Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Parker- Pharmacology block 2 > Sweatman antimicrobial reading > Flashcards

Sweatman antimicrobial reading Flashcards

1
Q

What are the 4 mechanisms of action for antibacterial agents?

A

Inhibition of cell wall synthesis
Inhibition of protein synthesis
Inhibition of folic acid biosynthetic pathways
Inhibition of DNA/RNA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Is penicillin bacteriostatic or bacteriocidal?

A

Bacteriocidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Of the 4 mechanisms of action by antibacterial agents, what is penicillin’s?

A

Inhibition of cell wall synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Penicillin binds to what to disrupt cell wall synthesis?

A

Transpeptidases in the cell wall (aka penicillin binding proteins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are 4 mechanisms of resistance to penicillin?

A
  1. Modification of PBP’s
  2. Active pumping of drug out of cell
  3. Cleavage of beta-lactam ring structure of penicillin by beta lactamases
  4. Altered porins that prevent penicillin from reaching PBP targets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

You are on your internal rotation. You prescribe penicillin along with tetracycline. The attending slaps you. Why?

A

Penicillin is bactericidal and only kills bacteria that are actively growing. Tetracycline is bacteriostatic (prevents bacteria from growing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do you think about taking antibiotics while on birth control?

A

Better check yourself. Antibiotics inhibit gut flora that normally metabolizes the contraceptive pill. She will get pregnant. Ask my friend Will…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name the subclasses of penicillins

A
  1. Natural penicillins
  2. Aminopenicillins
  3. Penicillinase resistant penicillins
  4. Antipseudomonal penicillins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What two subclasses of penicillin would typically be used to treat Gram + organisms?

A

Natural penicillins and penicillinase resistant penicillins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What subclasses would treat Gram - organisms?

A

Aminopenicillins and antipseudomonal penicillins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which natural penicillin (G or V) is given intravenously or intramuscularly?

A

Penicillin G (think G for Gastric and then remember that it is the opposite)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which natural Pn (from now on penicillin is Pn) is given orally?

A

Pn V (think V for vascular then remember that it is the opposite)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Ampicillin and amoxicillin fall under which subclass of Pn drugs?

A

AminoPn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Ampicillin and amoxicillin can both be given orally. Which must be taken on an empty stomach?

A

Ampicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

dicloxacillin, methicillin, oxacillin, nafcillin. What do those names do for u?

A

They is penicillinase-resistant penicillins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Whats the mechanism of action of penicillinase resistant Pn?

A

they contain side groups that protect the drug from being inactivated by bacterial beta-lactamases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What category of Pn are these drugs in: carbenicillin, ticarcillin, mezlocillin, and piperacillin?

A

Oh, well those are antipseudomonal Pn’s thanks for asking!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

can the antipseudomonal Pn’s be given orally?

A

No, hell no! Well actually carbenicillin is given orally. However, therapeutic levels are only found in the urinary tract (treats UTI’s and prostate infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the antimicrobial activity of irreversible beta lactamase inhibitors?

A

NONE! However, along with Pn’s they expand the coverage of antimicrobial therapy to fight against beta lactamase producing microorganisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is similar to Pn’s (has beta lactam backbone) but can be taken with or without food?

A

Cephalosporins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Are you gonna prescribe cephalosporins to someone who is allergic to Pn?

A

It is “unwise”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are some adverse effects of cephalosporins?

A

GI irritation, local irritation at site of injection, renal toxicity (don’t give to pts with pre-existing kidney disease). Some may cause seizures (usually only a concern for those with pre-existing kidney disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Difference between carbapenems and Pn/cephalasporins?

A

Carbapenems are resistant to beta lactamases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Telavancin and vancomycin also disrupt cell walls. How?

A

Bind to D-Ala-D-Ala portion of cell wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What cell wall disrupting drug is used to treat Mycobacterium tuberculosis that is resistant to first-line anti tubercular drugs?

A

Cycloserine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

You have a gram - bacilli. What do you treat it with?

A

Polymyxin B is bacteriocidal to nearly all gram - bacilli (except Proteus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Aminoglycosides, macrolides, and tetracyclines fall into which category of antimicrobial drug?

A

Protein synthesis inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Amikacin, gentamicin, kanamycin, netilmicin, streptomycin, tobramycin, and neomycin belong to which category of drugs (protein synthesis inhibitors)??

A

Aminoglycosides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

3 mechanisms of action of aminoglycosides?

A

Aminoglycosides bind to bacterial 30S ribosome and:

  1. interfere with formation of initiation complex
  2. misread mRNA and miscode AA’s
  3. cause ribosomes to separate from mRNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Are aminoglycosides given orally?

A

No, they are too water soluble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

where does accumulation of amino glycosides occur?

A

Inner ear and renal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the post antibiotic effect?

A

When microorganisms continue to die even as plasma levels of the antimicrobial drug decline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Aminoglycosides are typically used to treat gram - bacilli. Some anaerobes have developed resistance. How?

