Mechanisms of Action

Question 1

Reduce hyperkeratinization.

Answer 1

Keratolytics

Question 2

Reverse abnormal keratinization.

Answer 2

Retinoids

Question 3

Reduce microbial colonization and decrease inflammatory response.

Answer 3

Antibiotics

Question 4

Inhibits cholinesterase.

Answer 4

Malathion (Ovide)

Question 5

Vasoconstrictor effect.

Answer 5

Topical corticosteroids

Question 6

Inhibits phosphatase activity, resulting in inhibition of T-cell activation.

Answer 6

Calcineurin inhibitors

Question 7

Bind to sterols in the cell membrane of the fungus, causing increased membrane permeability and loss of intracellular contents.

Answer 7

Polyene antifungals

Question 8

Binds to ergosterol in fungi cell wall.

Answer 8

Amphotericin B

Question 9

Reduce ergosterol synthesis by inhibition of fungal cytochrome P450.

Answer 9

Triazole antifungals

Question 10

Reduce ergosterol synthesis by inhibition of fungal cytochrome P450, but less selective between human and fungal sterols, so more toxic.

Answer 10

Imidazole antifungals

Question 11

Inhibit the synthesis of ergosterol by

inhibiting squalene epoxidase.

Answer 11

Allylamine antifungals

Question 12

Inhibits epoxidation of squalene in fungi, so is toxic to fungi. Also reduces ergosterol and prevents synthesis of fungal
cell membrane.

Answer 12

Terbinafine (Lamisil)

Question 13

Inhibits fungal cell mitosis at metaphase by

interfering with cells mitotic spindle structure.

Answer 13

Griseofulvin

Question 14

Acts by chelating polyvalent cations (Fe+3) or (Al+3). Inhibits enzymes responsible for the breakdown of peroxidises within fungal cells.

Answer 14

Ciclopirox (Pen-Lac, Loprox)

Question 15

Mechanism of action unknown but may block

enzymes involved in growth of epithelial tissue.

Answer 15

Selenium sulfide

Question 16

These inhibit viral DNA synthesis.

Answer 16

Nucleoside analogues

Question 17

Inhibits DNA synthesis and viral replication. Competes with deoxyguanosine triphosphate binding. DNA templates into irreversible complexes. Causes chain termination following incorporation of viral DNA.

Answer 17

Acyclovir family

Question 18

Converted by body to acyclovir after oral administration via first pass.

Answer 18

Valacyclovir

Question 19

The diacetyl ester prodrug of 6-deoxypenciclovir.

Answer 19

Famciclovir

Question 20

Uses competitive inhibition of the viral DNA polymerase to block viral DNA synthesis.

Answer 20

Famciclovir

Question 21

Acyclovir family med that does NOT cause chain termination.

Answer 21

Famciclovir

Question 22

Activated in CMV infected cells. Inhibits viral DNA polymerase.

Answer 22

Ganciclovir

Question 23

Solubilizes cell surface proteins in stratum corneum. Possible desquamation.

Answer 23

Salicylic acid

Question 24

Possibly stimulates mononuclear cells to release interferon alpha and to stimluate macrophages to produce interleukins 1, 6, 8, and TNF alpha.

Answer 24

Imiquimod

Question 25

Cytotoxic with an affinity for the microtubule of the mitotic spindle. Interrupts in metaphase.

Answer 25

Podophyllum resin

Question 26

Block dopamine D2 receptors.

Answer 26

Typical antipsychotics (1st generation)

Question 27

Block D4, S2, and alpha-2 receptors.

Answer 27

Clozapine

Question 28

Block D4, D1, muscarinic, alpha-1, H1 receptors.

Answer 28

Olanzapine

Question 29

Block D2, S2, alpha-1, alpha-2, and H1 receptors.

Answer 29

Risperidone

Question 30

Decreases metabolic inactivation of catecholamines.

Answer 30

MAOIs

Question 31

Weak inhibitor of neuronal uptake of dopamine, NE, and serotonin.

Answer 31

Buproprion (Wellbutrin)

Question 32

Potently and selectively inhibit the serotonin uptake pump on presynaptic neuron. Increase concentration of 5-HT in synapse by inhibiting
reuptake, weak effect on NE and dopamine reuptake.

Answer 32

SSRIs

Question 33

At lower doses: primarily an SSRI.

Answer 33

Venlafaxine (Effexor)

Question 34

At higher doses: produces norepinephrine reuptake.

Answer 34

Venlafaxine (Effexor)

Question 35

Equivalent of adding an NSRI to an SSRI for augmented effects.

Answer 35

SNRIs (Effexor)

Question 36

Bind to molecular components of the gamma-aminobutyric acid (GABAA) receptors in the neuronal membranes in the CNS.

Answer 36

Benzodiazepines

Question 37

Potentiate GABA-ergic inhibition at all levels of the CNS. Leads to decreased firing rate of critical neurons in many regions of the brain.

Answer 37

Benzodiazepines

Question 38

Increase the amount of chloride current generated by GABAA receptor activation, potentiating the effects of GABA throughout the nervous system.

Answer 38

Benzodiazepines

Question 39

Blocks the reuptake of norepi and dopamine into presynaptic neurons.

Answer 39

Methylphenidate (Ritalin, Concerta, Daytrana)

Question 40

Noncatecholamine, sympathomimetic amines that promote release of catecholamines (primarily dopamine and norepi) from their storage sites in the presynaptic nerve terminals. Able to block reuptake of catecholamines.

Answer 40

Mixed amphetamine salts (Adderall)

Question 41

Noradrenergic reuptake inhibitor.

Answer 41

Strattera (Atomoxetine)

Question 42

Resorptive agents that block osteoclastic activity.

Answer 42

Bisphosphonates & Selective Estrogen Receptor Modulators

Question 43

Prevents the increased risk of breast and uterine cancer while maintaining bone integrity.

Answer 43

Raloxifine (Evista)

Question 44

Required for absorption of calcium from intestinal tract.

Answer 44

Vitamin D

Question 45

Regulates serum calcium and phosphate levels.

Answer 45

Calcitriol

Question 46

Critical in bone growth and remodeling.

Answer 46

Vitamin D

Question 47

Prevents thyroid hormone synthesis by blocking conversion of thyroxine (T4) to triiodthyroine (T3) in peripheral tissues.

Answer 47

Antithyroid drugs