All cards Flashcards

Question 1

Q

What are 3 features unique to gram-negative bacteria?

Answer

A

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

Question 2

Q

Which is easier for a drug to penetrate- gram positive or negative bacteria, and why?

Answer

A

Gram positive, low MW enter easily across exposed PG layer, itself a key target

Question 3

Q

How does the murein (peptidoglycan) layer differ between gram positive and negative bacteria?

Answer

A

Gram positive: thick PG

Gram negative: thin PG

Question 4

Q

How does gram staining distinguish between gram positive and negative bacteria?

Answer

A

Gram positive:purple dye

Gram negative: safranin (red)

Question 5

Q

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

Answer

A

bacteria vs humans:

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

Question 6

Q

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

Answer

A

Bactericidal: kills bacteria; irreversible (penicillin)

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

Question 7

Q

Describe 3(there are 4 in the lecture)categories of adverse effects of antibiotics – which is specific to antibiotics?

Answer

A

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

Question 8

Q

Contrast between prophylactic, pre-emptive, empiric and definitive / directed therapy.

Answer

A

Prophylactic: antibiotic used before an infection

Pre-emptive therapy: antibiotic used during symptoms occur to prevent anticipated infection or symptoms

Empiric therapy: selection of an antibiotic based onmost likely cause of infection

Definitive/directed therapy: selection of an antibiotic based on positive identification of the causative organisms

Question 9

Q

Define the terms “sensitivity”, “MIC”, and “clinical breakpoint”

Answer

A

Sensitivity: the ability of a bacteria to be inhibited/killed by a particular antibiotic; drug affects the bacteria atlowest concentration is the one to which it’smost sensitive

Minimum inhibitory concentration (MIC): lowest concentration of drug thatinhibitsgrowth of organism

Clinical breakpoint: highest plasma concentration that can safely be achieved in a patient

Question 10

Q

What is the purpose of broth dilution and disk diffusion testing?

Answer

A

Broth dilution: bacteria in liquid are exposed toincreasing concentrations of a drug - the lowest concentration that eliminates growth is MIC

Disk diffusion: bacteria are plated ontoagar studded with small disks containingdifferent antibiotics - if bacteria surrounding a disk are dead, they are susceptible to that drug

Question 11

Q

How are MIC and breakpoint concentrations used together to determine bacterial sensitivity?

Answer

A

Sensitive: MIC < breakpoint

Intermediate: MIC near breakpoint

Resistant: MIC > breakpoint

Question 12

Q

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

Answer

A

Broad spectrum: active against many types of bacteria

Narrow spectrum: active against only one or a few types of bacteria (might be more appropriate: tokill/inhibit only unwanted bacteria; lessen resistance)

Question 13

Q

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

Answer

A

Time dependent: constant rate of killing, provided that drug concentration exceeds MIC (beta lactams)

Concentration-dependent: rate of killing increase with drug concentration above MIC (aminoglycosides)

Question 14

Q

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

Answer

A

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

Question 15

Q

What is the difference between intrinsic and acquired resistance?

Answer

A

Intrinsic: trait that confers protection against antibiotic action, shared by all members of a bacterial species, not related to antibiotic exposure

Acquired: certain gene changed become favored as a result of pressure from antibiotic exposure

Question 16

Q

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

Answer

A

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

Question 17

Q

Can more than one resistance mechanism appear in the same strain of bacteria?

Answer

A

With in same species of bacteria, there may be multiple strains with varying types of resistance

A single species may have multiple acquired resistance mechanisms

Question 18

Q

What are the 3 main modes of horizontal transfer of acquired resistance, and how does each work?

Answer

A

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

Question 19

Q

Are resistance genes always acquired horizontally (from another organism)?

Answer

A

Bacterialproliferation andtransfer between hosts (poor hygiene, hospital acquired infections)

Increasedexposure of bacteria toantibiotics -> selection pressure (over prescription, wrong prescription, use in agriculture)

Question 20

Q

What is “antibiotic stewardship”?

Answer

A

coordinated data-driven programs that focus on reducing inappropriate antibiotic use in clinical settings and agriculture

Question 21

Q

What are two general categories of initiatives that are being supported to combat drug resistance development?

