High Yield Derm Pharm

Question 1

1–Clotrimazole/miconazole and 2–terbinafine(lamisil)/naftifine
What class are they?
3–What do they treat?
4–What is the MOA?

Answer 1

1– azoles

2–Allyamines

3–they are antifungal agents

4– MOA: inhibit squalene epoxidase, a key enzyme in ergosterol biosynthesis

Question 2

How do you treat MRSA?

Answer 2

–dependent on a thorough evaluation and requires oral or parenteral antibiotic therapy

Question 3

What are the most commonly used topical antibacterial agents? What are they treating?
Should you use them alone? Why?

Answer 3

–Clindamycin and Erythromycin used for acne

–DONT USE IN MONOTHERAPY!

–They should be used in combination with retinoids, benzoyl peroxide in order to decrease resistance

Question 4

**If you have a dry lesion you use a _____ agent, if you have a wet lesion you use a _____ agent

examples of each?

Answer 4

–wet/lubricating i.e. pastes, creams, ointments

–drying i.e. tinctures, wet dressings, lotions

Question 5

areas of body with highest absorption?

Answer 5

—face, scalp, axilla

Question 6

Why might you use a compress wrap along with topical treatments?

Answer 6

—Increased the absorption

Question 7

Amphotericin B treats what? why isn’t it used?

Answer 7

–Broad antifungal activity for systemic fungal infections

–Rarely used topically

–“amphoterrible”; cumulative organ toxicity

Question 8

Tolnaftate (Tinactin) used for?

Answer 8

–BOOM antifungal athletes foot

Question 9

Nystatin used for? why not used topically?

Answer 9

• -suspension antifungal against Oral thrush

- -limited bioavailability when used topically

Question 10

Oral antifungal agents?

Answer 10

–Azoles (Keto, Itra, Flucon, Voricon); systemic Yeast infxn

–Griseofulvin; dermatophyte infxn (hair, skin, nails). NOT CANDIDIA infxns

–Terbinafine; high first pass; builds up in skin, nails, fat. tinea infxns

Question 11

Antiviral agents?

How do they work?

What mode of application best treats herpes labialis, HSV, and VZV infxns?

Answer 11

—-Acyclocivr, valacyclovir, penciclovir, famiciclovir

–MOA: converted to pharmacological active triphosphate metabolites and inhibit viral DNA synthesis and viral replication

–Systemic is more effective than topical for these issues

Question 12

Imiquimod belongs to what class?

What does it treat?
What cancer does it treat?

MOA?

Answer 12

–Immunomodulators

–external genital and perinal warts in adults, actinic kearatosis of scalp

–basal cell carcinoma of the trunk/neck/extremities < 2cm in diameter

–Is an immune simulator but the exact MOA is unknown; see itching and redness because it is an immune stimulator

Question 13

Tacrolimus and Pimiecrolimus are what class?

What do they treat?

How do they work?

Answer 13

–Immunomodulator

– on boards = used in organ transplant rejection but may also be used for atopic dermatitis/psoriasis; they suppress immune response

–MOA; inhibit T-lymphocyte activation and prevent release of inflammatory cytokines and mediators from mast cells

Question 14

**Retinoic Acid, Adapalene, Tazarotene, and Isoretinoin are used for what?
MOA? What to watch out for?

**isoretinoinMOA? How do you give it? When to use/not use?

Answer 14

–acne TX

• -retinoids/retinoid derivatives react w/ retinoid nuclear receptor and increase/reduce gene transcription
• -avoid sun exposure (increase UV sunburn risk)
• -NOT 4 PREGO WOMEN
• *administer orally,
• *Isotretinoin MOA; reduces sebaceous gland size and reduces sebum production
• *used in unmanagable cystic acne and cutaneous/extracutaneous malignant neoplasms
• *dryness, itching of skin and membranes

Question 15

Acne prep:

Benzoyl peroxide MOA?

Answer 15

– release free-radical oxygen which oxidizes bacterial proteins in the sebaceous follicles decreasing the number of anaerobic bacteria and decreasing irritating-type free fatty acids

Question 16

Acne Prep:

Azelaic Acid MOA?

Answer 16

–antimicrobial against P. acnes as well as in vitro inhibitory effects on the conversion of testosterone to dihydrotestosterone

Question 17

Topical Psoriasis Drug classes

are topicals better than systemic drug txs?

