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Advanced Pharm > Chapter 24 > Flashcards

Chapter 24 Flashcards

Week 2

1
Q

What year and by who were penicillins discovered

A

1928, Alexander Flemming

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2
Q

What are 4 ways abx resistance is mediated?

A

1.Production and excretion of an enzyme that hydrolyzes the antimicrobial
2.Genetic alteration of the microbial site where antimicrobial binds
3.Alteration in cellular membrane proteins that prevent antimicrobials from penetrating into microbial cells
4.Transmembrane efflux pumps that transport antimicrobials from interior to exterior of the microbial cells

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3
Q

What is VRE and when did it emerge

A

vancomycin-resistant enterococci - emerged in 1980

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4
Q

What is CRE and when did it emerge

A

carbapenem-resistant enterobacterales - emerged in 2000s

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5
Q

Leading Risk Factors for having a drug-resistant pathogen:

A

Recent use of antimicrobials
Multiple medical comorbidities
Recent hospitalization or other skilled healthcare contact

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6
Q

Antibiotic Stewardship Strategies

A

Treatment for specific infectious disease
Formulary restrictions
Dose optimization
Prospective audits
Continuing education for prescribers

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7
Q

Define Antimicrobials:

A

The entire arsenal of drugs that have the activity to inhibit or kill microbes.

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8
Q

Define Antibiotic or Antibacterial

A

Specifically refers to antimicrobials that target bacteria

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9
Q

Define Bactericidal

A

Refers to 99.9% eradication of a bacterial colony in vitro in 24 hrs by an antimicrobial.
-No clinical utility in the designation. Not to be used for clinical decision-making.

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10
Q

Define Bacteriostatic:

A

Refers to an abx that kills bacteria but the result is less than 99.9% eradication in a 24hr period.
-No clinical utility in the designation. Not to be used for clinical decision-making.

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11
Q

What are Beta Lactams and what are they most effective at treating

A

Super class of abx and contains the most abx’s of any class. Most effective against rapidly replicating organisms.

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12
Q

What are the 4 major groups of abx within beta-lactams

A

Penicillins
Cephalosporins
Carbapenems
Monobactams

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13
Q

What is the active part of the beta-lactam abx

A

a 4-member ring known as the beta-lactam ring

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14
Q

What is the MOA of all beta-lactam abxs

A

B-lactams inhibit the biosynthesis of the bacterial cell wall by binding to bacterial enzymes, specifically the peptidoglycan structure, and leading to cell lysis.

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15
Q

What are three bacterial enzymes that help create cell wall/peptidoglycan synthesis

A

Transpeptidase
Carboxypeptidase
Endopeptidase

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16
Q

What is peptidoglycan?

A

a rigid envelope surrounding the cytoplasmic membrane of most bacterial species

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17
Q

What is minimum inhibitory concentration (MIC)?

A

the lowest concentration of an antimicrobial agent that will inhibit the visible growth of a microorganism after overnight incubation.

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18
Q

What are the 4 penicillin subclasses?

A
  1. Natural penicillins
  2. Aminopenicillins
  3. Antistaphylococcal penicillins
  4. Antipseudomonal or Extended-Spectrum penicillins
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19
Q

What are the four natural penicillins and how are they administered

A

Penicillin V - administered PO
Procaine penicillin - administered IM
Benzathine penicillin - administered IM
Penicillin G - administered IV

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20
Q

Penicillin G is reliable for treating which bacteria

A

reliable for treating Listeria monocytogenes

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21
Q

Natural penicillins are active against which organisms

A

active against aerobic, gram-positive organisms, including:
Streptococcus species such as S. pneumoniae and group A beta-hemolytic Streptococcus (GABHS)
Some Enterococcus strains
Some non–penicillinase-producing staphylococci

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22
Q

What is penicillinase?

A

the vast majority of organisms produce and excrete an enzyme called penicillinase. this enzyme hydrolyzes the beta-lactam ring of natural penicillins rendering them completely ineffective

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23
Q

Why has Penicillin-resistant Streptococcus pneumoniae has decreased in prevalence ?

A

widespread vaccination for Streptococcus pneumoniae (PCV-13, -15, -20)

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24
Q

Why do only 5% to 15% of community-acquired Staphylococcus aureus remain susceptible to natural penicillins?

A

the vast majority of organisms produce and excrete an enzyme commonly known as penicillinase

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25
Q

A Penicillin-resistant s. pneumoniae is also likely to be resistant to?

A

cephalosporins, macrolides, and sulfonamides, and, to a lesser extent, clindamycin; therefore, they are commonly called drug-resistant S. pneumoniae (DRSP)

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26
Q

What kind of organisms do Aminopenicillins target?