Answer

A

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

Question 22

Q

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

Answer

A

Penicillins: (-cillin) Cephalosporins: (-cef-) Carbapenems: (-penem) Monobactams (aztreonam)

Question 23

Q

What are the 4 major classes of penicillins?

Answer

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>

Question 24

Q

Name 4 examples of beta lactamase inhibitor drugs.

Answer

A

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

Question 25

Q

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

Answer

A

-van-

Question 26

Q

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

Answer

A

<ul><li>Other cell wall antibiotics: fosfomycin, bacitracin</li><li>Lipopeptides: dapotomycin</li><li>Polymyxins (-myxin)</li></ul>

Question 27

Q

Name 2 drugs that primarily target bacterial cell membranes.

Answer

A

Daptomycin: disrupts cytoplasmic membrane

Polymyxins: disrupt the outer membrane + cytoplasmic membrane

Question 28

Q

What are the two major components of peptidoglycan?

Answer

A

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

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

Question 29

Q

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

Answer

A

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

Question 30

Q

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

Answer

A

PBP often have bothtranspeptidase domain and glycosyltransferase domain

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

Flippase II enzymes:transportbuilding blocks to cell surface

Question 31

Q

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

Answer

A

Photo attached below

Question 32

Q

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

Answer

A

Daptomycin: disrupts cytoplasmic membrane

Polymyxins: disrupt the outer membrane + cytoplasmic membrane

Question 33

Q

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

Answer

A

<ol><li>Inactivation of antibiotic by bacterialbeta-lactamase: these enzyme catalyzedopening of the antibiotic’sbeta-lactam ring</li><li>Reduced uptake of antibiotic: specific togram-negative bacteria (imperviousouter membrane)</li><li>Antibiotic efflux:gram negative bacteria may producedrug efflux pumps which toss some beta-lactam antibiotics back out</li><li>Alteration of the antibiotic’s target: bacteria produce slightly different PBPs that antibiotics can’t bind to: development of anew PBP (PBP2a) by S. aureus is how the “superbug”MRSA arose</li></ol>

Question 34

Q

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

Answer

A

Inactivation of antibiotic by bacterialbeta-lactamase

Question 35

Q

What is the function of bacterial beta lactamase enzymes?

Answer

A

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

Question 36

Q

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

Answer

A

Gram negative. They have an impermeable outer membrane.

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

Question 37

Q

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

Answer

A

<ol><li>these enzymes catalyze opening of the antibiotic’s beta-lactam ring</li><li>most but not all bacteria produce beta-lactamase enzyme to defend themselves from antibiotics</li><li>bacteria make hundreds of different beta-lactamase enzymes, each degrades a particular range of beta-lactam antibiotics</li></ol>

Question 38

Q

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

Answer

A

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

Question 39

Q

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

Answer

A

Carbapenems (-penem): Imipenem, Meropenem

Question 40

Q

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

Answer

A

Monobactams: Aztreonam (gram negative only)

Question 41

Q

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

Answer

A

<ol><li>Narrow spectrum:<ol><li>Natural Penicillins: Penicillin G (IV), Penicillin V (PO)</li><li>Anti-Staphylococcal: Naficillin and Oxacillin (IV), Dicloxcillin (PO)</li></ol></li><li>Broadest spectrum:<ol><li>Extended Spectrum: Piperacillin + tazobactam (IV/IM)</li></ol></li></ol>

Question 42

Q

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

Answer

A

Gram Positive!

Question 43

Q

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

Answer

A

<ol>
<li>Cephalosporins (5th generation, IV): Ceftaroline, ceftolozane + tazobactam</li>
<li>Carbapenems: Imipenem (combine withbeta-lactam inhibitor to provide activity against MDR bacteria)</li>
<li>Glycopeptide: Vancomycin (more use recently due to rise in MDR bacteria)</li>
<li>Other cell wall agents: Fosfomycin</li>
<li>Cell membrane agents: Polymyxins</li>
<li>Daptomycin (Lipopeptide - cell membrane agent)</li>
</ol>

Question 44

Q

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

Answer

A

Monobactams: Aztreonam (NO CROSS REACTIVITY)

Question 45

Q

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

Answer

A

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

Question 46

Q

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

Answer

A

Glycopeptides: Vancomycin

Question 47

Q

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

Answer

A

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

Question 48

Q

Which β lactam drug is mainly cleared by renal metabolism?

