Sbm Pharmacology 1

Front 1

What is the most common mechanism of antiviral medicines?

Back 1

The most common mechanism of antiviral agents is interfering with DNA or RNA synthesis.

Front 2

What is Enfuvirtide’s mechanism of action with regards to HIV-1?

Back 2

Enfuvirtide blocks entry of HIV-1 into cells (preventing adsorption and penetration) by preventing the uncoiling of HIV’s gp41.

Front 3

Which two drugs stop influenza uncoating from happening?

Back 3

Amantidine and Ramantidine block Influenza’s M2 protein, a proton-pumping pore, which stops influenza uncoating.

Front 4

What drug blocks synthesis of the early proteins required to regulate CMV gene expression?

Back 4

Fomivirsen blocks early protein synthesis of proteins for CMV. It’s complementary to mRNA, but otherwise its mechanism has not been elucidated. Given systemically, the drug is toxic. It can be injected into eyeballs of pts with CMV retinitis, and it can act locally

Front 5

How do purine and pyrimidine analogues inhibit nucleic acid synthesis (2 mechanisms)?

Back 5

Purine and pyrimidine analogues:
1) Block viral polymerase
2) Some also cause chain termination

Front 6

What drug would be used to treat a flare up of herpes zoster, and what are its mechanisms?

Back 6

Acyclovir: 1) inhibits viral DNA polymerases and 2) acts as a chain terminator (same mechanisms as other purine and pyrimidine analogues).

Front 7

What are the 5 antiviral drugs given for CMV?

Back 7

1) Purine analogues (also effective against HSV and VZV)
a. Ganciclovir
i. Mechanism of action: viral enzymes phosphorylate the drugs to the monophosphate derivative. Ganciclovir triphosphate inhibits viral polymerase
b. Valganciclovir
2) Cidofovir
3) Foscarnet
4) fomivirsen

Front 8

What is the mechanism of action for Foscarnet, and what illnesses can it be used to treat?

Back 8

Foscarnet directly inhibits viral DNA polymerase, and it can be used for HSV 1 and 2, varicella-zoster virus and cytomegalovirus.

Front 9

What would you use to treat acyclovir-resistant HSV?

Back 9

Foscarnet would be used to treat acyclovir-resistant HSV. It directly inhibits viral DNA polymerase.

Front 10

How do Zanavir and Oseltamivir work, and what virus are they used against?

Back 10

Zanamivir and Oseltamivir work by inhibiting influenza (A&B) neuraminidase, and they both:
• block the release of virus from the host cell
• block spread within the respiratory tract
• promote viral clumping.

Front 11

Why couldn’t you use amantadine or rimantadine to treat influenza B?

Back 11

Amantadine and rimantidine only treat influenza A, because only influenza A has the M2 pore. Both drugs work by blocking Influenza A’s M2 proton-pumping pore.

Front 12

What is the composition of HAART in terms of drug classes?

Back 12

HAART is a “drug cocktail” composed of at least 3 drugs from at least 2 different classes.

Front 13

Can you name one nucleoside reverse transcriptase inhibitor and its mechanism of action?

Back 13

Zidovudine is an NRTI, and it works by inhibiting the unique reverse transcriptase enzyme (RNA->DNA).

Front 14

Can you name a non-nucleoside reverse transcriptase inhibitor and its mechanism of action?

Back 14

Efavirenz is a non-nucleoside reverse transcriptase inhibitor, and it binds to a site distant from the nucleotide binding site of reverse transcriptase enzyme and causes a conformational change that inactivates the reverse transcriptase enzyme.

Front 15

Can you name a protease inhibitor for treatment of HIV and its mechanism of action?

Back 15

atazanavir is a protease inhibitor, and it inhibits HIV protease. If the polyprotein remains uncleaved, the virions which are assembled are non-functional. A protease is essential for post-translational cleavage of gag and gag-pol polyproteins, producing active viral core proteins.

Front 16

What are 3 situations where HIV infection could be prevented by HIV antiviral medications?

Back 16

1) Maternal-infant transmission
2) Needle stick injuries
3) Sexual partner infection

Front 17

What is the definition of a noncompetitive allosteric site antagonist?

Back 17

The allosteric site is accessible in the absence of the agonist.

Front 18

What is the definition of an uncompetitive allosteric site antagonist?

Back 18

The allosteric site requires receptor activation before it becomes accessible to a drug.

Front 19

What is the definition of the therapeutic index?

Back 19

LD50/ED50 (therefore, a higher Therapeutic index is better).

Front 20

What does a Schild analysis do?

Back 20

A Schild analysis provides an agonist-independent measure of the equilibrium constant, Kb.

Front 21

What are 3 things that confer the selectivity of drug action?

Back 21

1. Drug structure
2. Receptor distribution
3. Pharmocokinetics

Front 22

Which way do Spare receptors shift the concentration curve?

Back 22

Spare receptors shift the curves to the right.

Front 23

How does the curve for a spare receptor vary in the presence of noncompetitive antagonists?

Back 23

It looks like the curve for increasing concentration of inhibitory antagonist.

Front 24

What is the law of mass action?

Back 24

The rate of a chemical reaction is directly proportional to the product of the effective concentrations of each participating molecule.

Front 25

How do noncompetitive antagonists affect the dose-response curve?

Back 25

It shifts it down, because the antagonist either binds irreversibly or at a site distinct from the agonist binding site such that it decreases the ability of the agonist to bind to its site. Thus, there is effectively less receptors available for the agonist to bind.

Front 26

How does a competitive antagonist affect the dose-response curve and why?

Back 26

Competitive agonists shift the dose-response curve to the right, because the bind reversibly, increasing the concentration of agonist necessary to achieve the same response as before.

Front 27

Describe the action of inverse agonists.

Back 27

Inverse agonists reduce constitutive activity of receptors.

Front 28

What’s the molecular nature of most drug targets?

Back 28

Most drugs target GPCRs

Front 29

What type of channels are GABA channels, and what type of molecule passes through them?

Back 29

GABA channels are chloride ionotropic channels with inhibitory activity (i.e., they hyperpolarize the membrane). They also happen to be pentameric.

Front 30

What type of stimulus is provided by glutamate receptors?

Back 30

Glutamate receptors provide excitatory stimulus, unlike GABA receptors.

Front 31

What’s the difference between the time scale of action of ionotropic versus metabotropic receptors?

Back 31

Ionotropic receptors act quickly (msec), whereas metabotropic receptors act more slowly (seconds-minutes)

Front 32

What does tachyphylaxis mean?

Back 32

Tachyphylaxis is a reduction in drug effectiveness in the continued presence of agonist or with repeated application (tachyphylaxis).