While bacteriocidal antibiotics frequently work by disrupting bacterial cell structure, what is the common mechanism through which bacteriostatic antibiotics impact bacteria?the common mechanism through which bacteriostatic antibiotics impact bacteria? a. disruption of their local tissue environment – not a mechanism of action by these drugs b. acidification of local tissue – nor a mechanism of action by these drugs *c. disruption of their metabolic processes - a slower process d. consumption of bacterial nutrients – not a mechanism of action by these drugs

*c. disruption of their metabolic processes - a slower process

While bacteriocidal antibiotics frequently work by disrupting bacterial cell structure, what is the common mechanism through which bacteriostatic antibiotics impact bacteria?the common mechanism through which bacteriostatic antibiotics impact bacteria?

a. disruption of their local tissue environment – not a mechanism of action by these drugs

b. acidification of local tissue – nor a mechanism of action by these drugs

c. disruption of their metabolic processes - a slower process

d. consumption of bacterial nutrients – not a mechanism of action by these drugs

*c. disruption of their metabolic processes - a slower process

Objective: demonstrate understanding of the differences between bacteriocidal and bacteriostatic antibiotic mechanism of action

2. Prodrugs require which of the following?

a. an acid environment – not required

b. metabolic conversion to their active form – required to convert the prodrug to activity

c. a second drug that activates them – not required

d. a second bacterial species to activate them – not required

*b. metabolic conversion to their active form – required to convert the prodrug to activity

 

Objective: demonstrate understanding of prodrug activity

3. Probiotics have which of the following properties or characteristics?

a. nonpathogenic bacteria

b. increase normal immune response

c. consume nutrients required by pathogens

d. all of the above – all of these mechanisms are involved

*d. all of the above – all of these mechanisms are involved

Objective: demonstrate an awareness of drug resistance mechanisms

5. Resistance of pneumococci to Penicillin G is due to:

a. alterations in porin structure – not a mechanism of resistance for Pen G

b. Beta-lactamase production – not a mechanism of resistance for Pen G

c. changes in the structure of target penicillin-binding proteins – mechanism of resistance for Pen G

d. decreased intracellular accumulation of penicillin G – not a mechanism of resistance for Pen G

*c. changes in the structure of target penicillin-binding proteins – mechanism of resistance for Pen G

Objective: demonstrate understanding of the mechanism of resistance to Pen G

4. Antibiotic drug resistance mechanisms include which of the following mechanisms?

a. production of enzymes that inactivate the drug

b. synthesis of a modified target for the drug

c. reduction of cell permeability for the drug

d. active drug export from the bacterial cell

e. all of the above – these are all potential mechanisms of drug resistance

*e. all of the above – these are all potential mechanisms of drug resistance

Objective: demonstrate an awareness of drug resistance mechanisms

6. Which of the following is true of the antibiotic vancomycin?

a. it is bacteriostatic – not bacteriostatic

b. it is active against methicillin-resistant staphylococci – it does have activity against MRSA

c. it binds to protein-binding protein – does not do this

d. it has oral systemic bioavailability- needs to be administered IV for systemic activity (only minimally absorbed orally)

 

 

*b. it is active against methicillin-resistant staphylococci – it does have activity against MRSA

Objective: demonstrate understanding of properties of vancomycin

7. Adding clavulanic acid to amoxicillin enables the combination drug to do which of the following?

a. prevents inactivation by stomach acids – doesn’t do this

b. decreases the frequency of side effects such as diarrhea – doesn’t do this

c. increases absorption of the combination drug – doesn’t do this

d. prevent inactivation by beta lactamase – clavulanate inactivates beta lactamase

 

*d. prevent inactivation by beta lactamase – clavulanate inactivates beta lactamase

Objective: demonstrate an understanding of the effect of clavulanic acid

8. Which of the following drugs is a cephalosporin antibiotic that can be administered either orally or intravenously?

a. Cephalexin [Keflex] – PO only

b. Cefuroxime [Ceftin] – PO  or IV

c. Ceftriaxone [Rocephin] – IM or IV

d. Cefixime [Suprax] – PO only

*b. Cefuroxime [Ceftin] – PO  or IV

Objective: demonstrate an understanding of administration routes for cephalosporins

9. Vancomycin can be used to treat infections of the gastrointestinal tract because:

a. it is well absorbed from the GI tract – not absorbed from GI tract

b. it is bacteriostatic - bacteriocidal

c. it is inhibited by gastric acid – not inhibited by gastric acid

d. it is minimally absorbed from the GI tract – only minimally absorbed from GI tract

 

*d. it is minimally absorbed from the GI tract – only minimally absorbed from GI tract

Objective: demonstrate understanding of the unique characteristics of vancomycin

10. The threshold of increased risk for each of the major adverse outcomes of chronic kidney disease is at estimated GFR’s of:

a. ≤ 40mL/min/1.73m²  - greater than threshold for increased risk

b. ≤ 90mL/min/1.73m²  - well above threshold for increased risk

c. ≤ 50 mL/min/q.73m²  - below threshold for increased risk

*d. ≤ 60 mL/min/1.73m²  - threshold for increased adverse outcome risk

  

*d. ≤ 60 mL/min/1.73m²  - threshold for increased adverse outcome risk

Objective: demonstrate an understanding of the threshold for increased risk of adverse outcomes in CKD