A

Alterations in receptor proteins on their ribosomes so that amino glycosides cannot bind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What class of drug inhibits protein synthesis through reversible binding to 30 S ribosomal subunits?

A

Tetracyclines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Tetracyclines bind to bacterial 30 S ribosomal subunits. So what? What does this do?

A

Prevents binding of incoming amino acids thereby inhibiting protein synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Which tetracycline derived drug is designed to overcome two common mechanisms of tetracycline resistance (resistance via efflux pumps and ribosomal protection)?

A

Glycylcyclines (Tigecycline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Tetracycline is bacteriostatic in both gram + and gram - bacteria. In which (gram + or gram -) does it get into the bacteria via passive diffusion?

A

Gram -

38
Q

Tetracycline may be inhibited by chelation to cations (Fe, Al, Mg). So do you want to take tetracycline on an empty stomach or full stomach?

A

Empty. Take tetracycline on an empty stomach

39
Q

How do gram + microorganisms acquire resistance to tetracycline?

A

Gram + organisms actively pump the drug out of the cell via an efflux pump

40
Q

How do gram - organisms develop resistance to tetracycline?

A

Gram - organisms develop alterations in their outer membrane that inhibits tetracycline from entering the cell

41
Q

Which tetracycline derived drug is not affected by tetracycline resistance mechanisms?

A

Tigecycline

42
Q

Describe chloramphenicol’s mechanism of action

A

Binds to 50 S ribosomal subunit and blocks linkage of incoming amino acids by interfering with the enzyme peptidyl transferase

43
Q

Clindamycin is under which class of drugs? And what is its mechanism of action?

A

Clindamycin is the common drug of Lincosamides. It binds to 50 S ribosomal subunits preventing translocation of incoming amino acids from the ribosomal A site to the P site

44
Q

Erythromycin, Clarithromycin and Azithromycin are under which class?

A

Macrolides

45
Q

What is the mechanism of action for macrolides?

A

Inhibit protein synthesis by binding to binding to 50 S ribosomal subunit

46
Q

Microorganisms can become resistant to macrolides in 3 ways. What are they?

A
  1. A microbe can alter its permeability for macrolides
  2. Microorganisms can methylate their 50 S ribosomal subunits
  3. Microorganisms can develop mechanisms to enzymatically destroy the drugs
47
Q

What are some possible side effects of macroclides (erythromycin in particular)?

A

GI distress, cholestatic hepatitis, inhibits CYP3A4, arrhythmias

48
Q

How is the mechanism of action of Ketolides (Telithromycin) different from that of the macrolides?

A

Ketolides (Telithromycin) inhibits protein synthesis by inhibiting the 50 S ribosomal subunit just like macrolides. However, Telithromycin binds to two separate domains of the 50 S

49
Q

What is more effective, macroclides or telithromycin? Why?

A

Telithromycin bc it binds to two domains of 50 S instead of one. Also, it is more resistant to bacterial efflux pumps. Thus, it is more difficult for bacteria to develop resistance to telithromycin

50
Q

Describe Retapamulin’s mechanism of action.

A

Binds to 50 S ribosomal subunit to prevent formation of the active 50 S ribosome.

51
Q

How is Retapamulin administered?

A

topical ointment

52
Q

What is the mech of action of Mupirocin?

A

Inhibits tRNA that transports isoleucine

53
Q

How is Mupirocin administered?

A

Topical ointment

54
Q

What two protein synthesis inhibiting antibiotics are administered via a topical ointment?

A

Retapamulin and Mupirocin

55
Q

How does Linezolid do its job of preventing protein synthesis in bacteria?

A

Binds to a unique site on the 50 S subunit preventing formation of the 70 S complex

56
Q

Which protein synthesis inhibiting drug is a combination of quinupristin and dalfopristin?

A

Streptogramins

57
Q

What is a Streptogramin’s mech of action? (hint: it is two-fold… the quinupristin does one thing and the dalfopristin does another)

A

The quinupristin blocks ribosomes and inhibits late phase of protein synthesis. Dalopristin inhibits early phase of protein synthesis.

58
Q

What is Streptogramin used to treat?

A

Vancomycin-resistant enterococci and skin infections caused by MRSA

59
Q

Why can we target Folic acid synthesis in bacteria?

A

Cuz human cells take in folate from their diet. Bacteria have to make their own folate… So they have folate synthesis, we don’t!

60
Q

Sulfonamides belong to what category? (of the big 4)

A

Folate synthesis inhibitor

61
Q

If a drug name starts with sulfa… is it a sulfonamide?

A

Yes, come on.. common sense

62
Q

Mech of action of sulfonamides?

A

compete with para-aminobenzoic acid at first step of folate synthesis pathway

63
Q

T/F Sulfonamides are highly protein bound in the plasma?

A

True

64
Q

The fact that sulfonamides are highly protein bound can lead to adverse effects with what common drugs?

