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Parker- Pharmacology block 2 > Sweatman antimicrobial reading > Flashcards

Sweatman antimicrobial reading Flashcards

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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

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2
Q

Is penicillin bacteriostatic or bacteriocidal?

A

Bacteriocidal

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3
Q

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

A

Inhibition of cell wall synthesis

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4
Q

Penicillin binds to what to disrupt cell wall synthesis?

A

Transpeptidases in the cell wall (aka penicillin binding proteins)

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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
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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)

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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…

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8
Q

Name the subclasses of penicillins

A
  1. Natural penicillins
  2. Aminopenicillins
  3. Penicillinase resistant penicillins
  4. Antipseudomonal penicillins
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9
Q

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

A

Natural penicillins and penicillinase resistant penicillins

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10
Q

What subclasses would treat Gram - organisms?

A

Aminopenicillins and antipseudomonal penicillins

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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)

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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)

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13
Q

Ampicillin and amoxicillin fall under which subclass of Pn drugs?

A

AminoPn

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14
Q

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

A

Ampicillin

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15
Q

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

A

They is penicillinase-resistant penicillins

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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

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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!

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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

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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

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20
Q

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

A

Cephalosporins

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21
Q

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

A

It is “unwise”

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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)

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23
Q

Difference between carbapenems and Pn/cephalasporins?

A

Carbapenems are resistant to beta lactamases

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24
Q

Telavancin and vancomycin also disrupt cell walls. How?

A

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

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25
What cell wall disrupting drug is used to treat Mycobacterium tuberculosis that is resistant to first-line anti tubercular drugs?
Cycloserine
26
You have a gram - bacilli. What do you treat it with?
Polymyxin B is bacteriocidal to nearly all gram - bacilli (except Proteus)
27
Aminoglycosides, macrolides, and tetracyclines fall into which category of antimicrobial drug?
Protein synthesis inhibitors
28
Amikacin, gentamicin, kanamycin, netilmicin, streptomycin, tobramycin, and neomycin belong to which category of drugs (protein synthesis inhibitors)??
Aminoglycosides
29
3 mechanisms of action of aminoglycosides?
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
30
Are aminoglycosides given orally?
No, they are too water soluble
31
where does accumulation of amino glycosides occur?
Inner ear and renal cortex
32
what is the post antibiotic effect?
When microorganisms continue to die even as plasma levels of the antimicrobial drug decline
33
Aminoglycosides are typically used to treat gram - bacilli. Some anaerobes have developed resistance. How?
Alterations in receptor proteins on their ribosomes so that amino glycosides cannot bind
34
What class of drug inhibits protein synthesis through reversible binding to 30 S ribosomal subunits?
Tetracyclines
35
Tetracyclines bind to bacterial 30 S ribosomal subunits. So what? What does this do?
Prevents binding of incoming amino acids thereby inhibiting protein synthesis
36
Which tetracycline derived drug is designed to overcome two common mechanisms of tetracycline resistance (resistance via efflux pumps and ribosomal protection)?
Glycylcyclines (Tigecycline)
37
Tetracycline is bacteriostatic in both gram + and gram - bacteria. In which (gram + or gram -) does it get into the bacteria via passive diffusion?
Gram -
38
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?
Empty. Take tetracycline on an empty stomach
39
How do gram + microorganisms acquire resistance to tetracycline?
Gram + organisms actively pump the drug out of the cell via an efflux pump
40
How do gram - organisms develop resistance to tetracycline?
Gram - organisms develop alterations in their outer membrane that inhibits tetracycline from entering the cell
41
Which tetracycline derived drug is not affected by tetracycline resistance mechanisms?
Tigecycline
42
Describe chloramphenicol's mechanism of action
Binds to 50 S ribosomal subunit and blocks linkage of incoming amino acids by interfering with the enzyme peptidyl transferase
43
Clindamycin is under which class of drugs? And what is its mechanism of action?
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
Erythromycin, Clarithromycin and Azithromycin are under which class?
Macrolides
45
What is the mechanism of action for macrolides?
Inhibit protein synthesis by binding to binding to 50 S ribosomal subunit
46
Microorganisms can become resistant to macrolides in 3 ways. What are they?
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
What are some possible side effects of macroclides (erythromycin in particular)?
GI distress, cholestatic hepatitis, inhibits CYP3A4, arrhythmias
48
How is the mechanism of action of Ketolides (Telithromycin) different from that of the macrolides?
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
What is more effective, macroclides or telithromycin? Why?
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
Describe Retapamulin's mechanism of action.
Binds to 50 S ribosomal subunit to prevent formation of the active 50 S ribosome.
51
How is Retapamulin administered?
topical ointment
52
What is the mech of action of Mupirocin?
Inhibits tRNA that transports isoleucine
53
How is Mupirocin administered?
Topical ointment
54
What two protein synthesis inhibiting antibiotics are administered via a topical ointment?
Retapamulin and Mupirocin
55
How does Linezolid do its job of preventing protein synthesis in bacteria?
Binds to a unique site on the 50 S subunit preventing formation of the 70 S complex
56
Which protein synthesis inhibiting drug is a combination of quinupristin and dalfopristin?
Streptogramins
57
What is a Streptogramin's mech of action? (hint: it is two-fold... the quinupristin does one thing and the dalfopristin does another)
The quinupristin blocks ribosomes and inhibits late phase of protein synthesis. Dalopristin inhibits early phase of protein synthesis.
58
What is Streptogramin used to treat?
Vancomycin-resistant enterococci and skin infections caused by MRSA
59
Why can we target Folic acid synthesis in bacteria?
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
Sulfonamides belong to what category? (of the big 4)
Folate synthesis inhibitor
61
If a drug name starts with sulfa... is it a sulfonamide?
Yes, come on.. common sense
62
Mech of action of sulfonamides?
compete with para-aminobenzoic acid at first step of folate synthesis pathway
63
T/F Sulfonamides are highly protein bound in the plasma?
True
64
The fact that sulfonamides are highly protein bound can lead to adverse effects with what common drugs?
Warfarin, NSAIDs, sulfonylureas
65
What are the 4 ways in which bacteria have developed resistance to sulfonamides?
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
Sulfonamides are metabolized hepatically by three mechs. What are they?
Acetylation, oxidation, and/or glucoronidation
67
Slow acetylators of sulfonamides may be at risk for??
Hypersensitivity reactions
68
What is most likely responsible for the adverse effects associated with sulfonamides?
Oxidation
69
What drug inhibits dihydrofolate reductase, the enzyme that catalyzes the last step of folic acid synthesis?
Trimethoprim
70
What are 3 ways in which bacteria may become resistant to trimethoprim?
1. Reduced uptake 2. Alterations/mutations in dihydrofolate reductase 3. Overproduction of dihydrofolate reductase
71
Besifloxacin, ciproflaxacin, gatifloxacin, gemifloxacin, etc... belong to which class of drug? What mechanism of action?
These are the Fluoroquinolones. They inhibit DNA/RNA synthesis
72
Fluoroquinolones are drugs that inhibit DNA/RNA synthesis. What two specific enzymes do they inhibit?
1. DNA gyrase (relaxes supercoiled DNA) | 2. Topoisomerase IV (separates DNA into daughter cells)
73
Of the fluoroquinoline family, which drug works best because it works on both DNA gyrase and topoisomerase IV?
Gemifloxacin
74
What is the name of the drug that binds to bacterial membranes and depolarizes them?
Daptomycin (a Lipopeptide drug)
75
There are 3 drugs with "distinct mechanisms". What are their names?
Metronidazole, nitazoxanide, tinidazole
76
Metronidazole works by being reduced (once inside an anaerobic bacteria) and thus becoming toxic. What does metronidazle react with in order to become reduced?
Ferredoxin- This reaction leads to reduction of metronidazole which becomes toxic. The toxicity messes with DNA synthesis
77
Nitazoxanide disrupts an enzyme-dependent electron transfer system that is key in anaerobic metabolism. What system does the drug disrupt?
Pyruvate/ferredoxin oxidoreductase dependent electron transfer
78
How does Tinidazole cause bacterial cytotoxicity?
Damages DNA and inhibits further DNA synthesis
79
Rifaximin is a rifampin derivative that inhibits bacterial RNA synthesis by??
Binding to bacterial RNA polymerase (think RNA.. R for Rifaximin)
80
What are two key differences between Rifaximin and Rifampin?
1. Rifaximin is not absorbed in the GI tract (like rifampin) | 2. Rifaximin does not interfere with hepatic CYP 450's
81
Rod-like gram + aerobic bacteria that form filamentous branching structures
Mycobacterials
82
Tuberculosis and Leprosy are examples of?
Mycobacterials
83
What are the 5 reasons that Mycobacterials are difficult to treat?
1. They grow slowly 2. Can lie dormant 3. Thick cell walls 4. Can reside inside host cells 5. Can become resistant quickly
84
Because of the difficulty of treating mycobacterials, describe how a physician should attempt to treat mycobacterials
Treat for long time. Use several different antibiotics simultaneously.
85
Isoniazid, rifampin, pyrazinamide, ethambutol, clofazimine belong to what class of drugs?
Antimycobacterials
86
Which of the antimycobacterials inhibits synthesis of my colic acid, an essential component for cell wall synthesis?
Isoniazid
87
Pharmacokinetics of Isoniazid?
1. Diffuses thru total body water | 2. Metabolism via acetylation
88
Which antimycobacterial inhibits RNA polymerase?
Rifampin
89
Should you be considerate of drug-drug interactions with Rifampin? Why?
Absolutely. Rifampin is a potent inducer of drug metabolism (I believe via CYP 450's)
90
This antimycobacterial drug has an unclear mech of action. It may lower the pH in the tubercle cavity
Pyrazinamide
91
Which antimycobacterial inhibits RNA synthesis and decreases replication of tubercle bacilli?
Ethambutol
92
Which antimycobacterial binds to mycobacterial DNA and inhibits RNA polymerase actions? Very slow activity, patients sometimes treated for life?
Clofazimine

Parker- Pharmacology block 2 (1 decks)

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