A

Have greater activity against gram-negative bacteria because of their enhanced ability to penetrate the outer cell membrane of these organisms.
(Like penicillins, they also have reliable activity against gram-positive organisms, including Streptococcus and Enterococcus species.)

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27
Q

What are the two most common aminopenicllins?

A

Ampicillin
Amoxicillin

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28
Q

Aminopenicllins are often paired with what to increase their effectiveness

A

Often paired with beta-lactamase inhibitors to prevent the destruction of beta-lactam antibiotics by serving as a competitive inhibitor of beta-lactamase. (sulbactam and clavulanate)

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29
Q

Ampicillin/sulbactam and amoxicillin/clavulanate have excellent activity against?

A

Staphylococcus aureus (MSSA), Streptococcus and Enterococcus species
Haemophilus influenzae, Neisseria meningitidis, Salmonella, some Shigella species

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30
Q

What are three Antistaphylococcal Penicillins and how are they administered?

A

Nafcillin (only available IV)
oxacillin (only available IV)
dicloxacillin (only available PO)

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31
Q

Are Antistaphylococcal penicillins stable in the presence of penicillinase produced by staphylococci?

A

yes

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32
Q

What is the difference between penicillinase and beta-lactamase?

A

Penicillinase is a specific subtype of β-lactamase, showing specificity to pencillins

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33
Q

Antistaphylococcal Penicillins are active against which organisms?

A

They are active against Streptococcus species, MSSA, and Peptostreptococcus.

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34
Q

What is the Antipseudomonal Penicillin abx

A

Piperacillin/tazobactam
comprised of a single combination product: piperacillin and a beta-lactamase inhibitor, tazobactam.

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35
Q

Piperacillin/tazobactam is active against?

A

Pseudomonas aeruginosa, Enterobacter, Escherichia coli, Klebsiella species.

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36
Q

What is the the most common mechanism of resistance to penicillins?

A

Beta-lactamase production. large group of enzymes with diverse ability to inactivate beta-lactams

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37
Q

Which bacteria are considered extended-spectrum beta-lactamases (ESBLs)? What is the consequence of this.

A

Enterobacterales such as E. coli, Klebsiella species, and Enterobacter produce ESBLs that have broader activity and not generally inhibited by beta-lactamase inhibitors.

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38
Q

Which natural penicillin can be given PO

A

Penicillin V

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39
Q

Which antistaphylococcal penicillin can be given PO

A

dicloxacillin

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40
Q

Which penicillins should be given IM, with a long half life

A

Penicillin G procaine and penicillin G benzathine

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41
Q

What could cause a cardiac arrest regarding penicillin administration

A

IM administration of Penicillin G procaine and penicillin G benzathine near a vein or artery

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42
Q

How are penicillins distributed throughout body

A

Varying degrees of plasma protein bonding

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43
Q

Can penicillins cross the placenta or be in breast milk?

A

Yes and Yes

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44
Q

Do penicillins readily cross the BBB?

A

No

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45
Q

What percent of renal excretion of penicillins is by active tubular secretion

A

90%

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46
Q

How readily are penicillins metabolized?

A

Excluding nafcillin and oxacillin, penicillins undergo negligible metabolism and are excreted primarily as unchanged drugs in the urine, achieving high urinary concentrations.

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47
Q

How should you treat C.Diff? What is the criteria for stool sampling?

A

if definitive diagnosis is made, treatment with oral vancomycin or fidaxomicin is required.
more than three watery, unformed stools per day or blood in the stool warrant stool testing to detect C. difficile toxin.

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48
Q

Piperacillin/tazobactam, when combined with vancomycin, leads to higher-than-expected rates of?

A

nephrotoxicity

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49
Q

the most commonly prescribed antibiotic in the United States

A

Amoxacillin

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50
Q

cross-sensitivity between penicillins and cephalosporins, carbapenems, or beta-lactamase inhibitors was thought to be much higher, data suggest that the rate is closer to?

A

1%

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51
Q

less than what percent of patients are truly allergic to penicillins?

A

1%

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52
Q

Type 1 rxns of penicillins usually occur within how much time post administration

A

2-30min

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53
Q

4 steps for Abx selection

A

Make clinical diagnosis
Obtain culture/specimens if able
Make microbial dx
Select drug based on sensitivity or usual susceptibility

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54
Q

Which 6 drugs are known to interact with penicillins

A

Diuretics
Methotrexate
Oral contraceptives
Probenecid
Tetracyclines
Warfarin

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55
Q

Ampicillin can interact with which two drugs

A

beta blockers and allopurinol

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56
Q

a rapid strep test, is testing for which organism

A

Group A Streptococcus Bacteria

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57
Q

How do cephalosporins compare chemically and structurally to penicillins?

