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Flashcards in Anti Infectives Deck (32)
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1
Q

B-lactams MOA

A

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

2
Q

4 mechanisms of B-lactam resistance are?

A
  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
3
Q

Cell wall inhibitor drug examples

A
  1. PCN
  2. cephalosporins
  3. ampicillin
4
Q

Cell metabolism inhibitor (protein synthesis) drug examples

A
  1. macrolides
  2. tetracyclines
  3. aminoglycosides
5
Q

B-lactam most serious adverse reaction

A

allergic reactions- anaphlyaxis

6
Q

Marcolid drug interaction

A

Increases serum levels of drugs metabolized in liver

7
Q

Aminoglycosides adverse reactions

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

Metal ions do what to anti-bacterials

A

reduce absorption ex. calcium supplements, vitamins, antacids

9
Q

Sulfonamides and trimethoprim have what MOA

A

cell metabolism inhibitors or folic acid inhibitors

10
Q

Examples of cell replication inhibitors

A

quinolones, fluoroquinolones, nitrofurans

11
Q

What makes nitrofurans unique?

A

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

12
Q

TB treatment

A

isoniazid and rifampin

13
Q

Polyenes MOA

A

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

14
Q

Polyenes specifically Amp B complications and drug interactions

A

Nephrotoxicity-major limitation to Amp B

15
Q

Azoles and allylamine MOA

A

ergosterol synthesis inhibitor

16
Q

Azoles complications and interactions

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

2. numerous and possibly fatal drug interactions

17
Q

Echinocandins MOA

A

glucan synthase inhibitors

18
Q

What are echinocandins commonly used for

A

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

19
Q

Antivirals MOA

A

inhibit nucleic acid synthesis

20
Q

Is there a cure for herpes?

A

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

21
Q

Ganciclovir primarily used to treat?

A

CMV

22
Q

Cidofovir primarily used to treat?

A

ACV resistant HSV infections

23
Q

Anti-influenze agents include

A

amantidine, rimantidine, oseltamivir, zanamivir

24
Q

Amantidine and rimantidine MOA

A

inhibition of viral replication primarily M2 protein

25
Q

Oseltamivir and zanamivir MOA

A

inhibits influenza neuraminidase

26
Q

How to treat hepatitis?

A

interferon and ribavirin

27
Q

Nucleoside and nucleotide reverse transcriptase inhibitors (NRTIs)

A

prevent infection of susceptible cells to HIV

28
Q

Non-nucleotide RT inhibitors (NNRTIs) major adverse effect

A

fatal hepatitis

29
Q

HIV protease inhibitors do what

A

prevent viral maturation to infectious form

30
Q

HIV protease inhibitors main adverse effect

A

crystalluria and nephrolithiasis from poor drug soluability

31
Q

HIV entry inhibitors examples

A

enfuviritide and miraviroc

32
Q

Raltegravir MOA

A

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