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PHAR 152* > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

How do Penicillins work?

A

They bind to PBP resulting in the inhibition of PG synthesis and activation of autolytic enzymes in the cell wall
They break down the wall and prevent wall repair
Bactericidal

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2
Q

How do bacteria become resistant to penicillins?

A

Production of beta-lactamases - destroy the drug
Lack of PBPs or altered PBPs - no target for drug
Efflux of drug out of cell - pump the drug out
Failure to synthesize PG such mycoplasmas or metabolically inactive bacteria - org not growing or maintaining cell walls

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3
Q

What is the structure that penicillins share?

A

6-aminopenicillanic acid (thiazolidine ring attached to a beta-lactam ring)
bonds need to be intact for AB to work

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4
Q

What is penicillin G most active against?

A

gram positive bacteria and spirochetes
ex) syphilis

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5
Q

What can penicillin G be destroyed by?

A

Beta-lactamases and stomach acids

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6
Q

Which Pen Gs are special? How?

A

Procaine and benzathine Pen G
They are both salts and administered Intramuscularly only
The salt prolongs their activity
If given thru IV, then you will kill the pt due to toxicity

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7
Q

What is Pen V? What is special about it?

A

It is an oral formulation
It is more acid stable but needs to be taken on an empty stomach

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8
Q

What are some groups/families that pen is good for?

A

streptococci, pneumococci, meningococci, spirochetes, clostridia, anaerobic +ve rods, actinomyces
enterococci

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9
Q

Explain Methicillin and its members

A

Isoxazolyl peniciliins “anti staph”
Designed for Staph aureus
Relative resistance to beta-lactamases
less gram +ve activity otherwise
IV and oral forms
Staphylococcal

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10
Q

What is MRSA

A

Methicillin resistant staph aureus (resistant to the whole class + penicillins too)
A lab marker

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11
Q

What is MSSA?

A

Methicillin susceptible staph aureus

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12
Q

Which antibiotic of the methicillin class is made in Canada?

A

Cloxacillin is from Canada

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13
Q

What types of organisms are aminopenicillins active/effective against?

A

gram positive and gram negative organisms (more broad than prev two)

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14
Q

What is a resistance strategy of orgs against aminopenicillins

A

Destroyed by beta-lactamases

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15
Q

What are the two main aminopenicillins?

A

ampicillin and amoxicillin

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16
Q

What is the difference between ampicillin and amoxicillin?

A

Ampicillin - used IV, more stable than natural pens but they have poor bioavailability (F)

amoxicillin - used orally, but they have better abs. than ampicillin, they are available combined with clavulanic acid (b-lactamase inhibitor)

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17
Q

Name some organisms that aminopenicillins works well against

A

Streptococci, enterococci, Neisseria sp., non-b-lactamase prod H. influenzae, E.coli, P mirabilis , Salmonella, etc

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18
Q

How do beta-lactamases work against penicillins and cephalosporins?

A

They open up the beta-lactam ring and render the AB no longer active

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19
Q

What does classification of beta-lactamases depend on?

A

genetics, biochemical properties and substrate affinity for a beta-lactamase inhibitor

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20
Q

What are ESBLs?

A

Extended-spectrum beta-lactamases found in e.coli and klebsiella pneumoniae
can deactivate lots of beta-lactams

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21
Q

What are NDM-like organisms? Provide an example

A

New Delhi metallo-beta-lactamase. Liinked to metals

Acinetobacter baumannii
(human pathogen)

MAY NEED TO UPDATE THIS CARD

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22
Q

What is the activity profile of ureidopenicillins?

A

Increased activity against gram negative rods
Also active against PSEUDOMONAS AERUGINOSA - The v. pathogenic gram -ve rod that not alot of ABs effective against

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23
Q

What is an example of a ureidopenicillin?

A

piperacillin

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24
Q

What is so special about piperacillin?

A

It is active against the pathogenic Pseudomonas aeruginosa

Parenteral administration only - IV only

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25
Q

What are ureidopenicillins combined with? Provide an example

A

Combined with a beta-lactamase inhibitor such as tazobactam (no activity against bacteria)

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26
Q

Discuss the pharmacokinetics of penicillins

A

oral bioavailability (F) varies
wide tissue distribution including CNS
Most are excreted by the kidney (if there are kidney probs, then adj the dose)

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27
Q

What is the only penicillin that can be taken with food?