A

Chemically and structurally similar to penicillins

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58
Q

What two drugs are included in the cephalosporin class but technically cephamycins?

A

Cefoxitin and cefotetan

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59
Q

What is the MOA of cephalosporins?

A

inhibit mucopeptide synthesis in the bacterial cell wall, making the bacterium osmotically unstable. Like penicillins, cephalosporins inhibit PBPs involved in cross-linking peptidoglycans in the cell wall

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60
Q

What are Penicillin Binding Proteins (PBPs)?

A

subgroup of enzymes of transpeptidases. Essential for bacterial cell wall synthesis. involved in the final stages of synthesizing peptidoglycan.
Inhibition of PBPs leads to defects in cell wall structure and irregularities in cell shape

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61
Q

What are cephalosporins most effective against?

A

They are most effective against rapidly growing organisms forming cell walls and when antibiotic concentrations exceed the pathogen’s MIC for at least 50% of the dosing interval

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62
Q

What is the only intravenous first-generation cephalosporin?

A

Cefazolin

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63
Q

What are the most commonly used first-generation cephalosporins?

A

cephalexin & cefadroxil

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64
Q

What organisms do 1st gen cephalosporins target?

A

active against gram-positive cocci, including S. aureus and S. epidermidis (excluding methicillin-resistant strains), and most streptococci.

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65
Q

What species are intrinsically resistant to cephalosporins?

A

Enterococcus species

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66
Q

Do 1st gen cephalosporins readily enter the CSF?

A

No

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67
Q

What are the three 2nd gen. cephalosporins?

A

cefaclor, cefprozil, and cefuroxime

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68
Q

2nd gen cephalosporins are active against?

A

active against the same organisms as the first generation but with increased activity against H. influenzae

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69
Q

Cephamycins are included in what generation of cephalosporins?

A

2nd generation

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70
Q

What are the two cephamycins?

A

cefotetan and cefoxitin

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71
Q

Cephamycins have what sort of activity?

A

activity similar to 1st gen. W/ limited activity against anaerobes including Bacteroides fragilis

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72
Q

What needs to be performed before ordering a second gen. cephalosporin?

A

2nd gens have variable activity, so susceptibility tests need to be performed

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73
Q

What are three 3rd gen. cephalosporin abx?

A

Cefotaxime, Ceftazidime, and Ceftriaxone

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74
Q

Third Generation Cephalosporins have activity against?

A

streptococcal species, Streptococcus pneumoniae, MSSA, H. influenzae (including beta-lactamase–producing strains), Moraxella, N. gonorrhoeae, N. meningitidis, E. coli, Klebsiella, Proteus, and Salmonella

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75
Q

What kind of activity do 3rd gen. cephalosporins have? What is the exception?

A

Similar spectrum of activity to other generations
*except for ceftazidime.
Ceftazidime - reduced gram-positive but increased gram-negative activity such as Pseudomonas aeruginosa

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76
Q

Do 3rd gen. cephalosporins have reliable activity against anaerobes?

A

None of the third-generation cephalosporins have reliable activity against anaerobes other than Peptostreptococcus

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77
Q

What generation of cephalosporins are used to treat meningitis?

A

Because they cross the blood-brain barrier, third-generation parenteral cephalosporins are used to treat meningitis

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78
Q

What is the 4th gen. cephalosporin?

A

cefepime

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79
Q

What is the 5th gen. cephalosporin?

A

ceftaroline

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80
Q

What are two nongenerational cephalosporins and how are they available?

A

ceftolozane/tazobactam and ceftazidime/avibactam are only available for IV administration.

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81
Q

What are the most common mechanisms of resistance to cephalosporins?

A

that bacteria express against cephalosporins are beta-lactamase production and altered target sites.

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82
Q

are cephalosporins stable in the presence of penicillinases produced by S. aureus?

A

yes

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83
Q

Which generation(s) are the most stable in the presence of most beta-lactamases produced by enteric gram-negative bacteria?

A

Third- and fourth generation cephalosporins

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84
Q

How well are cephalosporins absorbed through GI?

A

oral formulations are well-absorbed from the GI tract

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85
Q

How are cephalosporins distributed? What needs to be considered with ceftriaxone?

A

Protein binding varies, but ceftriaxone is so highly bound to albumin that it should be avoided in neonates at risk for hyperbilirubinemia, especially preterm infants

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86
Q

What generations of cephalosporins readily enter the CSF in the presence of meningeal inflammation

A

Third and fourth-generation drugs and cefuroxime

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87
Q

How significant is hepatic metabolism for cephalosporins?

