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Term 4: Infectious Diseases > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

What is the structure of penicillin?

A
  1. Thiazolidine ring
  2. B-lactam ring
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2
Q

What is the mechanism of action of B-lactams?

A
  • interact with enzymes localized in cell membrane whose action is to build the cell wall
  • prevents peptidoglycan synthesis (Gm +)
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3
Q

What is the dose of antibiotics limited by?

A

Toxicity

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4
Q

What is the minimum inhibitory concentration (MIC) of an antibiotic?

A

the lowest concentration of antibiotic that, under certain in vitro test conditions, inhibits further bacterial growth

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5
Q

What is the minimum bactericidal concentration (MBC) of an antibiotic?

A

lowest concentration that kills bacteria

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6
Q

In which diseases is the bactericidal effect thought to be important (relative to bacteriostatic effect)?

A
  • endocarditis (only bacterial infection for which bacterial effect is absolutely necessary for a cure)
  • meningitis or osteomylitis
  • neutropenia
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7
Q

What is Penicillin G?

A
  • benzyl penicillin
  • first form of penicillin used in humans
  • aqueous
  • most destroyed by gastric acid, so given IV
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8
Q

What is penicillin V?

A
  • add a phenoxy group to side chain of penicillin G
  • can be given orally b/c it resists acid
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9
Q

What does probenecid do?

A
  • delays excretion of penicillin at renal tubules
  • Musher has never used it, doesn’t think its necessary
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10
Q

Where does penicillin go in the body (distribution)?

A

-distributes to EFC (22% of lean body weight)

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11
Q

How rapidly is penicillin excreted (clearance)?

A

T1/2 = 20 minutes

-excreted via kidney

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12
Q

By percentage of body weight, how much ECF do we have?

A

22% (15 liters)

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13
Q

Why does penicillin only distribute to ECF?

A
  • cell membranes exclude it
  • polar molecule
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14
Q

What conditions are associated with greatly increased ECF?

A
  • Heart failure
  • cirrhosis w/ ascites
  • renal failure *doses of abx need to be adjusted to reflect this
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15
Q

How is penicillin excreted?

A

100% Kidney

*keep creatinine clearance and kidney failure in mind

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16
Q

Why is the peak concentration of penicillin much lower than expected?

A
  • half life of 20 minutes
  • infusion takes 20-30 minutes
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17
Q

How should penicillin be administered? Why?

A
  • IV at close intervals, usually 4hrs
  • Keeps concentration above MIC about 2/3 of the time
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18
Q

if you double the dose of IV penicillin, you only add ___________ of coverage

A

20 min (= one half-life)

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19
Q

So, if you want to increase the concentration of penicillin, how do you do it?

A
  • shorten the dosing interval
  • doubling dose will only add 20 min of coverage
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20
Q

How is nafcillin excreted?

A

-Kidney AND liver

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21
Q

What are the pharmakinetic advantages and disadvantages of amoxicillin over penicillin?

A
  • lower peak concentration
  • level above MIC may be more sustained because drug is being absorbed in GI tract as its being excreted
  • nearly 100% is absorbed in GI tract
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22
Q

What are procaine and benzathine penicillin designed for?

A

-slow absorption from injection site

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23
Q

What are the three factors that determine the outcome of treatment with antibiotics?

A

1) time that tissue levels exceed MIC
2) peak level of concentration (sometimes binding is irreversible above certain concentration)
3) area under the curve above MIC. (ex. both duration and height of level of quinolones)

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24
Q

Beta-lactams. Must exceed MIC for ______ of treatment period.

A

>60%

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25
Q

Antibiotic resistance may arise by __________ or by acquisition of ___________.

A
  • point mutation
  • genetic material
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26
Q

What are the general mechanisms of bacterial resistance to antibiotics?

A

1) make an enzyme that disrupts Abx at active site.
2) alter site at which abx act
3) generate new pathway that bypasses the one blocked by abx (MRSA)
4) alter entrance of antibiotic into bacterium (porins)
5) increase rate with which abx is pumped out of the bacterium

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27
Q

Resistance of pneumococci to beta-lactam antibiotics is of concern in ______________, not in pneumonia, sinusitis or otitis media

A

meningitis (antibiotic passage across blood-brain barrier)

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28
Q

What are bacterial porins?

A
  1. Porins are protein channels of outer membrane
  2. Transport polar molecules into periplasmic space; from there, diffuse through cell wall into cytoplasm
  3. Mechanism only for gram negative rods; Gram positive bacteria do not have them
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29
Q

Which -cillins are resistant to B-lactamase?

A
  • Methicillin
  • Nafcillin
  • oxacillin
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30
Q

What drug is usually used against methicillin-susceptible S. aureus?

A

Nafcillin

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31
Q

Which drugs is MRSA resistant to?

A
  • all penicilins
  • cephalosporins (except ceftaroline)
  • carbapenems
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32
Q

What is the half life of Amoxicillin?

A

45-60 minutes

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33
Q

What types of organisms is ampicillin good against?

A

Gm (-) organisms

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34
Q

What is piperacillin used against?

A
  • Gm (-) rods
  • pseudomonas

**widely used in TMC, especially with B-lactamase inhibitor (tazobactam)

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35
Q

What are the B-lactamase inhibitors?

A
  • clavulanic acid
  • sulbactam
  • tazobactam
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36
Q

What is Augmentin made of?

A

-Amoxicillin + Clavulanic acid (b-lactamase blocker)

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37
Q

Can Augmentin be used against MRSA?

A

no

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38
Q

What is Unasyn?

A

-Ampicillin + sulbactam

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39
Q

What is Zosyn?

A

Piperacililn + tazobactam

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40
Q

What are the adverse effects of penicillin?

A
  • skin rash (10%)
  • anaphylaxis (0.01%)
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41
Q

What is the structure of cephalospornis?

A
  • four membered ring attached to a six membered ring
  • side chain on four-membered ring
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42
Q

What are the first generation cephalosporins?

A
  • Cefazolin
  • Cephalexin (oral cefazolin)
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43
Q

What is Cefazolin used against?

A
  • non-MRSA Staph aureus
  • Group A strep, & other soft tissue infections
  • Gm (-) rods

**no effect against enterococcus

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44
Q

What is antibiotic prophylaxis for surgery?

A

-give abx before surgery so that it is in the tissues at the time of surgery

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45
Q

What is cephalexin?

A

-oral version of cefazolin

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46
Q

What are the third generation of cephalosporins?

A
  • cefotaxime (Claforan)
  • ceftriaxone (Rocephin)
  • cefpodoxime (Vantin) = oral
  • ceftazidime (pseudo)
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47
Q

What are third generation cephalosporins effective against?

A
  • Strep
  • pneumo
  • Haemophilus
  • Moraxella
  • Gonococci
  • Lyme disease
  • Gram negative rods (except Pseudomonas)
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48
Q

What is the half life of Ceftriaxone?

A

6-8 hours

*can be given every 24 hours

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49
Q

What cephalosporins are good against pseudomonas?

A
  • Ceftazidime (3G)
  • Cefepime (4G)
  • ceftaroline (5G) (MRSA)
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50
Q

Does penicillin cross the blood brain barrier?

A

Not very well

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51
Q

Inflammation decreases the rate at which the choroid plexus pump removes _________ from CSF, so, during meningitis, antibiotic levels persist whereas in the absence of meningitis they are rapidly cleared.

A

antibiotics

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52
Q

Does ceftriaxone cross the blood-brain barrier?

A
  • yes
  • good for meningitis
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53
Q

What is Cefpodoxime?

A

-Oral 3rd generation cephalosporin

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54
Q

What are the fourth generation cephalosporins?

A

-cefepime

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55
Q

When is cefepime used?

A

-like ceftriaxone, but with a good effect against pseudomonas

*really only used for pseudomonas

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56
Q

What is ceftaroline?

A
  • “fifth generation” cephalosporin
  • has all properties of cefepime, but ALSO active against MRSA
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57
Q

What are ESBL bacteria?

A
  • extended spectrum beta lactamase
  • resistant to all beta-lactamases (penicillins & cephalosporins)

*big problem

58
Q

Many cephalosporins have capacity to induce bacterial production of _____________.

A

cephalosporinases

59
Q

What are the side effects and drug reactions of cephalosporins?

A
  • most common is skin rash
  • drug fever is #2
  • don’t give ceph if pt has had life threatening rxn to penicillin)
60
Q

Which penicillins are good against pseudomonas?

A
  • piperacillin
  • ticarcillin
61
Q

How do we treat syphilis?

A

benzathine penicillin

62
Q

How do we know which antibiotics are carbapenems?

A

-they all end in penem

63
Q

What is Primaxin?

A

-Compination of imipenem and cilastatin

64
Q

How do carbapenems work?

A

-bind all known penicillin binding proteins EXCEPT PBP2a (MRSA)

65
Q

Are carbapenems effective against bacteria with beta-lactamases?

A

-yes

*carbapenemases have appeared though

66
Q

Are carbapenems effective against E. faecalis?

A

Yes

67
Q

Are carbapenems effective against MRSA?

A

No

68
Q

Are carbapenems effective against pseudomonas?

A

yes

69
Q

What is Aztreonam useful against?

A
  • Pseudomonas
  • NOT enterococcus
70
Q

What element do aminoglycosides require?

A

oxygen

71
Q

How do aminoglycosides work?

A

Irreversibly bind to 30s ribosomal subunit at interface of 30s and 50s subunits

72
Q

What is an example of synergism involving aminoglycosides?

A
  • Aminoglycosides + B-lactams
  • B-lactam alters cell wall, allows high concentrations of aminoglycoside to enter cell
  • fights Enterococcus and other Gm (+) bacteria
73
Q

What class of abx is streptomycin?

A

Aminoglycoside

74
Q

What was streptomycin first developed as?

A

an antituberculosis agent

75
Q

What kind of bacteria is streptomycin good against?

A

Gm (-) rods

*limited by rapid selection to resistance

76
Q

What are the adverse effects of all aminoglycosides?

A
  • Nephrotoxicity
  • CN 8 damage

***dosage must be reduced in renal insufficiency

77
Q

What organ clears aminoglycosides?

A

Kidneys

78
Q

What bugs is gentamicin good against?

A
  • nearly all communit Gm (-) rods and most nosocomial
  • pseudomonas
79
Q

What is a good initial therapy for serious UTI?

A

Gentamicin

80
Q

What class of drug is gentamicin?

A

Aminoglycoside

81
Q

Why is it ok if aminoglycoside levels are not above the MIC for the majority of time?

A
  • irreverisbly binds ribosome
  • bacteriocidial capability depends on peak concentration, NOT time above MIC
82
Q

What class of drug is Amikacin?

A

Aminoglycoside

83
Q

What is Amikacin used for?

A

-nosocomial or comm acquired Gm (-) infection

84
Q

When are aminoglycosides used?

A

-againsed Gm (-) rod infections but generally only if not susceptible to other drugs (fear of toxicity)

85
Q

Vancomycin resistant bacteria have gene ______ which encodes formation of terminal ________ instead of D-ala; thus vancomcyin does not bind.

A
  • VanA
  • lactate
86
Q

What is vancomycin good against?

A
  • MRSA
  • NOT better than penicillins in staph infection s that are methicillin susceptible
  • works on pretty much everything except VRE
87
Q

Why do we need to measure Vancomycin levels when giving to patients?

A
  • It distributes to fat as well
  • need to base dosage on TOTAL body mass, not just lean mass
88
Q

What drug is added to vancomycin for synergy against Staph aureus?

A

gentamicin

89
Q

Do not use vancomycin for “empiric” therapy unless:

A
  • infection is serious AND
  • there is good reason to believe that it is due to an organism that will be resistant to other Abx
90
Q

(T/F) Every pneumococcus is susceptible to vancomycin.

A

True

*but still give ceftriaxone b/c vanc can’t cross BBB as well

91
Q

What is Panton-Valentine Toxin?

A
  • seen in CA-MRSA
  • causes necrotic lesions of skin and mucos

**produced from genetic material of a bacteriophage

92
Q

PNEUMOLYSIN

A
  • know that all pneumococci produce it
  • if we block its production, pneumococci are no longer virulent
  • animal studies show cure to pneumococcal disease if they have antibody to it
  • inhibits PMN function
93
Q

What toxicities do we watch for with Polymyxins?

A

-Nephro and neurotoxic

94
Q

What are Polymyxins good against?

A

Gm (-) rods, especially ones that are resistant to other abx

95
Q

What drugs are Polymyxins?

A
  • Polymyxin
  • colistin
96
Q

What drugs are the advanced macrolides?

A
  • clarithromycin (Biaxin)
  • azithromycin (Zithromax/Z-pack)
97
Q

Macrolides are ________for Staph aureus. __________for pneumococcus, Haemophilus

A
  • bacteriostatic
  • Bactericidal
98
Q

How do macrolides prevent biofilm production by pseudomonas?

A

-block alginate

99
Q

Why are macrolides used in CF patients?

A

-it prevents biofilm production by pseudomonas

100
Q

What are the two clinically important forms of resistance to macrolides?

A
  • efflux pump (mef gene)
  • Erythromycin ribosome methylation, alters attachment site (erm gene)
101
Q

What is azithromycin useful against?

A
  • Haemophilus
  • Moraxella
  • N. gonorrhoeae
  • Legionella
  • Mycoplasma
  • Chlamydia
  • Mycobacterium avium-intracellulare (MAC)
102
Q

Why are macrolides good against intracellular pathogens?

A

-they are taken up by macrophages

103
Q

What are the adverse effects of Macrolides?

A
  • nausea
  • vomiting
  • prolonged Q-T interval
  • sudden death (VERY rare)
104
Q

What class of drug is Clindamycin?

A

-lincosamide

105
Q

What is clyindamycin effective against?

A
  • Gm (+) bacteria
  • Most CA-MRSA
  • most anaerobic bacteria
106
Q

In which clinical scenarios is clindamycin useful?

A
  • Intraabdominal infection
  • aspiration pneumonia
  • w/ penicillin in Streptococcal gangrene (necrotizing fasciitis (group A))
107
Q

What drug is most likely to cause C. diff colitis?

A

Clindamycin

108
Q

What is the black box warning on Ketolides for?

A

Liver failure

109
Q

What is linezolid effective against?

A
  • Gm (+) organisms
  • S. aureus & MRSA
  • Coag (-) staph
  • pneumococci
  • enterococci

**expensive

110
Q

What are the adverse effects of linezolid?

A

-bone marrow suppression, especially platelets

111
Q

What drug is used for N. meningitis prophylaxis of nasal carriage in an outbreak situation?

A

Rifampin

112
Q

Why can’t rifampin be used as a single drug?

A

rapid emergence of resistance

113
Q

What is Rifabutin used for?

A

Mycobacterium avium/intracellular (MAC)

114
Q

When is rifampin used?

A
  • TB
  • Meningococci prophylaxis
  • Difficult staph associated with foreign body (prosthetics)
  • Coating of impregnating implantable devices
115
Q

What are the adverse effects of rifampin?

A
  • turns urine and tears orange
  • Stains soft contact lenses
116
Q

What are the tetracyclines?

A
  • doxycycline
  • minocycline
117
Q

What are tetracyclines effective against?

A
  • pneumococci
  • Haemophilus & moraxella
  • Staph aureus including MRSA
  • Legionella, mycoplasma, chlamydia
  • brucella
  • Rickettsiae, ehrlichia, anaplasma
118
Q

What is Septra/Bactrim?

A

-combination of sulfamethoxazole plus trimethoprim

119
Q

How does sulfamethoxazole work?

A

-inhibits synthesis of tetrahydrofolic acid (needed for synthesis of thymidine)

120
Q

What bugs are sulfa drugs and trimethoprim effective against?

A
  • S. aureus soft tissue infections (including MRSA)
  • Group A strep in vitro, poor in vivo though (strep break down human tissue to get thymidine)
121
Q

What are the recommended clinical uses for sulfa/trimethoprim?

A
  • uncomplicated UTI
  • pneumonia caused by Pneumocystis jiroveci
  • Nocardosis
122
Q

What are the adverse effects of sulfa/trimethoprim?

A
  • Stevens Johnson syndrome (idiosyncratic)
  • Renal insufficiency (dose-related)
123
Q

How are quinolones given?

A

-orally, they are well absorbed

*except in surgical pt’s who cannot swallow

124
Q

What bugs are quinolones good against?

A
  • Gram (-) rods
  • good against biofilms
125
Q

What clinical scenarios are quinolones used?

A
  • UTI
  • CA-intraabdominal infection
  • biofilm
  • Atypical pneumonia
126
Q

What antibiotic is causing problems because farmers are adding it to animal feed?

A

quinolones

127
Q

What’s a super awesome treatment against biofilm formation?

A

-combination of quinolone with rifampin

128
Q

What are the adverse effects of quinolones?

A
  • prolonged Q-T interval (be careful in conjunction w/ Ca channel blockers)
  • Tendonitis & achilles rupture
  • Drug-drug interaction; increased risk of bleeding in pt’s on warfarin (vitamin K)

**prophylaxis in pt’s w/ prolonged neutropenia or cirrhosis, ascites, and prior spont. bacterial peritonitis

129
Q

What drug is in the class of Lipopeptides?

A

Daptomycin

130
Q

What class of drug is Daptomycin?

A

Lipopeptide

131
Q

What class of drug is Daptomycin?

A

Lipopeptide

132
Q

Why can’t we use daptomycin to treat pneumonia?

A

-it is inactivated by surfactant

133
Q

What is Daptomycin good against?

A

-S. aureus and MRSA

134
Q

What are the adverse effects of Daptomycin?

A
  • muscle pain
  • elevation of enzymes indicating muscle damage (Cr. phosphokinase)
135
Q

What class of antibiotics ends in “-vancin”?

A

Lipoglycopeptides

136
Q

What is the mechanism of action of Lipoglycopeptides?

A

1) block peptidoglycan synthesis (same as vanc)
2) alter cell membrane (dame as daptomycin)

137
Q

What is metronidazole good against?

A
  • intraabdominal infections
  • Trichomonas vaginalis
138
Q

What are the adverse effects of metronidazole?

A
  • relatively nontoxic
  • causes a bad taste in the mouth
139
Q

What is fidaxomycin used to treat?

A
  • C. diff ONLY
  • better than vanc (lower rate of relapse)
140
Q

What are the two topical antibiotics?

A
  • Bacitracin
  • Mupurocin

Term 4: Infectious Diseases (21 decks)

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