A

Warfarin, NSAIDs, sulfonylureas

65
Q

What are the 4 ways in which bacteria have developed resistance to sulfonamides?

A
  1. Reduced uptake
  2. Development of alternative metabolic pathways to synthesize folic acid
  3. Production of excessive amounts of para-aminobenzoic acid to compete with sulfonamides for folic acid synthesis
  4. Alterations or mutations in diydropteronate synthase, the enzyme that catalyzes the ratae limiting step of folate synthesis
66
Q

Sulfonamides are metabolized hepatically by three mechs. What are they?

A

Acetylation, oxidation, and/or glucoronidation

67
Q

Slow acetylators of sulfonamides may be at risk for??

A

Hypersensitivity reactions

68
Q

What is most likely responsible for the adverse effects associated with sulfonamides?

A

Oxidation

69
Q

What drug inhibits dihydrofolate reductase, the enzyme that catalyzes the last step of folic acid synthesis?

A

Trimethoprim

70
Q

What are 3 ways in which bacteria may become resistant to trimethoprim?

A
  1. Reduced uptake
  2. Alterations/mutations in dihydrofolate reductase
  3. Overproduction of dihydrofolate reductase
71
Q

Besifloxacin, ciproflaxacin, gatifloxacin, gemifloxacin, etc… belong to which class of drug? What mechanism of action?

A

These are the Fluoroquinolones. They inhibit DNA/RNA synthesis

72
Q

Fluoroquinolones are drugs that inhibit DNA/RNA synthesis. What two specific enzymes do they inhibit?

A
  1. DNA gyrase (relaxes supercoiled DNA)

2. Topoisomerase IV (separates DNA into daughter cells)

73
Q

Of the fluoroquinoline family, which drug works best because it works on both DNA gyrase and topoisomerase IV?

A

Gemifloxacin

74
Q

What is the name of the drug that binds to bacterial membranes and depolarizes them?

A

Daptomycin (a Lipopeptide drug)

75
Q

There are 3 drugs with “distinct mechanisms”. What are their names?

A

Metronidazole, nitazoxanide, tinidazole

76
Q

Metronidazole works by being reduced (once inside an anaerobic bacteria) and thus becoming toxic. What does metronidazle react with in order to become reduced?

A

Ferredoxin- This reaction leads to reduction of metronidazole which becomes toxic. The toxicity messes with DNA synthesis

77
Q

Nitazoxanide disrupts an enzyme-dependent electron transfer system that is key in anaerobic metabolism. What system does the drug disrupt?

A

Pyruvate/ferredoxin oxidoreductase dependent electron transfer

78
Q

How does Tinidazole cause bacterial cytotoxicity?

A

Damages DNA and inhibits further DNA synthesis

79
Q

Rifaximin is a rifampin derivative that inhibits bacterial RNA synthesis by??

A

Binding to bacterial RNA polymerase (think RNA.. R for Rifaximin)

80
Q

What are two key differences between Rifaximin and Rifampin?

A
  1. Rifaximin is not absorbed in the GI tract (like rifampin)

2. Rifaximin does not interfere with hepatic CYP 450’s

81
Q

Rod-like gram + aerobic bacteria that form filamentous branching structures

A

Mycobacterials

82
Q

Tuberculosis and Leprosy are examples of?

A

Mycobacterials

83
Q

What are the 5 reasons that Mycobacterials are difficult to treat?

A
  1. They grow slowly
  2. Can lie dormant
  3. Thick cell walls
  4. Can reside inside host cells
  5. Can become resistant quickly
84
Q

Because of the difficulty of treating mycobacterials, describe how a physician should attempt to treat mycobacterials

A

Treat for long time. Use several different antibiotics simultaneously.

85
Q

Isoniazid, rifampin, pyrazinamide, ethambutol, clofazimine belong to what class of drugs?

A

Antimycobacterials

86
Q

Which of the antimycobacterials inhibits synthesis of my colic acid, an essential component for cell wall synthesis?

A

Isoniazid

87
Q

Pharmacokinetics of Isoniazid?

A
  1. Diffuses thru total body water

2. Metabolism via acetylation

88
Q

Which antimycobacterial inhibits RNA polymerase?

A

Rifampin

89
Q

Should you be considerate of drug-drug interactions with Rifampin? Why?

A

Absolutely. Rifampin is a potent inducer of drug metabolism (I believe via CYP 450’s)

90
Q

This antimycobacterial drug has an unclear mech of action. It may lower the pH in the tubercle cavity

A

Pyrazinamide

91
Q

Which antimycobacterial inhibits RNA synthesis and decreases replication of tubercle bacilli?

A

Ethambutol

92
Q

Which antimycobacterial binds to mycobacterial DNA and inhibits RNA polymerase actions? Very slow activity, patients sometimes treated for life?

A

Clofazimine

Parker- Pharmacology block 2 (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions