glucocorticoids - control inflammation and itching

topical!

97
Q

treatment of systemic psoriasis (>5% of body surface area)

A

methotrexate- don’t use in kidney or liver dysfunction

acitretin -don’t use in pregnancy and heavy alcohol use

cyclosporine - don’t use in kidney dysfunction and HTN

MSK II Exam I (6 decks)

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