Answer 17

• -Emollients (keep skin moist)
• -Corticosteroids
• -Vitamin D

–NO, systemic drugs are better for this issue

Question 18

Systemic Psoriasis Drugs

When are they used?

Answer 18

• -Methotrexate
• -Acitretin
• -Cyclosporine

–used when it covers > 10% of body or in the more debilitating cases

Question 19

Methotrexate MOA?

Answer 19

–inhibit dihydrofolate reductase

Question 20

Cyclosporine MOA?

Answer 20

inhibit calcineurin and thereby inhibits transcription of interleukin-1 and -2 receptors; blocks T-cell activation

Question 21

Etanercept, infliximab, adalimumab are what class?

What do they treat?

MOA?

Why are they risky?

Answer 21

–TNF inhibitors

–Treat psoriasis

–MOA; prevent TNF-mediated immune response

–might cause lymphoma and other cancers

Question 22

Alefacept is a what?

treats what?

MOA?

Answer 22

–immunosuppressive

–psoriasis

–fusion protein that interferes with lymphocyte activation

–stop when CD4 counts remain below 250cells/uL

Question 23

Ustekinumab treats what?

MOA?

Is a newer drug and probably wont be on the boards or on the test but will see in our third year rotations

Answer 23

– psoriasis

–interferes with proinflammatory cytokines IL-12 and IL-23

–linked to cardiovascular events

Question 24

Corticosteroids do what?

lowest efficacy?
Medium efficacy?
highest efficacy?

Answer 24

–anti-
inflammatory/immunosuppressive agents

–lowest = hydrocortisone (seb. dermatitis)

–medium = hydrocortisone valerate (seb. dermatitis)

– highest = Clobetasol propionate (psoriasis, sarcoidosis)

Question 25

Salicyclic Acid and Fluorouracil are what class?

Answer 25

–Keratolytic Agents

Question 26

How do Keratolytic agents work?

Answer 26

–peeling agent causing softening and dissolution/peeling of the stratum corneum

Question 27

Fluorouracil MOA?

Answer 27

–MOA; inhibits thymidylate synthetase and blocks the synthesis of DNA and RNA

Question 28

**FIRST generation H1-receptor antagonists Antipruritic agents?

MOA?

Answer 28

–Diphenhydramine and Promethazine

–MOA; antocholinergic activity and are sedating, making them useful for the control of pruritis

Question 29

**SECOND generation H1-receptor antagonists Antipruritic agents?

MOA?

how are they processed?

When not to give?

Answer 29

–Cetrizine, Loratadine, Desloratidine, Fexofenadine hydrochloride

–MOA; NONsedating and LACK antocholonergic effects b/c they dont cross Blood brain barrier

–metabolized by CYP34A and CYP2D6

–dont give with imidazole antifungals or macrolide antibiotics

Question 30

Trichogenic agents?

used for what?

MOA?

What happens when you stop treatment?

Answer 30

–Minoxidil (rogaine) and Finasteride (propecia)

– Hair growth

–MOA for Rogaine; unknown

–MOA for Propecia; competitive/selective inhibitor of type 2 isoenzyme of steroid of 5a-reductase; blocks the conversion of testosterone to DHT

–hair loss resumes when you stop these drugs

Question 31

Agents for Melanoma?

Answer 31

–BRAF inhibitors (vemurafenib, dabrafenib, trametinib)

–Ipilimumab

–Pegylated interferon

Question 32

BRAF inhibitors MOA?

Answer 32

–Vemura and Dabra MOA; Kinase inhibitors of BRAF V600E mutation

– Trameti MOA; Kinase inhibitor of BRAF V600E or V600K mutations

Question 33

When to use BRAF inhibitors?

Answer 33

–indicated in TX of UNresectable or metastatic melanoma with BRAF mutations and NOT for BRAF wild-type melanoma

Question 34

Ipilimumab MOA?

When is it used?

Answer 34

–MOA; CTLA-4 blocker antibody

–approved for TX of UNresectable or metastatic melanoma

Question 35

Vismodegib is a what?

MOA?

What does it treat?

Why didn’t i list the other antineoplastic drugs?

Answer 35

–Antineoplastic agent

– inhibits hedgehog pathway

–basal cell carcinoma or locally advanced basal cell carcinoma in adults who are not candidates for for surgery/radiation

– he said he only wanted to highlight Vismodegib on the slide and didn’t want to “spend alot of time” on the others