1. In the article by Munar (Drug Dosing Adjustments in Patients with Chronic Kidney Disease, AFP, 2007, Table 1), the K/DOQI (Kidney Disease Outcomes Quality Initiative) threshold eGFR for the onset of Kidney failure is:

a. <15 mL/min/m² – threshold for kidney failure

b. < 30 mL/min/m²  - above threshold for kidney failure

c. < 60 mL/min/m²  - above threshold for kidney failure

d. <90 mL/min/m²  - well above threshold for kidney failure

*a. <15 mL/min/m² – threshold for kidney failure

Objective: demonstrate an understanding of the eGFR threshold for kidney failure

 

2. Which of the following classes of antibiotics acts by inhibiting protein synthesis?

a. Penicillin – disrupts cell wall synthesis

b. Macrolides – inhibits protein synthesis

c. Fluoroquinolones – disrupt DNA gyrase to block bacterial DNA dsynthesis

d. Sulfonamides – disrupts foliate synthesis

*b. Macrolides – inhibits protein synthesis

Objective: demonstrate an understanding of bacterial drug classes

3. Which of the following antibiotics inhibits bacterial growth by blocking transpeptidation involving the 50S subunit of the bacterial ribosome?

a. Tetracycline – binds to 30s subunit

b. Azithromycin [Zithromax] – binds to the 50s subunit

c. Penicillin  - binds to PBP

d. Minocycline [Minocin] – binds to 30s subunit

 

*b. Azithromycin [Zithromax] – binds to the 50s subunit

Objective: demonstrate an understanding of macrolide MoA

4. Which of the following classes of antibiotics is commonly added at low doses to animal feed contributing to the development of widespread bacterial resistance?

a. Erythromycin

b. Penicillin

c. Clindamycin

d. Tetracycline – common animal feed additive

 

*d. Tetracycline – common animal feed additive

Objective: demonstrate an understanding of sources of antibiotic resistance

5. Which of the following antibiotics has the advantage of being minimally renally excreted (i.e. ~20% renally excreted)?

a. Azithromycin [Zithromax] – largely excreted in bile

b. Penicillin – renal excretion

c. Doxycycline [Vibramycin or Doryx] – minimally renal excretion; significant fecal excretion

d. Clarithromycin [Biaxin] – largely excreted in bile

 

*c. Doxycycline [Vibramycin or Doryx] – minimally renal excretion; significant fecal excretion

Objective: demonstrate understanding of the unique features of doxycycline

6.  Which of the following is a macrolide antibiotic that has a long tissue half-life and a 10 to 100 fold increased tissue concentration (compared to serum)?

a. Erythromycin [E.E.S.] - does not concentrate in tissue to this extent

b. Azithromycin [Zithromax] – unique quality of azithromycin

c. Clarithromycin [Biaxin] - does not concentrate in tissue to this extent

d. Amoxicillin - does not concentrate in tissue to this extent

 

*b. Azithromycin [Zithromax] – unique quality of azithromycin

Objective: demonstrate understanding of characteristics of azithromycin

7. Which of the following antibiotics is a drug of choice for treating pharyngeal streptococcus infections in patients allergic to penicillin?

a. Tetracycline – not a DoC

b. Clindamycin [Cleocin] – streptococci are sensitive to Cleocin

c. Penicillin G – would be allergic to this

d. Bacitracin [Bactroban] – topical use only

 

*b. Clindamycin [Cleocin] – streptococci are sensitive to Cleocin

Objective: demonstrate understanding of the clinical characteristics of clindamycin

8. Which of the following antibiotics is an Oxazolidinone category antibiotic that can precipitate Serotonin Syndrome if used with other drugs that increase serum serotonin levels?

a. Clindamycin [Cleocin] – doesn’t precipitate serotonin syndrome

b. Doxycyline [Vibramycin or Doryx] – doesn’t precipitate serotonin syndrome

c. Linzolid [Zyvox] – can precipitate serotonin syndrome in appropriate circumstances

d. Amoxicillin/Clavulanate [Augmentin] – doesn’t precipitate serotonin syndrome 

*c. Linzolid [Zyvox] – can precipitate serotonin syndrome in appropriate circumstances

Objective: demonstrate understanding of potential adverse effects of Linzolid

9. In patients with a history of an anaphylactic reaction to penicillin, which of the following classes of antibiotic should not be used due to concerns of cross-allergenicity?

a. Tetracycline – not contraindicated

b. Macrolides– not contraindicated

c. Cephalosporin’s – low rate of cross-allergenicity but could be fatal

d. Lincosamides– not contraindicated

 

*c. Cephalosporin’s – low rate of cross-allergenicity but could be fatal

Objective: demonstrate understanding of potential for cross-reactivity of antibiotic classes

 

10. Which class of antibiotics needs to be dosed 2 hours before, or 6 hours after, taking an antacid to prevent binding of the antibiotic by the antacid?

a. Penicillins –  don’t bind avidly to antacids

b. Cephalosporins – don’t bind avidly to antacids

c. Lincosamides – don’t bind avidly to antacids

d. Tetracyclines – bound readily by antacids

 

*d. Tetracyclines – bound readily by antacids

Objective: demonstrate understanding of antacid binding of tetracyclines