A

Amoxicillin

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28
Q

What are some pharmacokinetic properties of penicillins?

A

Generally short half-lives, so there needs to be frequent dosing
They have concentration-independent pharmacodynamics

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29
Q

What are concentration independent pharmacodynamics? How about dependent ones?

A

They are effective above a certain threshold, so we want to maintain the drug above this level. For penicillins we want to maintain this level thru continuous IV drip infusion

Dependent means that the higher the concentration, the better the killing action or effectiveness. They need the highest dose possible, no maintenance really

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30
Q

Are penicillins safe in pregnancy? How about during breastfeeding? How about with oral contraceptives?

A

Safe in pregnancies
Distributed in breast milk, so may affect baby’s microflora
There is a drug interaction with oral contraceptive -> destruction of estrogen, no entero recirculation

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31
Q

What are the adverse effects of penicillins?

A

Allergic rxns - many ppl report allergies, most aren’t real ones tho
Anaphylactic shock
Serum sickness -> fever and joint stiffness
Rashes
Fever, nephritis (nephron inflammation), eosinophilia
Seizures, encephalopathy delirium
electrolyte imbalances
neutropenia, thrombocytopenia in longer courses of therapy
Diarrhea, GI upset = these are the most common side effects

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32
Q

What is the main structure of cephalosporins?

A

7-aminocephalosporanic acid

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33
Q

What is a structural difference in cephamycins?

A

There is an oxygen in place of the sulfur in the ring
ppl say that this isn’t a true cephalosporin

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34
Q

What is the mechanism of action for cephalosporins?

A

Same as penicillin, so they bind to PBP’s disrupt the cell wall, PG inhibition
They are also bactericidal

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35
Q

What are some of the resistance strategies employed by bacteria against cephalosporins?

A

Lack of PBP or altered PBP with reduced affinity
Production of beta-lactamases (produced by staph aureus and gram negative bacilli)
Efflux - pumping out the AB
Inability of the drug to penetrate

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36
Q

What are examples of first generation cephalosporins? How is the first gen ceph cefazolin administered?

A

oral - cephalexin (common) and cefadroxil
Cefazolin - IV/IM

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37
Q

What are first gen cephalosporins effective against?

A

Active against gram positive cocci (but not enterococci or MRSA) and some gram negative bacilli such as E. coli, proteus and klebsiella

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38
Q

What are the exceptions for gram positive cocci bacteria that are not affected by first generation cephalosporins?

A

enterococci or MRSA

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39
Q

True of false 1st gen cephs penetrate the CNS

A

They don’t penetrate the CNS

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40
Q

What is the only drug of choice in the 1st gen gen cephs for surgical prophylaxis?

A

Cefazolin

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41
Q

What are the second generation oral cephalosporins?

A

Cefuroxime axetil, cefprozil (cefaclor)

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42
Q

What is an IV/IM second generation cephalosporin?

A

Cefuroxime

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43
Q

What is the second generation cephalosporin cephamycin?

A

cefoxitin, it has good anaerobic coverage

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44
Q

What is the coverage of second generation cephalosporins?

A

Active against the same orgs from the first gen cephs
There is a greater coverage of gram negative bacteria, but it DOES NOT cover Pseudomonas aeruginosa

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45
Q

When are cephamycins used? Provide an example

A

in mixed aerobic and anerobic infections

In the gut or diabetic foot infxn - there are lots of aerobic and non-aerobic species here

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46
Q

How are third generation cephalosporins administered?

A

IV or IM injections

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47
Q

What are examples of third generation cephalosporins? Which one is an oral agent? Which one do we reserve for Ps. aeruginosa?

A

Cefotaxime, ceftriaxone, ceftazidime, cefixime

Ceftazidime for aeruginosa
Cefixime is the oral agent

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48
Q

What is the spectrum for third generation cephalosporins?