Answer

A

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

Question 49

Q

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

Answer

A

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

Because they have very short half lives

Question 50

Q

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

Answer

A

<ol><li>Natural Penicillins: Penicillin G (IV or IM)</li><li>Carbapenems (-penem): concentration-dependent seizure risk (Imipenem, Merapenem, Doripenem, Ertapenem) [Imipenem highest risk]</li></ol>

Question 51

Q

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

Answer

A

<ol><li>Beta Lactamase inhibitor (usually-bactam):<ol><li>Sulbactam, Tazobactam, Avibactam</li></ol></li></ol>

Exception: Clavulanic Acid

Question 52

Q

What is the purpose of beta lactamase inhibitor drugs?

Answer

A

Combined with beta lactam antibiotics to overcome bacterial drug resistance

Question 53

Q

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

Answer

A

No, it is usually administered with beta lactam antibiotics

Question 54

Q

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

Answer

A

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

Question 55

Q

What is the major class of bactericidal protein synthesis-inhibiting antibiotics, and how can one recognize names of drugs in each class?

Answer

A

Aminoglycosides (-mycin/-micin): gentamicin, tobramycin, amikacin

Question 56

Q

Name 6 classes (and 1 additional drug) that are examples of bacteriostatic protein synthesis inhibiting antibiotics.

Answer

A

Tetracyclines (-cycline)
Macroclides (-thromycin/-xomycin)
Lincosamides (-lin-)
Streptogramins (-prisitin) 
Oxazolodonones (-zolid)
Chloramphenicol

The Man Loves Strep Of Course

Question 57

Q

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.

Answer

A

Tetracyclines (-cycline) : Doxycycline, Minocycline

Macroclides (-thromycin/-xomycin): Erythromycin, Clarithromycin, Azithromycin, Fidaxomycin

Lincosamides (-lin-): Clindamycin

Streptogramins (-prisitin): Dalfoprisitn/ Quinupristin

Oxazolodonones (-zolid): Linezolid, Tedizolid

Chloramphenicol

Question 58

Q

Name one aminoglycoside antibiotic that does not follow the aminoglycoside naming convention.

Question 59

Q

What are the two major subunits of the bacterial ribosome?

Answer

A

Large ribsomoal subunit and small ribosomal subunit

Question 60

Q

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

Answer

A

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

Question 61

Q

Interferes with Initiation complex function (1 class):

Answer

A

Aminoglycosides (16S and 30S)

Question 62

Q

impairs Proofreading (1 class):

Answer

A

Aminoglycosides

Question 63

Q

interferes/ inhibits tRNA binding at the A site and / or peptide bond formation (6 classes

Answer

A

Tetracyclines (16S on 30S)
Glycylclines
Lincosamides (23S on 50S)
Streptogramins (23S on 50S)
Oxazolidinones (23S on 50S)
Chloramphenicol (23S on 50S)

Question 64

Q

block Exit of the polypeptide from the ribosome (2 classes)

Answer

A

Macrolides (23S on 50S)

Streptogramins

Answer 64

A

Formation of free radicals, which damage the cell
Formation of holes in the cell membrane
Formation of toxic aggregates inside the cell

Answer 65

A

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

Answer 66

A

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

Answer 67

A

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

Answer 68

A

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

Answer 69

A

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

Answer 70

A

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

Answer 71

A

Ribosomal protection proteins prevent tetracyclines from binding to the ribosome, allowing translation and protein synthesis to continue
Part of tetracycline resistance

Answer 72

A

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

Answer 73

A

TetR prevents accumulation by increasing efflux which confers resistance to all tetracyclines

Answer 74

A

Transferase enzymes will chemically modify the aminoglycosides to develop resistance

