Wk 6. Antibiotics part 1 Flashcards

1
Q
  1. What is selective toxicity? Why is it important?
A

Injuring a target cell or organism without injuring other cells or organisms in intimate contact with the target. Makes antibiotics safer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  1. What is the difference between bactericidal and bacteriostatic?
A

Bactericidal – kills bacteria

Bacteriostatic – slows growth, phagocytes eliminate bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. What are ranges and chances of drug resistance with narrow-spectrum and broad-spectrum antibiotics?
A

Narrow: smaller range
less resistance
Broad: larger range
more resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  1. What is acquired resistance? What are four ways bacteria become resistant to antibiotics? How do we lessen the chance for resistance?
A

Bacteria become less susceptible or lose sensitivity to drug.
1) Reduce drug concentration at sites, 2) Alter drug receptors, 3) Synthesize an antagonist, & 4) Produce drug-metabolizing enzymes.
Treat infection, not colonization, and use correct drug in correct concentration for entire course of therapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  1. What is the difference between the MIC and MBC?
A

MIC – amount of drug required to halt growth

MBC – amount of drug required to kill 99.9%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. Explain the importance of conjugation. What bacteria are most affected?
A

Conjugation allows the DNA code for drug resistance to be passed to other bacteria. Gram negative bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  1. What are two examples of suprainfections?
A

Candidiasis (yeast infection), Clostridium difficile infection (CDI) – 3 or more unformed stools in 24 hours with C. difficile or toxin from C. difficile in stools.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. What is the difference between an additive and potentiative effect?
A

Additive – sum of the effect

Potentiative – greater than the sum of the effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. How do penicillins kill bacteria?
A

Disrupts cell wall (inhibits cross-linkages between peptidoglycan strands and lyses cell wall bonds)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. What is the major adverse effect of penicillins?
A

Allergic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. What are some common signs and symptoms of anaphylaxis and serum sickness to penicillins?
A

Laryngeal edema, bronchoconstriction, severe hypotension, nausea and vomiting, tachycardia
Rash, hives, pruritis, arthralgias, fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. Which three penicillins can be taken with food?
A

Penicillin V, Amoxicillin, Augmentin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. Why is Penicillin G given IM?
A

Destroyed by gastric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  1. What lab abnormality can occur with Penicillin G or V when administered with potassium supplements?
A

Hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. What types of enzymes can destroy the penicillin molecule?
A

General beta-lactamases and penicillinases. Cephalosporinases deactivate cephalosporins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. What is the advantage of Nafcillin over other penicillins?
A

Penicillinase-resistant

17
Q
  1. Amoxicillin has what kind of bacterial spectrum?
A

Broad-spectrum

18
Q
  1. How does clavulanic acid prevent amoxicillin from being deactivated?
A

Clavulanic acid inhibits beta-lactamase

19
Q
  1. What are other beta-lactam antibiotic groups other than the penicillins?
A

Cephalosporins, carbapenems

20
Q
  1. How do cephalosporins kill bacteria?
A

Inhibits cell wall synthesis

21
Q
  1. Each subsequent generation of cephalosporins show more activity against what type of bacteria? How does each subsequent generation penetrate into the cerebral spinal fluid?
A

Gram negative bacteria and anaerobes, more resistant to beta-lactamases.
Each subsequent generation is more likely to reach the cerebral spinal fluid.

22
Q
  1. What percentage of penicillin-allergic patients will have an allergic reaction to a cephalosporin?
A

1%

23
Q
  1. What is the adverse effect seen with some cephalosporins and alcohol?
A

Antabuse-like effects: weakness, pulsating headache, chest pain, abdominal cramps

24
Q
  1. What is the drug interaction is seen between IV calcium and IV cephalosporins?
A

Lung and renal precipitates.

25
Q
  1. How does vancomycin kill bacteria? What bacteria does it kill?
A

Inhibits cell wall synthesis. Gram-positive bacteria.

26
Q
  1. For what types of infection is vancomycin reserved? How is it given for CDI?
A

Severe C. difficile infections (CDIs), MRSA, & Staph. Epidermidis. Must be given PO for CDI, because cannot cross between GI tract and bloodstream.

27
Q
  1. What are the signs and symptoms of Red Man Syndrome seen with the rapid infusion of vancomycin?
A

Red rash, hives, flushing, and pruritis on face & upper body. Hypotension, tachycardia. From histamine release, NOT an allergic reaction.

28
Q
  1. Creatinine (Cr) is monitored with vancomycin therapy to avoid what? What is an indication for stopping vancomycin?
A

Renal failure. Stop if Cr rises 50%.

29
Q
  1. Aztreonam is used to treat what type of infection? Why?
A

Gram-negative aerobic bacteria. Only attaches to PBPs on gram-negative aerobic bacteria.