A

The feature enhanced activity against gram negative bacilli
Decreased activity against gram-positive cocci extra strep pneumoniae

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49
Q

Which third generation cephalosporin has the ability to penetrate the CNS?

A

All of them

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50
Q

What are the three main fourth generation cephalosporins?

A

Cefepime, Ceftaroline and ceftobiprole

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51
Q

What is the activity of cefepime?

A

Enhanced activity against Enterobacter and Citrobacter
Active against Ps. aeruginosa

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52
Q

What is so special about ceftaroline and ceftobiprole?

A

they are broad spectrum and have activity against MRSA, ampicillin sensitive E. faecalis and penicillin resistant S. pneumoniae

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53
Q

What are the adverse effects of cephalosporins?

A

Hypersensitivity
Diarrhea
Skin rash
Other - fever, granulocytopenia, hemolytic anemia
Biliary pseudolithiasis for ceftriaxone

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54
Q

What is biliary pseudolithiasis and what AB is responsible for this condition?

A

The crystallization of the drug, which mimics a gallstone
Ceftriaxone - because it is eliminated thru the biliary and has a long half-life

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55
Q

What class of antibiotics are structurally related to beta-lactams?

A

carbapenems

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56
Q

What are some examples of carbapenems?

A

Imipenem-cilastatin, meropenem, ertapenem

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57
Q

What is the spectrum of carbapenems?

A

gram positive, gram negative
including pseudomonas, and other anaerobes

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58
Q

What is so special about ertapenem?

A

Long half life
dosed once daily
poor activity against enterococcus sp and P. aeruginosa

monkey-cillin because it doesn’t cover APE

*Gorilla = APE = meropenem

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59
Q

Explain monobactams

A

Monocyclic beta-lactam ring
Resistant to beta-lactamases
Aztreonam not available in Canada

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60
Q

What is the spectrum of monobactams?

A

Gram-negative bacilli
Includes Ps. Aeruginosa

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61
Q

What do monobactams not cover?

A

ESBL or AmpC producers

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62
Q

What are the macrolides?

A

Erythromycin, clarithromycin, and azithromycin

63
Q

How macrolides work?

A

They attach to the 23s rRNA on the 50S subunit of the bacterial ribosome resulting in the inhibition of protein synthesis
Bacteriostatic, time dependent killing

64
Q

How do organisms evade macrolides?

A

Methylation of the rRNA receptor
inactivating enzymes
active efflux

65
Q

What is the spectrum of macrolides?

A

Gram positive pneumococci, streptococci and corynebacterial (reserved for penicillin allergic patients)

M penumonias
Chlamydia trachomatis
C. penumophilia
Bordatella pertussis
Campylobacter jejuni
Helicobacter pylori

66
Q

Do erythromycin base penetrate the CNS?

A

No, they are super big molecules

67
Q

How is erythromycin administered?

A

IV or oral
the IV causes severe phlebitis which is characterized by pain in the veins

68
Q

What are the adverse effects of erythromycin?

A

GI - nausea, acid burning, dyspepsia
Increased liver function tests (LFTs)
Cholestatic hepatitis
QT prolongation and cardia arrhythmias

69
Q

What causes increased cholestatic hepatits?

A

Using estolate and/or if pregnant

70
Q

What is the drug interaction with erythromycin that causes QT prolongation or cardiac arrhythmias?

A

When combined with CYP3A inhibitors

71
Q

What is the dosing for clarithromycin and azithromycin?

A

BID and OD

72
Q

What enhanced activity do clarithromycin and azithromycin have?

A

Chlamydia, Moraxella, H. influenzar, mycobacteriums
Useful for some MRSA

73
Q

What can be said if an organism is resistant to erythromycin?

A

it is resistant to clarithromycin and azithromycin too

74
Q

Which antibiotic(s) of the macrolides have a higher rate of GI adverse effects?

A

erythromycin

75
Q

What is the erythromycin base with the longest half life?

A

azithromycin

76
Q

What are the main uses for macrolides?

A

URTIs
STI
Acne

77
Q

Of the three erythromycin bases, which one has the least drug interactions?

A

Azithromycin

78
Q

Which erythromycin bases are substrates and inhibitors for CYP 3A4?