A

Hepatic metabolism is not significant for cephalosporin drug elimination.

88
Q

How are most cephalosporins excreted? What is one exception?

A

Most cephalosporins are excreted via the kidney in varying degrees as unchanged drug. Renal impairment significantly extends the half-life of these drugs.
Ceftriaxone elimination is mainly extrarenal, via biliary, making its half-life stable to changes in renal function

89
Q

What lab value signifies a renal dosing adjustment is needed for cephalosporins?

A

Dosage adjustments are recommended for most oral agents when the glomerular filtration rate reaches less than 30 mL/min

90
Q

How does renal impairment affect cephalosporin elimination?

A

Renal function impairment significantly affects the half-life of most cephalosporins

91
Q

Are cephalosporins safe in pregnancy?

A

Generally safe in pregnancy. Does cross placenta and small portions into breast milk.

92
Q

Are cephalosporins recommended for those who have had a type 1 (immediate, anaphylactic) reaction to any penicillin?

A

Despite this low cross-reactivity (1%), cephalosporins are still generally not recommended

93
Q

What adverse event has occurred when renal impairment is not adjusted for when administering cephalosporins?

A

Several parenteral cephalosporins have been associated with induction of seizure activity, especially in the presence of renal impairment when the dose was not adjusted

94
Q

Who are at risk for coagulation abnormalities from cephalosporin administration?

A

those with impaired renal function, cancer, impaired vitamin K synthesis, low vitamin K stores, or malnutrition.

95
Q

Is C. diff development a possible sequela of cephalosporin admin?

A

yes

96
Q

What are some clinical uses for cephalosporins?

A

Active against many respiratory pathogens, including those that cause acute otitis media, sinusitis and group A streptococcal pharyngitis, pneumonia, and chronic bronchitis
Active against most UTI pathogens

97
Q

What cephalosporin is used to treat gonorrhea?

A

Ceftriaxone (IM) is the recommended treatment for gonorrhea - resistant to others

98
Q

Staphylococcal skin infections often respond to which generation of cephalosporins?

A

first-generation cephalosporins such as cephalexin.

99
Q

What is the drug of choice for surgical prophylaxis?

A

Parenteral cefazolin

100
Q

What is the “definitive approach” to drug selection?

A

the microbial diagnosis is based on valid and reliable tests such as culture or antigen assays, and drug selection is based on laboratory and susceptibility results. The goal of susceptibility testing is to identify the most effective antibiotics.

101
Q

What is the “empirical approach” to drug selection?

A

the microbial diagnosis and drug regimen are determined with epidemiological studies. These references identify the drug with the narrowest spectrum that covers the most likely microbiological pathogens for a specific clinical diagnosis.

102
Q

What goes into the drug selection process of cephalosporin selection?

A

Selection of cephalosporins, like selection of any antimicrobial, is based on the organism that is present (in the definitive approach) or most likely present (in the empirical approach), site of infection, resistance patterns, adverse effects, pharmacokinetics, cost, and convenience

103
Q

Which generation of cephalosporins is the preferred empirical treatment for skin and tissue infections?

A

Second-generation oral cephalosporins are slightly less active against gram-positive cocci than first-generation oral cephalosporins, so the latter are the preferred empirical treatment

104
Q

What cephalosporins are effective against the most resistant strains of pneumococcus

A

Parenteral ceftriaxone and cefotaxime are used empirically in serious infections presumed to be caused by these strains.

105
Q

What is Clindamycin and does it have much utility?

A

Derivative of Lincomycin and only drug of its class
Limited indications due to potential for severe diarrhea/CDI, resistance, and better-tolerated alternatives

106
Q

MOA of Clindamycin

A

Binds to 50S subunit of bacterial ribosome; Suppresses protein synthesis

107
Q

What kind of organisms does Clindamycin affect?

A

Primarily Gram-Positive and select anaerobic organisms

108
Q

How well is Clindamycin absorbed?

A

PO: Complete absorption, not affected by gastric acid or food

109
Q

How is Clindamycin distributed?

A

Distributes to pleural/peritoneal fluids w/high conc in bile/bone
Highly protein bound

110
Q

What is Clindamycin’s presence in CSF, placenta, and breast milk?

A

Poor CSF penetration
Crosses placenta and found in breast milk

111
Q

How is Clindamycin metabolized and eliminated?

A

metabolized by the liver to active and inactive metabolites
Excreted in bile/urine(10%)

112
Q

Clinical uses of Clindamycin

A

Bacterial Vaginosis
first-line therapy to treat odontogenic infections including dental abscesses
Bacterial Endocarditis prophy as alternative for penicillin allergic pt
Drug-Resistant Penumococcal Infections

112
Q

Does Clindamycin need to have renal or hepatic dosage adjustments?