Answer 75

A

Glycylcyclines are designed to avoid tetracycline resistance; not affected by ribosomal protection pumps (RPPs) or efflux pumps

Answer 76

A

Aminoglycosides do not have activity against anaerobes because there is no oxygen to drive the process

Answer 77

A

Tetracyclines

Answer 78

A

Streptogramins (-pristin): Dalforpristin / quinupristin

Oxazolidinones (-zolid): Linezolid / Tedizolid

Macrolides (-thromcin / -xomycin): Erythromycin /Clarithromycin / Azithromycin / Fidaxomycin

Answer 79

A

Aminoglycosides: tobramycin and gentamicin

Answer 80

A

Macrolides: due to anti-inflammatory and immunomodulating characteristics; erythromycin, clarithromycin, azithromycin, fidaxomycin

Answer 81

A

Tobramycin: treat P. aeruginosa in cystic fibrosis

Monobactam, aztreonam is used similarly

Answer 82

A

Aminoglycosides

Answer 83

A

Aminoglycosides→ entire oral dose goes to feces; usually given IM or IV

Answer 84

A

Streptogramins (dalfopristin/quinupristin) and Glycylcyclines (tigecycline)

Answer 85

A

Tetracyclines; dairy products impair absorption

- Multivalent cations and alkaline pH also impair absorption

Answer 86

A

Macrolides

Answer 87

A

Aminoglycosides

Answer 88

A

Macrolides: GI effects (due to stimulation of gut motility via motion receptors), heart rhythm, hepatic toxicity, and drug interactions (P450 inhibitors)

Answer 89

A

Tetracyclines

Answer 90

A

Tetracyclines

Answer 91

A

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

Answer 92

A

Glycylcyclines (Tigecycline)

Answer 93

A

Linezolid (PO/IV); caution with antidepressants

Answer 94

A

Chloramphenicol; broad spectrum

Answer 95

A

Combined with B lactams when needing to treat gram positive bacteria to create holes in peptidoglycan cell wall, allowing aminoglycosides to enter

Answer 96

A

Streptogramins: Dalfopristin / Quinupristin→ synergistic effects = rapidly bactericidal

Answer 97

A

Sulfonamides, (sulfa)

Answer 98

A

Trimethoprim

Answer 99

A

Fluoroquinolones (flox)

Answer 100

A

Nitrofurantoin

Answer 101

A

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

Answer 102

A

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

Answer 103

A

Sulfonamides-DHPS Trimethoprim-bacterial DHFR blocking folate synthesis

Answer 104

A

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

Answer 105

A

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

Answer 106

A

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

Answer 107

A

<ul><li>Overproduction of PABA</li><li>Structural changes to DHPS enzyme to reduce its affinity to sulfonamides</li><li>Changes in permeability that reduce the ability of sulfonamides to enter the bacterial cell</li></ul>

Answer 108

A

<ol><li>Reduced cell permeability</li><li>Overproduction of DHFR</li><li>Production of an altered reductase that doesn't bind trimethoprim well</li></ol>

Answer 109

A

Rare

Answer 110

A

Fluoroquinolones

Answer 111

A

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

Answer 112

A

Fluoroquinolones

Answer 113

A

UTI

Answer 114

A

Sulfonamides

Answer 115

A

Sulfonamides

Answer 116

A

Sulfonamides

Answer 117

A

Nitrofurantoin

Answer 118

A

<ol><li>Fluoroquinolones<ol><li>Tendinitis and tendon rupture</li><li>Peripheral neuropathy</li><li>CNS effects</li><li>Aortic aneurysm/dissection</li></ol></li></ol>

Answer 119

A

Nitrofurantoin

Answer 120

A

<ol><li>Trimethoprim-sulfamethoxazole (TMP-SMX)<ol><li>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)</li><li>Used for severe pneumocystis pneumonia, alternate therapy for some multidrug-resistant infections (IV)</li></ol></li></ol>

Answer 121

A

<ol><li>Trimethoprim-sulfamethoxazole (TMP-SMX)<ol><li>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)</li><li>Used for severe pneumocystis pneumonia, alternate therapy for some multidrug-resistant infections (IV)</li></ol></li></ol>

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