A

erythromycin and clarithromycin

79
Q

What are some drugs that are metabolized by CYP3A4?

A

antiarrhythmics, antidepressants, benzodiazepines, anticonvulsants, statins

Using with E or C will increase these drugs’ toxicity

80
Q

What is the mechanism of action of clindamycin?

A

Same as macrolides

80
Q

What is the mechanism of action of clindamycin?

A

Same as macrolides

They attach to the 23s rRNA on the 50S subunit of the bacterial ribosome resulting in the inhibition of protein synthesis

81
Q

What is the spectrum of clindamycin?

A

anaerobes, S. aureus, MRSA, streptococci

82
Q

Clindamycin is not the drug of choice for any infections. When would it be an appropriate time to use them in patients?

A

When the patient has a penicillin allergy or when dealing with resistant organisms

83
Q

How is clindamycin administered?

A

Orally or parneteral

84
Q

True or False: Clindamycin is associated with antibiotic-associated diarrhea

A

Ture, and its called C. difficile diarrhea

85
Q

What are the adverse effects of clindamycin?

A

nausea, vomiting, diarrhea
rash
elevated LFTs
esophageal irritation
C. difficile diarrhea

86
Q

How to prevent esophageal irritation?

A

Always take the med with water and sit upright

87
Q

What are examples of tetracylines?

A

tetracycline, monocycline, doxycycline

88
Q

What is the mechanism of action for tetracyclines?

A

inhibit binding of aminoacyl-tRNA to the 30s unit of ribosome to inhibit protein synthesis
bacteriostatic

89
Q

What are strategies employed by bacteria against tetracyclines?

A

Unknown

90
Q

What is the spectrum for tetracyclines?

A

many gram positive and negative orgs
Very broad spectrum

there are high rates of resistance

91
Q

What are tetracyclines the drug of choice for?

A

rickettsiae, bartonella, chlamydiae, m. pneumoniae
Nocardia
P. acnes

92
Q

What are the adverse effects of tetracyclines?

A

GI upset (nausea, vomiting, diarrhea)
Skin rashes
Photosensitivity
Yeast overgrowth
Deposited in bones and teeth so there may be teeth yellowing
Hepatitis
Vestibular toxicity (dizziness, vertigo, ataxia) seen in minocycline

93
Q

Does minocycline have more or less hypersensitivity?

A

More hypersensitivity

94
Q

Who do we avoid using tetracyclines in?

A

Children less than 8 years old

95
Q

What are the drug interactions with tetracyclines?

A

Anticonvulsants (phenobarbital, phenytoin, carbamazepine) may reduce Tetra levels
Divalent and trivalent cations reduce abs; need to dose separately
Increase INR and bleeding seen with warfarin

96
Q

What are glycylcyclines?

A

synthetic analogue of tetracycline - tigecycline
active against many gram positive and negative orgs including MRSA, s.pneumoniae, enterococci, salmonella, shigella, Acinetobacter, anaerobes

97
Q

How are glycylcyclines administered?

A

IV or IM
eliminated thru biliary tract and feces

98
Q

When are glycylcyclines used?

A

reserved for resistant organisms

99
Q

What is the main glycopeptide?

A

Vancomycin

100
Q

What is the MOA of glycopeptides?

A

inhibits cell wall PG synthesis
bactericidal
DIFFERENT THAN THAT OF PENICILLIN

101
Q

What is the spectrum of glycopeptides/vancomycin?

A

gram positive cocci in particular enterococci, Penicillin resistant strep pneumoniae, MRSA
Active against clostridia, clostrioides, and some bacilli

102
Q

What are resistant species to vancomycin?

A

vanco-resistant enterococci (VRE) and S. aureus (VISA)

103
Q

How can vancomycin be administered?

A

IV - for serious infxn
PO - only for C. difficile (as not orally absorbed)

104
Q

What are the adverse effects of vancomycin?

A

Nephrotoxicity (kidney damage) especially in combination with nephrotoxins
Ototoxicity - heating loss and off balance
Red man syndrome - person turns red + uncomfortable due to hypotension
Granulocytopenia

105
Q

How to prevent ototoxicity in vancomycin?

A

Avoid the use with furosemide, which can increase oto effects

106
Q

How to avoid or prevent red-man syndrome?

A

reduce the infusion rate of vancomycin

107
Q

What is a similar structure drug to vancomycin?

A

Teicoplanin

108
Q

What is daptomycin?

A

lipopeptide (same class as vancomycin)
parenteral
OD dosing
major adverse effect is myopathy

109
Q

What class of drugs is considered to be the opposite of vancomycin?

A

Aminoglycosides

110
Q

What happens if vancomycin is administered alongside an aminoglycoside?

A

the nephrotoxicity is synergistic = dangerous for the pt

111
Q

What are examples of aminoglycosides?

A

streptomycin, gentamicin, tobramycin, and amikacin
The work horse drug is gentamicin

112
Q

What is the MOA of aminoglycosides?

A

inhibit protein synthesis by inhibiting the 30S subunit of bacterial ribosome

113
Q

What are the resistance strategies against aminoglycosides?

A

mutation or methylation of the 16s rRNA-binding site
Enzymatic destruction of the drug
lack of permeability of the drug molecule
active efflux (or lack of active transport)

114
Q

Aminoglycosides are not effective against gram +ve species. What could we do to help with activity?

A

Destroy the cell wall first and then use the aminoglycoside to attack the ribosome
Seen in endocarditis

115
Q

What is the spectrum of aminoglycosides?

A

aerobic gram negative bacilli

116
Q

Discuss the pharmacokinetics of aminoglycosides

A

IV/IM
penetrate the tissues relatively poorly, no CNS
Renal elimination (adj the dose with renal dysfxn)

117
Q

Are aminoglycosides synergistic with penicillins for enterococci and streptococci?

A

Yes

118
Q

What are the adverse effects of aminoglycosides?

A

Nephrotoxicity
Ototoxicity
Neuromuscular blockade
allergies rare

119
Q

What are some drug interactions with aminoglycosides?

A

Other nephrotoxic drugs
other ototoxic drugs
neuromuscular blocking agents

120
Q

What are examples of fluoroquinolones?

A

Ciprofloxacin, levofloxacin, moxifloxacin

121
Q

What is the MOA of fluoroquinolones?

A

Inhibit DNA gyrase or topoisomerase II and IV
Bactericidal; conc dependent killing

122
Q

What are the strategies for fluoroquinolone resistance?

A

alteration of the A or B subunit of DNA gyrase
mutation in ParC or ParE of topoisomerase IV
Change in outer membrane permeability
efflux pumps

123
Q

What is the spectrum of fluroroquinolones?

A

highly active against gram negative bacteria
Haemophilus sp, Neisseriae, chlamydiae, etc

124
Q

Of the fluroquinolones what is the most active against P. aeruginosa? S. pneumoniae? Anaerobes?

A

P. aeruginosa -> ciprofloxacin
S. pneumoniae -> levofloxacin
anaerobes -> moxifloxacin

125
Q

What conditions are commonly treated with fluoroquinolones?

A

UTI, STI, lower resp tract infxn, enteritis or travelers diarrhea, drug resistant mycobacterial infection

126
Q

How are fluoroquinolones administered?

A

IV or PO, parenteral use not commonly required
Excellent oral bioavailability

127
Q

How are ciprofloxacin, levofloxacin, and moxifloxacin eliminated?

A

ciprofloxacin and, levofloxacin - eliminated renally
moxifloxacin - biliary pathway (doesn’t get to the urine and not for UTI’s)

128
Q

What are the adverse effects of fluoroquinolones?

A

Nausea, vomiting, diarrhea
insomnia, headache, dizziness
Other CNS effects including seizures (goes to the brain and causes jitters, dizzy, scattered thoughts)
skin rashes
impaired liver fxn
tendinitis, tendon rupture
QTc interval prolongation
Hypo/hyperglycemia - hypo is linked to the seizures
C. difficile diarrhea
Peripheral neuropathy = tingles and numbness in extremities

129
Q

What are the drug interactions with fluroquinolones?