A

No dosage modification unless severe renal/hepatic impairment

113
Q

What are three known drug interactions with Clindamycin?

A

Erythromycin: Antagonist effects
Kaolin-pectin: Delays GI absorption
NMB: Severe respiratory depression

114
Q

What makes Clindamycin a treatment option in septic shock?

A

Its inhibition of protein synthesis, clindamycin can decrease toxin production in the setting of septic shock caused by Streptococcus, susceptible Staphylococcus, and Clostridium

115
Q

What is the mechanism of resistance against Clindamycin?

A

Mechanisms of resistance include mutation or modification of the ribosomal receptor site and enzymatic inactivation of clindamycin. Modification of the ribosomal receptor site also confers macrolide resistance as these two classes of antibiotics have overlapping binding sites on the 50S ribosomal subunits

116
Q

What are a few adverse reactions due to Clindamycin

A

GI-related, including nausea, vomiting, and a bitter or metallic taste. GI intolerance is dose-limiting. The most serious is the risk for CDI.

117
Q

What is an anesthesia consideration of Clindamycin?

A

If surgery or general anesthesia is planned during or within a day or so after therapy, the anesthetist or anesthesiologist must be advised because clindamycin can intensify neuromuscular blockade.

118
Q

What kind of antibiotics are fluoroquinolones?

A

synthetic, broad-spectrum antibiotics

119
Q

Fluoroquinolones are divided into two groups. What are the older fluoroquinolones?

A

ciprofloxacin [Cipro]
ofloxacin [Floxin]

120
Q

Fluoroquinolones are divided into two groups. What are the newer fluoroquinolones? What are they often referred to as?

A

(often referred to as the respiratory fluoroquinolones because of their activity against S. pneumoniae)
levofloxacin [Levaquin]
moxifloxacin [Avelox]
delafloxacin [Baxdela]

121
Q

What is the MOA of fluoroquinolones?

A

bactericidal through interference with enzymes required for the synthesis and repair of bacterial deoxyribonucleic acid (DNA)
extra info: inhibit bacterial topoisomerase II (DNA gyrase) and topoisomerase IV. Inhibition of DNA gyrase prevents the relaxation of positively supercoiled DNA that is required for normal transcription and replication

122
Q

What effect does the fluorine molecule have on fluoroquinolone activity?

A

Fluorine molecule added to create the fluoroquinolones provides increased potency against gram-negative organisms and broadens the spectrum to include gram-positive organisms as well.

123
Q

What are the two fluoroquinolones that have activity against P. Aeruginosa?

A

Only ciprofloxacin and levofloxacin

124
Q

Fluoroquinolones have notable activity against?

A

notable for their extensive gram-negative activity
Ex: E. Coli, Klebsiella, +more

125
Q

How is resistance mediated against fluoroquinolones?

A

Resistance is mediated by mutations in the quinolone-binding region of the target enzyme or by a change in the permeability of the organism. Overuse of these agents has already eroded the utility of this group of drugs.

126
Q

How well are fluoroquinolones absorbed PO?

A

All drugs in this class are well-absorbed after oral administration

127
Q

How are fluoroquinolones distributed?

A

All drugs in this class are widely distributed, with high tissue and urinary levels.
Tissue concentrations > than plasma concentrations

128
Q

Do fluoroquinolones readily cross BBB and placenta?

A

Minimal BBB crossing. All apear to cross to placenta.

129
Q

How much are fluoroquinolones metabolized?

A

Very minimal metabolism

130
Q

How are fluoroquinolones excreted?

A

Predominant route of elimination varies widely between fluoroquinolones.
Ofloxacin and levofloxacin have predominant renal excretion with minimal (less than 10%) metabolism

131
Q

At what CrCl level should fluoroquinolones be renally dosed?

A

For patients with CrCl of 50 mL/min or less, dosage adjustments are necessary for all fluoroquinolones, except for moxifloxacin

132
Q

What is the boxed warning for fluoroquinolones?

A

All fluoroquinolones have a boxed warning regarding the risk of tendon rupture and tendonitis. The risk is increased in older patients, patients taking corticosteroids, and patients immunosuppressed. An additional boxed warning has been issued to avoid all fluoroquinolones in patients with myasthenia gravis.

133
Q

What is the age recommendations for fluoroquinolones?

A

Fluoroquinolones are not recommended for children younger than 18 years.

134
Q

What are three possible adverse effects of fluoroquinolones?

