Anti Infectives

Question 1

B-lactams MOA

Answer 1

cell wall inhibitors- attach to PBPs (penicillin binding proteins) and weaken cell wall to cause cell lysis

Question 2

4 mechanisms of B-lactam resistance are?

Answer 2

1. inactivation of B-lactam ring
2. alteration of PBPs
3. reduction of antibiotic access to PBPs
4. elaboration of efflux mechanisms- kick antibiotics out

Question 3

Cell wall inhibitor drug examples

Answer 3

1. PCN
2. cephalosporins
3. ampicillin

Question 4

Cell metabolism inhibitor (protein synthesis) drug examples

Answer 4

1. macrolides
2. tetracyclines
3. aminoglycosides

Question 5

B-lactam most serious adverse reaction

Answer 5

allergic reactions- anaphlyaxis

Question 6

Marcolid drug interaction

Answer 6

Increases serum levels of drugs metabolized in liver

Question 7

Aminoglycosides adverse reactions

Answer 7

1. ototoxicity- toxic to 8th cranial nerve leading to audio and vestibular disturbances
2. nephrotoxicity
   * commonly used for in-patients or after transplant surgery**

Question 8

Metal ions do what to anti-bacterials

Answer 8

reduce absorption ex. calcium supplements, vitamins, antacids

Question 9

Sulfonamides and trimethoprim have what MOA

Answer 9

cell metabolism inhibitors or folic acid inhibitors

Question 10

Examples of cell replication inhibitors

Answer 10

quinolones, fluoroquinolones, nitrofurans

Question 11

What makes nitrofurans unique?

Answer 11

not an antibiotic, its metabolites are selectively toxic to DNA/RNA synthesis and protein synthesis of bacteria

Question 12

TB treatment

Answer 12

isoniazid and rifampin

Question 13

Polyenes MOA

Answer 13

binds sterols (ergosterol) and disrupts osmotic integrity of cell–fungicidal

Question 14

Polyenes specifically Amp B complications and drug interactions

Answer 14

Nephrotoxicity-major limitation to Amp B

Question 15

Azoles and allylamine MOA

Answer 15

ergosterol synthesis inhibitor

Question 16

Azoles complications and interactions

Answer 16

1. resistance b/c impair growth rather then cause cell death

2. numerous and possibly fatal drug interactions

Question 17

Echinocandins MOA

Answer 17

glucan synthase inhibitors

Question 18

What are echinocandins commonly used for

Answer 18

salvage therapy for HIV and AIDS patient with multi-drug resistant candidiasis

Question 19

Antivirals MOA

Answer 19

inhibit nucleic acid synthesis

Question 20

Is there a cure for herpes?

Answer 20

No. Antivirals work on replication process to reduce duration of symptoms

Question 21

Ganciclovir primarily used to treat?

Answer 21

CMV

Question 22

Cidofovir primarily used to treat?

Answer 22

ACV resistant HSV infections

Question 23

Anti-influenze agents include

Answer 23

amantidine, rimantidine, oseltamivir, zanamivir

Question 24

Amantidine and rimantidine MOA

Answer 24

inhibition of viral replication primarily M2 protein

Question 25

Oseltamivir and zanamivir MOA

Answer 25

inhibits influenza neuraminidase

Question 26

How to treat hepatitis?

Answer 26

interferon and ribavirin

Question 27

Nucleoside and nucleotide reverse transcriptase inhibitors (NRTIs)

Answer 27

prevent infection of susceptible cells to HIV

Question 28

Non-nucleotide RT inhibitors (NNRTIs) major adverse effect

Answer 28

fatal hepatitis

Question 29

HIV protease inhibitors do what

Answer 29

prevent viral maturation to infectious form

Question 30

HIV protease inhibitors main adverse effect

Answer 30

crystalluria and nephrolithiasis from poor drug soluability

Question 31

HIV entry inhibitors examples

Answer 31

enfuviritide and miraviroc

Question 32

Raltegravir MOA

Answer 32

HIV integrase inhibitor-prevents the formation of covalent bonds between host and viral DNA thus preventing virus integration into host chromosomes