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1
Q

<p><span>What are 3 features unique to gram-negative bacteria?</span></p>

A

<ol>
<li><span>thin peptidoglycan (PG)</span></li>
<li><span>Safranin (red)</span></li>
<li><span>outer lipid rich membrane + lipoproteinsrepel many drug: polar drugs enter through porins to access PG</span></li>
</ol>

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2
Q

<p><span>Which is easier for a drug to penetrate- gram positive or negative bacteria, and why?</span></p>

A

<p><span>Gram positive, low MW enter easily across exposed PG layer, itself a key target</span></p>

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3
Q

<p><span>How does the murein (peptidoglycan) layer differ between gram positive and negative bacteria?</span></p>

A

<p><span>Gram positive: thick PG</span></p>

<p><span>Gram negative: thin PG</span></p>

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4
Q

<p><span>How does gram staining distinguish between gram positive and negative bacteria?</span></p>

A

<p><span>Gram<u> p</u>ositive:<u>p</u>urple dye</span></p>

<p><span>Gram negative: safranin (red)</span></p>

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5
Q

<p><span>Ribosomes and cell walls are common targets for antibiotics – which is unique to bacteria, and which is slightly different from its human counterpart?</span></p>

A

<p><span>bacteria vs humans:</span></p>

<ul>
<li><span>cell wall (humans have no cell walls) </span></li>
<li><span>70Sribosome (humans: 80S)</span></li>
<li><span>outer membrane (gram negative only)</span></li>
<li><span>Different needs for substrates</span></li>
</ul>

<p></p>

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6
Q

<p><span>What are the differences between bactericidal and bacteriostatic antibiotics, and which one requires a competent immune system to resolve the infection?</span></p>

A

<p><span>Bactericidal: kills bacteria; irreversible (penicillin)</span></p>

<p><span>Bacteriostatic: prevent replication; reversible (tetracycline) - the patient’s own immune system must deal with getting rid of rest of the infection</span></p>

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7
Q

<p><span>Describe 3</span><span><u>(there are 4 in the lecture)</u></span><span><u></u></span><span>categories of adverse effects of antibiotics – which is specific to antibiotics?</span></p>

A

<ol><li><span><u>Direct toxicity</u>: aminoglycosides generate free radicals that damage neurons in inner ear</span></li><li><span><u>Allergic reactions</u>: rapid, immune-mediated development of rash, hives</span></li><li><span><u>Idiosyncratic reactions</u>: hemolysis in G-6-PD-deficient patients treated with sulfonamides</span></li><li><span><u>Changes in normal body flora</u>: killing some bacteria allows other to proliferate; vaginal yeast infections<strong>(this is specific to antibiotics)</strong></span></li></ol>

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8
Q

<p><span>Contrast between prophylactic, pre-emptive, empiric and definitive / directed therapy.</span></p>

A

<p><span><u>Prophylactic</u>: antibiotic used before an infection</span></p>

<p><span><u>Pre-emptive therapy</u>: antibiotic used during symptoms occur to prevent anticipated infection or symptoms</span></p>

<p><span><u>Empiric therapy</u>: selection of an antibiotic based on<strong>most likely</strong> cause of infection</span></p>

<p><span><u>Definitive/directed therapy</u>: selection of an antibiotic based on<strong> positive identification</strong> of the causative organisms</span></p>

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9
Q

<p><span>Define the terms “sensitivity”, “MIC”, and “clinical breakpoint”</span></p>

A

<p><span><u>Sensitivity</u>: the ability of a bacteria to be inhibited/killed by a particular antibiotic; drug affects the bacteria at<strong>lowest concentration</strong> is the one to which it’s<strong>most sensitive</strong></span></p>

<p><span><u>Minimum inhibitory concentration (MIC)</u>: lowest concentration of drug that<strong>inhibits</strong>growth of organism</span></p>

<p><span><u>Clinical breakpoint</u>: highest plasma concentration that can safely be achieved in a patient</span></p>

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10
Q

<p><span>What is the purpose of broth dilution and disk diffusion testing?</span></p>

A

<p><span><u>Broth dilution</u>: bacteria in<strong> liquid</strong> are exposed to<strong>increasing concentrations</strong> of a drug - the lowest concentration that eliminates growth is MIC</span></p>

<p><span><u>Disk diffusion</u>: bacteria are plated onto<strong>agar studded</strong> with small disks containing<strong>different antibiotics</strong> - if bacteria surrounding a disk are dead, they are susceptible to that drug</span></p>

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11
Q

<p><span>How are MIC and breakpoint concentrations used together to determine bacterial sensitivity?</span></p>

A

<p><span><u>Sensitive</u>: MIC < breakpoint</span></p>

<p><span><u>Intermediate</u>: MIC near breakpoint</span></p>

<p><span><u>Resistant</u>: MIC > breakpoint</span></p>

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12
Q

<p><span>Contrast between the terms “broad spectrum” and “narrow spectrum” – why would a narrow spectrum drug sometimes be more appropriate?</span></p>

A

<p><span><u>Broad spectrum</u>: active against many types of bacteria</span></p>

<p><span><u>Narrow spectrum</u>: active against only one or a few types of bacteria (might be more appropriate: to<strong>kill/inhibit only unwanted</strong> bacteria; lessen resistance)</span></p>

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13
Q

<p><span>Contrast between time- and concentration-dependent antibiotic effects, and the dosing strategy required for each – give an example drug for each.</span></p>

A

<p><span><u>Time dependent</u>: constant rate of killing, provided that drug concentration exceeds MIC (beta lactams)</span></p>

<p><span><u>Concentration-dependent</u>: rate of killing increase with drug concentration above MIC (aminoglycosides)</span></p>

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14
Q

<p><span>State 3 advantages of combining antibiotic drugs - are all combinations of antibiotics equally beneficial, or can some be detrimental?</span></p>

A

<ol><li><span><strong>both MOA</strong> to produce a<strong>synergistic</strong> effect (greater than sum of individual drugs), in some cases combined antibiotics can<strong>antagonize</strong> each other’s effects</span></li><li><span>Combining antibiotics can also<strong>minimize risk of resistance</strong> development</span></li><li><span><strong>Lower doses</strong> of each agent can be used,<strong>minimizing side effect severity</strong></span></li></ol>

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15
Q

<p><span>What is the difference between intrinsic and acquired resistance?</span></p>

A

<p><span><u>Intrinsic:</u> trait that confers protection against antibiotic action, shared by all members of a bacterial species, not related to antibiotic exposure</span></p>

<p><span><u>Acquired</u>: certain gene changed become favored as a result of pressure from antibiotic exposure</span></p>

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16
Q

<p><span>What are 4 general mechanisms by which bacteria can become resistant to antibiotics, and which one of these is specific to gram negative bacteria?</span></p>

A

<ol><li><span><u>Altered receptors or targets</u> so drugs cannot bind (vancomycin)</span></li><li><span><u>Drug destruction</u> or inactivation (beta lactams)</span></li><li><span><u>New resistant pathway</u> (sulfonamides)</span></li><li><span><u>Decreased drug exposure</u>: less uptake/more efflux (regulating outer membrane pore function, or efflux transporter expression) - this mechanism is relevant to</span><span> gram negative</span><span> bacteria</span></li></ol>

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17
Q

<p><span>Can more than one resistance mechanism appear in the same strain of bacteria?</span></p>

A

<p><span>With in same species of bacteria, there may be multiple strains with varying types of resistance</span></p>

<p><span>A single species may have multiple acquired resistance mechanisms</span></p>

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18
Q

<p><span>What are the 3 main modes of horizontal transfer of acquired resistance, and how does each work?</span></p>

A

<ol><li><span><u>Transformation</u>: uptake of naked DNA containing resistance genes</span></li><li><span><u>Transduction</u>: DNA transferred by infection with viruses</span></li><li><span><u>Conjugation</u>: DNA transfer between bacterial cells via plasmid exchange</span></li></ol>

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19
Q

<p><span>Are resistance genes always acquired horizontally (from another organism)?</span></p>

A

<p><span>Bacterial<strong>proliferation</strong> and<strong>transfer</strong> between hosts (poor hygiene, hospital acquired infections)</span></p>

<p><span>Increased<strong>exposure</strong> of bacteria to<strong>antibiotics</strong> -> selection pressure (over prescription, wrong prescription, use in agriculture)</span></p>

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20
Q

<p><span>What is “antibiotic stewardship”?</span></p>

A

<p><span>coordinated data-driven programs that focus on reducing inappropriate antibiotic use in clinical settings and agriculture</span></p>

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21
Q

<p><span>What are two general categories of initiatives that are being supported to combat drug resistance development?</span></p>

A

<ol><li><span>Government</span></li><li><span>WHO, World Bank</span></li></ol>

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22
Q

<p>What are the 4 major classes of beta lactam antibiotics, and how can one recognize names of drugs in each class?</p>

A

<p>Penicillins: (-cillin)<br></br>Cephalosporins: (-cef-)<br></br>Carbapenems: (-penem)<br></br>Monobactams (aztreonam)</p>

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23
Q

What are the 4 major classes of penicillins?

A

<ul><li>Natural Penicillins:<ul><li>Penicillin G</li><li>Penicillin V</li></ul></li><li>Anti-staphylococcal:<ul><li>Nafcillin and Oxacillin</li><li>Dicloxacillin</li></ul></li><li>Amino/ Broad spectrum:<ul><li>Ampicillin</li><li>Amoxicillin</li></ul></li><li>Extended Spectrum:<ul><li>Piperacillin + tazobactam</li></ul></li></ul>

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24
Q

<p><span>Name 4 examples of beta lactamase inhibitor drugs.</span></p>

A

<ul><li><span>Clavulinic Acid</span></li><li><span>Sulbactam</span></li><li><span>Tazobactam</span></li><li><span>Avibactam</span></li></ul>

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25

What feature is shared in the names of all glycopeptide antibiotics?

-van-

26

Name the classes (and the 2 additional “other” drugs) that target bacterial cell membranes.

  • Other cell wall antibiotics: fosfomycin, bacitracin
  • Lipopeptides: dapotomycin
  • Polymyxins (-myxin)
27

Name 2 drugs that primarily target bacterial cell membranes.

Daptomycin: disrupts cytoplasmic membrane

Polymyxins: disrupt the outer membrane + cytoplasmic membrane

28

What are the two major components of peptidoglycan?  

Polysaccharides: 2 alternating sugars - N-acetylglucosamine (G) and N-acetylmuramic acid (M)

Peptides: five amino acid chain, linked N-acetylmuramic acid sugar

29

What are the 3 major steps in PG synthesis – what happens in each step?

Monomer synthesis & transport: in cytoplasm, building blocks are made from amino acids & sugar by enzyme (Mur enzyme), then transported to the cell surface by lipid carriers.

Glycan polymerization: at cell surface, N and M sugars are connected into strands via transglycosylation by penicillin binding proteins (PBPs)

Polymer cross-linking: strands are linked by transpeptidation, when penicillin binding proteins (PBPs) remove the peptide’s terminal D-alanine to cross-link it to another peptide

30

What are the roles of PBP (both roles), Mur enzymes, and flippase II enzymes?

PBP often have both transpeptidase domain and glycosyltransferase domain

Mur A enzyme: building blocks made from amino acids and sugar

Flippase II enzymes: transport building blocks to cell surface

31

Which steps in the PG synthesis pathway are targeted by:  β lactams, glycopeptides, fosfomycin and bacitracin - and to what target does each one bind?

Photo attached below

32

What are 2 drugs that target the cell membrane, and how does each work?

Daptomycin: disrupts cytoplasmic membrane

Polymyxins: disrupt the outer membrane + cytoplasmic membrane

33

What are the 4 primary mechanisms by which bacteria become resistant to β lactam drugs?

  1. Inactivation of antibiotic by bacterial beta-lactamase:   these enzyme catalyzed opening of the antibiotic’s beta-lactam ring
  2. Reduced uptake of antibiotic: specific to gram-negative bacteria (impervious outer membrane)
  3. Antibiotic efflux: gram negative bacteria may produce drug efflux pumps which toss some beta-lactam antibiotics back out
  4. Alteration of the antibiotic’s target: bacteria produce slightly different PBPs that antibiotics can’t bind to:    development of a new PBP (PBP2a) by S. aureus is how the “superbug” MRSA arose
34

Which of the 4 mechanisms of how bacterial resistance develops against cell wall / membrane-targeted agents is the most common?

Inactivation of antibiotic by bacterial beta-lactamase

35

What is the function of bacterial beta lactamase enzymes?

they protect beta-lactam antibiotics from ring-destruction (counter-defense)

36

What type of bacteria are more likely to develop antibiotic resistance by altering drug uptake / efflux – gram positive or negative (and why)?

Gram negative. They have an impermeable outer membrane.

Example: development of a new PBP (PBP2a) by S. aureus is how the “superbug” MRSA arose

37

Give 3 examples of how bacteria can develop antibiotic resistance by altering antibiotic binding targets.

  1. these enzymes catalyze opening of the antibiotic’s beta-lactam ring
  2. most but not all bacteria produce beta-lactamase enzyme to defend themselves from antibiotics
  3. bacteria make hundreds of different beta-lactamase enzymes, each degrades a particular range of beta-lactam antibiotics
38

What is the mechanism by which MRSA developed resistance to penicillins?

Alteration of the antibiotic’s target: bacteria produce slightly different PBPs that antibiotics can’t bind to

-all available beta lactam antibiotics (except two new cephalosporins) fail to bind to MRSA’s new PBP (PBP2a)

-MRSA is currently treatable with vancomycin, daptomycin and ceftaroline

39

Which class of beta lactam antibiotics has the broadest spectrum of activity? 

Carbapenems (-penem): Imipenem, Meropenem

40

Which 1 class of beta lactams antibiotics has activity against gram negative bacteria only?  

Monobactams: Aztreonam (gram negative only)

41

Among the 4 categories of penicillins, which 2 have a narrow spectrum of activity, and which 1 has the broadest spectrum of activity?

  1. Narrow spectrum: 
    1. Natural Penicillins: Penicillin G (IV), Penicillin V (PO)
    2. Anti-Staphylococcal: Naficillin and Oxacillin (IV), Dicloxcillin (PO)
  2. Broadest spectrum: 
    1. Extended Spectrum: Piperacillin + tazobactam (IV/IM)
42

All penicillins have activity against which type of bacteria – gram positive or gram negative?

Gram Positive!

43

Name 6 antibiotic classes / subclasses / drugs that can be used to treat MDR strains of bacteria 

  1. Cephalosporins (5th generation, IV): Ceftaroline, ceftolozane + tazobactam 
  2. Carbapenems: Imipenem (combine with beta-lactam inhibitor to provide activity against MDR bacteria)
  3. Glycopeptide: Vancomycin (more use recently due to rise in MDR bacteria)
  4. Other cell wall agents: Fosfomycin
  5. Cell membrane agents: Polymyxins
  6.  Daptomycin (Lipopeptide - cell membrane agent)
44

Which of the β lactams is least likely to have cross-reactivity in patients with penicillin allergy?

Monobactams: Aztreonam (NO CROSS REACTIVITY)

45

Which β lactam drug class is associated with the highest risk of C difficile colitis?  

Cephalosporins (3rd generation): cefituten (PO), cefotaxime, ceftriaxone (-one, -ten, -ime)

46

Which antibiotic drug produces a classic constellation of side effects including histamine-mediated flushing, ototoxicity and nephrotoxicity?

Glycopeptides: Vancomycin

47

Which β lactam subclass can cause alcohol intolerance, hemolysis, impaired coagulation and C diff. colonic overgrowth?

Cephalosporins (3rd generation): cefituten (PO), cefotaxime, ceftriaxone (-one, -ten, -ime)

48

Which β lactam drug is mainly cleared by renal metabolism?

Carbapenems (-penem): Imipenem, Merapenem, Doripenem, Ertapenem

49

Which one of the 4 classes of beta lactam antibiotics is only available IV (and why)?

Carbapenems (-penem): Imipenem, Merapenem, Doripenem, Ertapenem

Because they have very short half lives

50

Give examples of 2 antibiotics that are more likely to cause concentration-dependent risk of seizures? 

  1. Natural Penicillins: Penicillin G (IV or IM)
  2. Carbapenems (-penem): concentration-dependent seizure risk (Imipenem, Merapenem, Doripenem, Ertapenem) [Imipenem highest risk]
51

How can one recognize the names of beta lactamase inhibitor drugs, and what is the one exception to this rule?

  1. Beta Lactamase inhibitor (usually-bactam): 
    1. Sulbactam, Tazobactam, Avibactam 

Exception: Clavulanic Acid

52

What is the purpose of beta lactamase inhibitor drugs?

Combined with beta lactam antibiotics to overcome bacterial drug resistance

53

Are beta lactamase inhibitors generally administered with non-beta lactam antibiotics?

No, it is usually administered with beta lactam antibiotics

54

Which antibiotic must be administered in combination with cilastatin, and what is the purpose of cilastatin in this combination?

Carbapenems: Imipenem (must combine with cilastatin (DHP-1 inhibitor) to achieve therapeutic concentration because DHP-1 metabolizes carbezenems

55
What is the major class of bactericidal protein synthesis-inhibiting antibiotics, and how can one recognize names of drugs in each class?
Aminoglycosides (-mycin/-micin): gentamicin, tobramycin, amikacin
56
Name 6 classes (and 1 additional drug) that are examples of bacteriostatic protein synthesis inhibiting antibiotics.
``` Tetracyclines (-cycline) Macroclides (-thromycin/-xomycin) Lincosamides (-lin-) Streptogramins (-prisitin) Oxazolodonones (-zolid) Chloramphenicol ``` The Man Loves Strep Of Course
57
For each of the classes of bacteriostatic protein synthesis inhibitors (except glycylcyclines, which have only one member), list the portion of the name that is similar among the drugs in each class.
Tetracyclines (-cycline) : Doxycycline, Minocycline Macroclides (-thromycin/-xomycin): Erythromycin, Clarithromycin, Azithromycin, Fidaxomycin Lincosamides (-lin-): Clindamycin Streptogramins (-prisitin): Dalfoprisitn/ Quinupristin Oxazolodonones (-zolid): Linezolid, Tedizolid Chloramphenicol
58
Name one aminoglycoside antibiotic that does not follow the aminoglycoside naming convention.
Amikacin
59
What are the two major subunits of the bacterial ribosome?
Large ribsomoal subunit and small ribosomal subunit
60
What are the 3 major steps in protein synthesis – what happens in each step?
Initiation: tRNA brings first amino acid in polypeptide chain to bind to start codon on mRNA Elongation: tRNAs bring amino acids one by one to add to polypeptide Termination: release factor recognizes stop codon, translational complex dissociates and completed polypeptide is released
61
Interferes with Initiation complex function (1 class):
Aminoglycosides (16S and 30S)
62
impairs Proofreading (1 class):
Aminoglycosides
63
interferes/ inhibits tRNA binding at the A site and / or peptide bond formation (6 classes
- Tetracyclines (16S on 30S) - Glycylclines - Lincosamides (23S on 50S) - Streptogramins (23S on 50S) - Oxazolidinones (23S on 50S) - Chloramphenicol (23S on 50S)
64
block Exit of the polypeptide from the ribosome (2 classes)
Macrolides (23S on 50S) | Streptogramins
65
For the bactericidal class of protein synthesis-inhibiting antibiotics, what 3 types of processes are thought to contribute to the bactericidal effect?
- Formation of free radicals, which damage the cell - Formation of holes in the cell membrane - Formation of toxic aggregates inside the cell
66
What 2 steps are required for aminoglycoside antibiotics to reach their target site in gram negative bacteria?
1) Passive diffusion across outer membrane - Normal entry through porins OR can disrupt lipopolysaccharides (LPS) function to enable movement across outer membrane 2) Active transport across cell membrane into cytoplasm (O2 dependent) - Anaerobes cannot bring aminoglycosides, requires energy gradient created by proton pump - Low extracelleular pH and lack of O2 dissipate that gradient
67
How do each of the following impact cellular uptake of aminoglycosides in gram negative bacteria?
- LPS : disrupting LPS allows for movement across outer membrane - Porins : polar drugs cannot cross membrane except through porins - Oxygen : lack of oxygen dissipates gradient - pH: low extracellular pH dissipates gradient
68
Are anaerobic bacteria susceptible to aminoglycoside antibiotics? Why or why not?
Anaerobic bacteria cannot bring aminoglycosides in because oxygen is required to drive the transport process, therefore they are not susceptible. - Active transport across cell membrane is O2 dependent
69
What is the basis for gram positive bacteria’s intrinsic resistance to aminoglycosides?
1)Alteration or deletion of the target receptor protein on the 30S 2) Impaired drug uptake by: - Mutation or deletion of a porin - Mutation of struction involved in electrochemical gradient maintenance - Growth conditions where O2 dependent transport process is not functional 3)Production of transferase enzymes that inactivate the aminoglycoside
70
Compare the process of cellular uptake between aminoglycoside and tetracycline antibiotics.
Aminoglycosides: combined with B lactam to create holes in peptidoglycan cell wall, allowing aminoglycoside to enter Tetracycline: complexes with metal cations and attracts them to specific porins → accumulation in periplasm -Uptake into cytopalsm is energy-dependent, driven by the pH gradient difference
71
Describe how bacteria alter (or protect) their antibiotic binding targets against aminoglycosides vs. tetracyclines
Aminoglycoside: antibiotics target the small 30S subunit and bind at the 16S rRNA site causing: - Interference with the initiation complex - Production of faulty miscoded proteins, by interfering with proofreading Tetracycline: bind reversibly to 16S site on small 30S subunit Drug blocks the site
72
What is the function of a ribosomal protection protein?
Ribosomal protection proteins prevent tetracyclines from binding to the ribosome, allowing translation and protein synthesis to continue Part of tetracycline resistance
73
Compare the resistance mechanisms by which bacteria limit concentrations of aminoglycosides vs. tetracyclines.
Aminoglycosides: inactivation from chemical modification by transferase enzymes -Generally transferred horizontally between bacteria by plasmids Tetracyclines: bind to repressor protein (Tet(R)) resulting in dissociation from mRNA and facilitates teh expression of tetracyline specific efflux pump
74
What is a TetR protein and what is its role in antibiotic resistance?
TetR prevents accumulation by increasing efflux which confers resistance to all tetracyclines
75
How do bacteria alter aminoglycosides to develop resistance to them (what’s the category of enzyme that is responsible)?
Transferase enzymes will chemically modify the aminoglycosides to develop resistance
76
Are glycylcyclines affected by the resistance mechanisms that affect other protein synthesis-inhibiting antibiotics?
Glycylcyclines are designed to avoid tetracycline resistance; not affected by ribosomal protection pumps (RPPs) or efflux pumps
77
Do aminoglycosides have activity against anaerobes? Why or why not?
Aminoglycosides do not have activity against anaerobes because there is no oxygen to drive the process
78
Which class of protein synthesis inhibiting antibiotics has particularly good activity against atypical pathogens like rickettsieae and Vibrio?
Tetracyclines
79
In addition to clindamycin (linocosamides) and gentamicin (aminoglycosides), what 3 classes of protein synthesis inhibiting antibiotics have particularly good activity against drug-resistant pathogens?
Streptogramins (-pristin): Dalforpristin / quinupristin Oxazolidinones (-zolid): Linezolid / Tedizolid Macrolides (-thromcin / -xomycin): Erythromycin /Clarithromycin / Azithromycin / Fidaxomycin
80
Which class is often used as eyedrops for eye infections?
Aminoglycosides: tobramycin and gentamicin
81
Which class is useful for COPD / asthma exacerbations?
Macrolides: due to anti-inflammatory and immunomodulating characteristics; erythromycin, clarithromycin, azithromycin, fidaxomycin
82
Which DRUG is used in inhaled form for treating bacterial infections in cystic fibrosis?
Tobramycin: treat P. aeruginosa in cystic fibrosis | Monobactam, aztreonam is used similarly
83
Which drug class, due to dependence on renal clearance, is dosed based on body weight and creatinine clearance and requires concentration monitoring?
Aminoglycosides
84
Which class has basically no oral absorption?
Aminoglycosides→ entire oral dose goes to feces; usually given IM or IV
85
Which 2 classes are only available by IV route?
Streptogramins (dalfopristin/quinupristin) and Glycylcyclines (tigecycline)
86
Which class cannot be taken with dairy products or antacids, and why?
Tetracyclines; dairy products impair absorption | - Multivalent cations and alkaline pH also impair absorption
87
Which class must be enteric coated to avoid destruction by stomach acid?
Macrolides
88
Which class is associated with nephrotoxicity and ototoxicity?
Aminoglycosides
89
Which class is associated with GI effects (and why?), hepatic toxicity, QT interval prolongation, and hearing loss?
Macrolides: GI effects (due to stimulation of gut motility via motion receptors), heart rhythm, hepatic toxicity, and drug interactions (P450 inhibitors)
90
Which class is associated with phototoxicity, bone / tooth toxicity, and hepatic toxicity?
Tetracyclines
91
Which class should not be administered to children or pregnant women, and why?
Tetracyclines
92
What are 5 advantages of docycyline vs. most other tetracyclines?
- Available PO and IV - Can be administered with food - Less likely to produce photosensitivity - Less calcium binding ( only tetracycline that can be given to kids under 8 yers old) - Clearance is non-renal
93
What two protein synthesis-inhibiting antibiotic agents have been associated with increased mortality risk?
Glycylcyclines (Tigecycline)
94
Which drug presents a risk for development of serotonin syndrome?
Linezolid (PO/IV); caution with antidepressants
95
Which drug is rarely used now, due to risk of bone marrow suppression, fatal aplastic anemia and gray baby syndrome?
Chloramphenicol; broad spectrum
96
Which protein synthesis-inhibiting antibiotic class is given with aminoglycosides, and why?
Combined with B lactams when needing to treat gram positive bacteria to create holes in peptidoglycan cell wall, allowing aminoglycosides to enter
97
Which protein synthesis-inhibiting agent is available as a 2-drug combination, and what is the advantage of combining the two?
Streptogramins: Dalfopristin / Quinupristin→ synergistic effects = rapidly bactericidal
98
What is the major class of folate antagonist antibiotics, and how do you recognize their names?

Sulfonamides, (sulfa)

 

99

What additional drug is also considered a folate antagonist?

Trimethoprim

100

What is the major class of DNA synthesis inhibiting antibiotics, and how do you recognize their names?

Fluoroquinolones (flox)

101

What is one agent that is considered a urinary antiseptic?

Nitrofurantoin

102

What are the functions of dihydropteroate synthase (DHPS) and dihydrofolate reductase (DHFR) enzymes (which one metabolizes PABA and which one metabolizes dihydrofolic acid)?

DHPS is the enzyme that converts a precursor, PABA, to dihydrofolic acid. DHFR metabolizes dihydrofolic acid to tetrahydrofolic acid (folates!).

103

Is folate synthesis from PABA a bacteria specific process? Which portion of the pathway is shared by both bacteria and humans?

Yes, the portion where dihydrofolic acid is converted into folates is shared by both bacteria and humans.

104

Which enzyme is inhibited by sulfonamides, and which by trimethoprim?

Sulfonamides-DHPS
Trimethoprim-bacterial DHFR blocking folate synthesis

105

What is the function of the topoisomerase enzymes (DNA gyrase and Top IV)?

The unwinding process is done by topoisomerase, DNA gyrase (alters DNA supercoiling), topoisomerase IV (separates interlocked strands)

106

Do humans have topoisomerases? If so, how do antibiotics target topoisomerases without affecting human cells?

Yes, humans do have topoisomerase. Fluoroquinolones are specific inhibitors of bacterial topoisomerases.

107

How does nitrofurantoin selectively target bacterial vs. human cells?

Bacterial selectivity is due to more rapid bacterial conversion to reactive intermediates in bacteria vs humans

108
What 3 mechanisms provide bacteria with resistance to sulfonamides?
  • Overproduction of PABA 
  • Structural changes to DHPS enzyme to reduce its affinity to sulfonamides 
  • Changes in permeability that reduce the ability of sulfonamides to enter the bacterial cell
109

What 3 mechanisms provide bacteria with resistance to trimethoprim?

  1. Reduced cell permeability
  2. Overproduction of DHFR
  3. Production of an altered reductase that doesn't bind trimethoprim well
110

Is resistance to nitrofurantoin common or rare?

Rare

111

Among the drugs/classes covered in this lecture, which has the broadest spectrum of activity?  

Fluoroquinolones

112

Name one class and one combination (class + drug) that have activity against multi-drug resistant bacteria

Fluoroquinolones (one class) Trimethoprim-Sulfamethoxazole (class+drug)

113

For which class is use limited to serious or treatment-resistant infections, and why?

Fluoroquinolones

114

What is the one use of nitrofurantoin?

UTI

115

What class is used topically for burns and as eyedrops for eye infections?

Sulfonamides

116

Which class tends to have cross-allergenicity with many other drug classes?

Sulfonamides

117

Which class tends to produce urine crystals, hematologic toxicity and hemolytic reactions in G6PD deficient individuals?

Sulfonamides

118

Which other drug can also produce hemolytic reactions in G6PD deficient individuals?

Nitrofurantoin

119

Which class is generally well tolerated, but has many FDA warnings for rare serious side effects?  (Name 4 examples of rare serious side effects with this class of drug).

  1. Fluoroquinolones
    1. Tendinitis and tendon rupture
    2. Peripheral neuropathy
    3. CNS effects
    4. Aortic aneurysm/dissection
120

Which class is generally well tolerated, but can produce neuropathy / pulmonary toxicity if the drug can’t be cleared by kidneys?

Nitrofurantoin

121

What drug is often given with sulfonamides, and what are the 2 advantages of this combination

  1. Trimethoprim-sulfamethoxazole (TMP-SMX)
    1. Effective for a wide variety of infections, including pneumonia and most respiration tract infections, otitis media, UTI’s, prostatitis, uncomplicated skin and soft tissue infections (oral)
    2. Used for severe pneumocystis pneumonia, alternate therapy for some multidrug-resistant infections (IV)
122

What drug is often given with sulfonamides, and what are the 2 advantages of this combination

  1. Trimethoprim-sulfamethoxazole (TMP-SMX)
    1. Effective for a wide variety of infections, including pneumonia and most respiration tract infections, otitis media, UTI’s, prostatitis, uncomplicated skin and soft tissue infections (oral)
    2. Used for severe pneumocystis pneumonia, alternate therapy for some multidrug-resistant infections (IV)

pharm exam 3 (9 decks)

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