A

C. Diff
Serious and occasionally fatal hypersensitivity reactions, including Stevens–Johnson syndrome and anaphylaxis
Phototoxicity has been observed with all fluoroquinolones

135
Q

Fluoroquinolones are first-line therapy in the treatment of?

A

traveler’s diarrhea and severe diarrhea not associated with antibiotic therapy.

136
Q

Which respiratory fluoroquinolones are used for community-acquired pneumonia?

A

levofloxacin and moxifloxacin

137
Q

What drug is termed an OXAZOLIDINONE?

A

Linezolid (Zyvox)
approved in the United States in 2000, is the first drug in a new class of antibiotics,
a unique class of synthetic antibiotics.

138
Q

MOA of Linezolid (Zyvox)

A

inhibitors of bacterial ribosomal protein synthesis, but unlike other antibiotics, they stop the first step in synthesis in which bacteria assemble ribosomes from their dissociated subunits.
(Linezolid does this by binding to the 50S ribosomal subunit, thus preventing the formation of a 70S initiation complex required for protein synthesis. No other known antibiotic uses this process.)

139
Q

What is Linezolid (Zyvox) active against?

A

most effective against aerobic gram-positive bacteria.
group A and B Streptococcus, S. aureus (both MSSA and MRSA.
retains activity against the most resistant forms of Enterococcus including VRE

140
Q

What is the resistance activity against Linezolid (Zyvox)

A

resistance is not widespread and considered uncommon

141
Q

What is the absorption of Linezolid (Zyvox)

A

Linezolid is rapidly and completely absorbed after oral administration

142
Q

What is the distribution of Linezolid (Zyvox)

A

only 31% protein bound and the binding is dependent on concentration. High drug concentrations are found in the skin and other well-perfused tissues. Peripheral tissue concentrations far exceed plasma concentrations

143
Q

How do Linezolid (zyvox) concentrations compare between maternal plasma and placenta?

A

Breast milk concentrations are similar to those in the maternal plasma

144
Q

What is the metabolism of Linezolid (Zyvox)

A

two inactive metabolites of linezolid created by oxidation of the morpholine ring. Because this is a nonenzymatic oxidation, this drug does not induce the CYP system

145
Q

What is the excretion of Linezolid (Zyvox)? Is renal or hepatic dosing needed?

A

Nonrenal excretion accounts for 65% of the total clearance; of the remainder, 30% is excreted unchanged in urine. No dosage adjustments are required for impaired hepatic or renal function

146
Q

When is Linezolid (Zyvox) contraindicated?

A

Concomitant use or use within 2 weeks of a monoamine oxidase inhibitor (MAOI) with linezolid is contraindicated.
Serotonin syndrome or hypertension

147
Q

What are the recommendations for children using Linezolid (Zyvox)?

A

Linezolid is approved for use in children from birth. Preterm infants and neonates require reduced dosing because of slower clearance.

148
Q

What is a unique precaution clinicians need to be aware of before prescribing Linezolid (Zyvox) ?

A

Bone marrow activity suppression AKA Myelosuppression (anemia, leukopenia, pancytopenia, and thrombocytopenia) has been reported in patients receiving linezolid

149
Q

What kind of food must be avoided when receiving Linezolid (Zyvox)?

A

Because significantly elevated blood pressure may occur if taken with tyramine-rich foods, the amount of tyramine consumed at any one meal should be limited (less than 100 mg/meal).

150
Q

The most common adverse effect of Linezolid (Zyvox)?

A

most common adverse reactions reported were diarrhea, headache, and nausea.
C diff.

151
Q

What drug interactions does Linezolid (Zyvox) have?

A

Because linezolid is a reversible, nonselective inhibitor of monoamine oxidase, it also has potential interactions with serotonergics such as selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants, ondansetron, meperidine, buspirone, methadone, and tramadol
Watch for s/s of serotonin syndrome

152
Q

Clinical use of Linezolid (Zyvox)?

A

Shown to have greater clinical cure rates for MRSA pneumonia compared with vancomycin.
one of only several agents that are first line for treating VRE infections

153
Q

Drug Selection Rationale for Linezolid (Zyvox)?

A

Linezolid’s use should be reserved for moderate to severe infections in which alternative antibiotics are less desirable secondary to efficacy, resistance, safety, route, or $$cost.

154
Q

Why has the use of sulfonamides decreased?

A

Use of sulfonamides has decreased due to resistance and the incidence of allergic reactions to sulfa drugs.

155
Q

What are two sulfonamide topical agents used to prevent infection in patients with burns?

A

Mafenide (Sulfamylon) and silver sulfadiazine (Silvadene)

156
Q

MOA of Sulfonamides

A

Competitive inhibition synthesis enzymes. Inhibition of this pathway prevents folic acid synthesis, which is required by susceptible organisms for the production of purines and nucleic acids.
If a bacteria doesn’t require folic acid, sulfa is ineffective.