A

They bind to di and tri-valent cations
QTc prolongation
CYP 1A2 inhibition -> increased levels of many drugs
Increase INR with warfarin

130
Q

Is the use of fluroquinolones common?

A

No, many toxicities and a lot have been removed from the market
Only for resistant organisms, not really a drug of choice overall
Not used in children under 18 years

131
Q

True or false: sulfamethoxazole and trimethoprim are commonly combined together as TMP/SMX

A

True, normally they are static drugs, but when combined, they become cidal drugs

132
Q

What is the mechanism of SMX?

A

structural analogue of PABA and competitively inhibits dihydrofolic acid synthesis

133
Q

What is the mechanism of TMP?

A

binds to dihydrofolate reductase therefore inhibiting the reduction of dihydrofolic acid to tetrahydrofolic acid

134
Q

What is the resistance for SMX and TMP?

A

the ability for the cell to use preformed folic acid, don’t need to make it

135
Q

What is the spectrum of SMX and or TMP?

A

wide spectrum of gram positives, gram negatives, chlamydia, nocardiae, and protozoa

136
Q

What are some examples of organisms affected by SMX/TMP?

A

staphylococci including MRSA
Streptococcus pneumonia, not group A strep
S. maltophilia
Moraxella
H. influenza
Enterobacteriaceae
Brucella
pneumocystis jirovecii

137
Q

What is Pneumocystis jirovecii?

A

An opportunistic pathogen in HIV infected patients

138
Q

What are the uses of SMX/TMP?

A

UTI, MRSA infections, PJP, other

139
Q

What are the adverse effects of SMX and TMP?

A

skin rashes, which can be severe/ life-threatening
Hypersensitivity - due to the sulfa component
headache
GI issues (N,V,D)
bone marrow suppression - decreases in WBC and platelets, anemia too
Hyperkalemia and hyponatremia
photosensitivity

140
Q

What are the drug interactions of TMP/SMX?

A

2C9 inhibitor and 3A4 substrate causing increased levels of carvedilol, digoxin, and phenytoin
Increased INR and bleeding with warfarin
Hypoglycemic agents - increased risk of hypoglycemia
Drugs that increase potassium levels

141
Q

What are some cautions and contraindications with TMP/SMX?

A

Caution with those with renal dysfunction (folic acid development and unbinding to bilirubin causing increased toxic free forms)
Contraindicated in first and third trimester of pregnancy

142
Q

What is the MOA of metronidazole?

A

Unknown, possible inhibition of nucleic acid synthesis and disruption of DNA
Resistance is unknown

143
Q

What is the spectrum of metronidazole?

A

anaerobes including C. difficile
protozoa - trichomonas, Giardia, etc.
Propionibacterium are resistant

144
Q

How is metronidazole administered?

A

IV and PO
The PO has excellent bioavailability

145
Q

What are the adverse effects of metronidazole?

A

GI
metallic taste
headache
dark urine
peripheral neuropathy (after a couple weeks of use)
Disulfiram-like rxn with alcohol
Insomnia
stomatitis - mouth sores

146
Q

What are disulfiram-like reactions and which anitbiotic may cause this?

A

You feel sick -> nausea, vomiting, sweating
Can be seen in patient who use metronidazole

147
Q

What are the drug interactions with metronidazole?

A

alcohol - disulfiram rxn
warfarin - increased INR and bleeding

148
Q

What is the MOA of linezolid?

A

inhibits protein synthesis
bacteriostatic, but cidal for strptococci

149
Q

What is the spectrum for linezolid?

A

Streptococci, enterococci( includes VRE), Staphylococci (including MRSA)
Reserved for multi-drug resistant organisms
An alternative for vancomycin
expensive

150
Q

What is the administration for linezolid?

A

IV and Oral

151
Q

What are the adverse effects of linezolid?

A

Headache
nausea, vomiting, diarrhea
Rash
increased LFT’s
myelosuppression - low platelets and anemia
Optic or peripheral neuropathy
Lactic acidosis
decreased seizure threshold

152
Q

What are some drug interactions with linezolid?

A

Increased serotonin syndrome risk with SSRIs and MAOIs
Rifampin decreases linezolid levels

PHAR 152* (16 decks)

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