157
Q

Activity of Sulfonamides

A

inhibit both gram-positive and gram-negative bacteria.
Protazoa - Toxoplasma gondii

158
Q

Resistance to sulfonamides is mediated by?

A

Mutations that result in excessive production of PABA cause organisms to develop resistance.

159
Q

MOA of Trimethoprim

A

inhibits bacterial dihydrofolic acid reductase. Dihydrofolic acid reductases convert dihydrofolic acid to tetrahydrofolic acid, a stage leading to the synthesis of purines and ultimately to DNA

160
Q

What happens when a Sulfonamide and Trimethoprim are giving together?

A

results in synergistic activity of both drugs

161
Q

Activity of Trimethoprim

A

active against both gram-positive and gram-negative organisms

162
Q

Resistance of Trimethoprim

A

results from reduced cell permeability, overproduction of dihydrofolate reductase, or production of an altered reductase with less drug-binding ability
most common cause is plasmid-encoded resistant reductases

163
Q

Nitrofurantoin use is limited to? Is it a sulfonamide?

A

UTIs, Not a sulfonamide

164
Q

MOA of Nitrofurantoin

A

Ultimately, protein synthesis, aerobic energy metabolism, DNA and RNA synthesis, and cell wall synthesis are inhibited

165
Q

Activity of Nitrofurantoin

A

Active against most gram-positive cocci and gram-negative bacilli that cause UTIs
Many bacteria including E.Coli

166
Q

Resisitance of Nitrofurantoin

A

Resistant mutants are rare

167
Q

What is Fosfomycin and is it a sulfonamide?

A

a bactericidal antibiotic available in the United States only as an oral formulation for the treatment of UTIs
Not a sulfanamide

168
Q

MOA of Fosfomycin

A

ultimately leads to inhibition of cell wall synthesis. beneficial in the treatment of UTIs because it reduces adherence of bacteria to the epithelial cells in the urinary tract.

169
Q

Activity of Fosfomycin

A

activity against most urinary pathogens

170
Q

Resistance of Fosfomycin

A

uncommon but has been reported. The bacterial mechanisms of resistance most commonly described are enzymatic modification of fosfomycin.

171
Q

Absorption of Sulfonamides

A

Oral sulfonamides are absorbed readily from the GI tract.

172
Q

Distribution of Sulfonamides

A

They are distributed widely throughout the body and found in all body tissues. They readily enter the CSF, pleura, synovial fluids, and the eye. They cross the placenta and enter breast milk.

173
Q

Absorption of Trimethoprim

A

well-absorbed following oral administration. .

174
Q

Distribution of Trimethoprim

A

It is widely distributed in body tissues, including prostatic tissues, and crosses the placenta. Distribution into breast milk occurs with high concentrations.

175
Q

Absorption of Nitrofurantoin

A

readily absorbed via oral administration.

176
Q

Absorption of Fosfomycin

A

oral bioavailability of 34% to 58%

177
Q

Distribution of Fosfomycin

A

Very little drug is protein-bound. Fosfomycin distributes into the kidneys, bladder wall, prostate, and CSF fluid if the meninges are inflamed.

178
Q

Metabolism of Sulfinamide

A

Metabolism in the liver by conjugation and acetylation to inactive metabolites

179
Q

Excretion of Sulfinamide

A

Renal excretion is mainly by glomerular filtration

180
Q

Metabolism of Nitrofurantoin

A

Approximately 50% to 70% is rapidly metabolized by body tissues to inactive metabolites.

181
Q

Excretion of Nitrofurantoin

A

Renal excretion is via glomerular filtration and tubular secretion. Needs renal dosing for CrCl <30

182
Q

Excretion of Fosfomycin

A

eliminated as unchanged drug primarily through renal excretion (up to 60% of an oral dose) and in feces (18%)

183
Q

What abx should be used with caution for patients with folate deficiency.

A

Trimethoprim

184
Q

What electrolyte should be monitored when using Trimethoprim

A

Potassium. risk for hyperkalemia

185
Q

What are tetracyclines?

A

broad-spectrum antibiotics that are used extensively throughout the world.

186
Q

What drugs are in the tetracycline group

A

tetracycline, demeclocycline, doxycycline (Doxy, Doxychel, Vibramycin), and minocycline (Minocin)

187
Q

which tetracycline is used primarily for syndrome of inappropriate antidiuretic hormone.

A

Demeclocycline

188
Q

MOA of tetracyclines

A

inhibit protein synthesis by reversibly binding to the 30S subunit of the bacterial ribosome and preventing the addition of amino acids to growing peptides.

189
Q

Activity of tetracyclines

A

good activity against gram-positive organisms, activity against some gram-negative bacteria

190
Q

mechanism of resistance to tetracyclines

A

The mechanisms of resistance to tetracyclines are (1) decreased intracellular accumulation due to impaired influx or increased efflux of an active transport protein pump, (2) ribosome protection by proteins that interfere with drug binding, and (3) enzymatic inactivation. Resistance to tetracycline generally predicts resistance to the entire class

191
Q

Absorption of tetracyclines

A

adequately. The percentage of oral dose absorbed is highest for doxycycline and minocycline (95% to 100%) and intermediate for tetracycline (60% to 70%)

192
Q

Distribution of tetracyclines

A

Doxycycline and minocycline are highly lipid soluble. found in tissues

193
Q

Which tetracycline needs to be renally dosed? Which does not?

A

Tetracycline needs renal dosing. doxycycline and minocycline do not significantly accumulate or require dosage reductions for renal impairment.

194
Q

Metabolism of tetracyclines

A

liver metabolism

195
Q

Excretion of tetracyclines

A

Tetracyclines are eliminated by the kidney via glomerular filtration and undergo enterohepatic recirculation with excretion in the bile and feces

196
Q

Can tetracyclines be used during pregnancy and breastfeeding?

A

Doxycycline and other tetracyclines should not be used in pregnancy.
Short term breastfeeding ok

197
Q

Can children use tetracyclines

A

Children younger than 8 years generally should not use tetracyclines. These drugs form a stable calcium complex in any bone-forming tissue, decreasing bone growth.

198
Q

Besides GI upset, what adverse reactions are related tot tetracycline use

A

GI Symptoms including C. Diff
Pseudotumor cerebri (benign intracranial hypertension) has also been associated with tetracyclines. Symptoms are headache and blurred vision
Photosensivity, SJS

199
Q

What drug interactions do tetracyclines have?

A

Mainly with elements.
with divalent and trivalent cations that are found in antacids, iron salts, sevelamer, magnesium-containing laxatives, and zinc supplements.

200
Q

Clinical use of tetracylines

A

STIs, Acne, H. Pylori

201
Q

Doxycycline is the primary drug choice for which conditions/infections

A

ehrlichiosis and rickettsial infections (e.g., Rocky Mountain spotted fever, typhus, Q fever, and trench fever caused by B. quintana)

202
Q

What drug level should be closely monitored when taking a tetracycline

A

digoxin

203
Q

What is the primary glycopeptide

A

Vancomycin

204
Q

When are glycopeptide abx’s used?

A

group of antibiotics is used for gram-positive infections that are resistant to first-line antibiotics.

205
Q

MOA of vancomycin

A

inhibits cell wall synthesis by binding firmly to a portion of peptidoglycan synthesis enzymes.
result is a weakened cell wall susceptible to lysis

206
Q

Activity of Vanco

A

bactericidal for gram-positive organisms

207
Q

Resistance to Vanco

A

Resistance is due to a modification of the binding site of the peptidoglycan building block

208
Q

Absorption of vanco

A

Poor PO absorption.
Oral bioavailability is approximately 1%

209
Q

When vanco is given IV, how quickly is onset? What influences the duration?

A

When administered intravenously, onset of action is rapid, with peak concentrations in 1 hour and a duration of effect that is highly variable and directly correlated to renal clearance

210
Q

Distribution of Vanco

A

It is 52% to 56% protein bound. Distribution is wide, with 20% to 30% penetration of the CSF. The drug crosses the placenta.

211
Q

Excretion of Vanco

A

Because minimal oral absorption occurs, most oral doses of vancomycin are excreted in feces. Intravenously administered vancomycin is eliminated renally, with more than 90% via glomerular filtration

212
Q

Precautions using vanco

A

nephrotoxic and should be used with caution in patients with impaired renal function or patients receiving other nephrotoxic agents

213
Q

What is Vancomycin Infusion Syndrome

A

includes potentially severe hypotension, and red man syndrome, has been associated with rapid intravenous administration of vancomycin

214
Q

When can vancomycin be used in pregnancy

A

Oral vancomycin is generally considered safe in pregnancy, whereas the IV form should only be used if the benefits outweigh the risk.

215
Q

What drug, when administered with Vanco, leads to a three-fold higher risk of AKI

A

Pip/Taz aka Zosyn

216
Q

Clinical use of Vanco

A

Oral vancomycin is used to treat CDI
IV dosing of vancomycin is complex and extremely patient specific.

Advanced Pharm (50 decks)

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