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Antibiotics Flashcards

0
Q

Antibiotics

A

naturally occurring agent that inhibits growth of bacteria

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1
Q

Chemotherapeutics

A

agent that inhibits rapidly dividing cells

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2
Q

Antibacterials

A

semi- or synthetic agent that inhibits bacterial growth

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3
Q

Antibiotics take advantage of the difference between the host organism and the microbe
In certain instances the selectivity is relative
In order to choose the most appropriate antibiotic, the following information is vital:

A

The identity of the pathogenic organism
The susceptibility to various antibiotics (C&S)
Site of infection
Comorbid condition and other drugs prescribed
Safety of the antibiotic
Cost factors

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4
Q

CULTURE and SENSITIVITY

A

The fastest way to identify an organism is by Gram staining. This may not identify the organism thoroughly but it can suggest guideline on treatment
Culture of the organism and identification of sensitivity to various antibiotics is the most effective way to ensure that the choice of antibiotic is most appropriate
Starting antibiotic therapy prior to obtaining samples for culture runs the risk of delayed or inability to identify the pathogenic organism

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5
Q

EMPIRIC THERAPY

A

Often empiric therapy is started before final identification of an organism because further delay can have significant adverse consequences
Choice of antibiotic is based on Gram staining, site of infection, recent history including travel history, co-morbid conditions, immune status, whether the infection was nosocomial (hospital-acquired) or community acquired.
Once positive identification is achieved, then the choice of antibiotic can be changed if necessary

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6
Q

MIC

A

minimum inhibitory conc. is the smallest concentration necessary to inhibit growth in culture

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7
Q

MBC

A

minimum bacteriocidal conc. is the smallest concentration necessary to kill the bacteria (99.9%)

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8
Q

Bacteriostatic drugs

A
  • inhibit the growth of the organism, giving the immune system time to work and eliminate the organism.
  • All inhibitors of protein synthesis except aminoglycosides
  • Bacteriostatic agents interfere with the efficacy of bactericidal agents (cells must be actively dividing).

Effects can be antagonistic, additive or synergistic

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9
Q

Bactericidal drugs

A
  • are drugs that kill the organism in the plasma levels achieved in vivo.
  • All inhibitors of cell wall synthesis

Some antibiotics can be bacteriostatic for one organism but bactericidal for another

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10
Q

Some antibiotics cross the blood-brain barrier easily:

A

chloramphenicol, metronidazole, 3rd generation cephalosporin, etc.

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11
Q

Some antibiotics cross the blood-brain barrier poorly:

A

vancomycin, penicillins (unless there is meningitis), 1st generation cephalosporin, etc.

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12
Q

Antibiotic must get to the site of action

A

If infection is in the CNS, antibiotic must cross the blood-brain barrier

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13
Q

Protein binding

A

many antibiotics are highly protein bound

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14
Q

Metabolism and excretion

A
  • drugs that undergo hepatic metabolism or are concentrated in the liver can accumulate in hepatic dysfunction and cause toxicity (erythromycin, tetracycline).
  • Drugs that are eliminated by the kidneys should be used with caution when renal function decreases because of accumulation and toxicity
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15
Q

Immune status

A

if the patient has a co-morbid condition that interferes with immune function, this may alter the choice of antibiotics

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16
Q

Very young and very old patients

A

have decreased ability to metabolize and excrete antibiotics, so the choice and dosage must be altered

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17
Q

Pregnancy and lactation can alter the choice of antibiotics. The following drugs should be avoided in pregnancy:

A

tetracyclines, quinolones, chloramphenicol, aminoglycosides, folic acid inhibitors, etc.

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18
Q

ROUTE OF ADMINISTRATION

A

Depending on the route of administration, the bioavailability of various antibiotics will change significantly
Some antibiotics can only be given parenterally because they are peptides or they are poorly absorbed by the GI tract
Other important routes of administration: intrathecal injections, topical application (eye & ear), intraocular
The dosage and frequency of administration will reflect the elimination of these antibiotics from their reservoirs

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19
Q

POST-ANTIBIOTIC EFFECT

A

Some antibiotics continue to work long after the MIC has been breached. The antibiotics that exhibit the PAE include aminoglycosides, fluoroquinolones, tigecycline

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20
Q

TIME DEPENDENT vs. CONCENTRATION DEPENDENT

Some antibiotics are found to have a direct concentration dependent efficacy. The amount of organisms killed is proportional to the plasma concentration of the anitbiotic: aminoglycosides, fluoroquinolones.

A

Other antibiotics have a time dependent efficacy. The major factor that affect bactericidal activity is the amount of time the drug’s plasma concentration is above a minimum level.
Increasing the concentration does not significantly increase activity: β-lactams, macrolides, glycopeptides, linezolid, clindamycin.

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21
Q

Narrow spectrum antibiotics

A

isoniazid

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22
Q

Extended spectrum antibiotics

A

ampicillin

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23
Q

Broad spectrum antibiotics

A

tetracycline, fluoroquinolones, macrolides, chloramphenicol

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24
Q

RESISTANCE

A

Most organisms have evolved a mechanism of resistance to various antibiotics.
Some specific organisms are always resistant to certain antibiotics
Other organisms acquire resistance to specific antibiotics (or classes of antibiotics that have the same mechanism of action)

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25
Q

Genetic alterations leading to drug resistance

A

Spontaneous mutations
Transfer of genes between organisms via plasmids, transduction or conjugation
Inappropriate use of antibiotics increases risk by selection process

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26
Q

Altered expression of proteins in resistance

A

Modification of target site, hence antibiotic inefficacy
Decreased accumulation of antibiotic intracellularly
Enzymatic inactivation of antibiotics

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27
Q

Antibiotics are given prophylactically for various situations:

A

surgery, MVP, traveling to endemic regions, high-risk situations

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28
Q

CLASSES OF ANTIBIOTICS

A 
Cell wall inhibitors
Inhibitors of protein synthesis
Inhibitors of folate metabolism
Inhibitors of bacterial DNA synthesis
Inhibitors  of cell membrane function
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29
Q

SIDE EFFECTS

A

Hypersensitivity reaction
Jarisch-Herxheimer reaction and Mazzotti Rxn
Direct toxicity - aminoglycosides
Superinfections – Broad spectrum antibiotics

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30
Q

Carbapenems

A

Doripenem
Ertapenem
Imipenem
Meropenem

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31
Q

Beta-Lactamase Inhibitors

A

Clavulanic Acid
Sulbactam
Tazobactam

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32
Q

Monobactams

A

Aztreonem

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33
Q

PENICILLINS

A

Beta lactam antibiotics including penicillins prevent the last step in peptidoglycan synthesis
Inhibition of the transpeptidase prevents the cross-linking of the D-alanine to the L-glycine
There are other PBPs aside from the transpeptidase which also contribute to the efficacy of penicillins as antibiotics

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34
Q

NATURAL PENICILLINS

A

Penicillin G is a salt that is dosed in unit.
1 unit= 0.6 μg
Penicillin G is very effective against non lactamase producing gram positive organisms: Streptococci, Neisseria, spirochetes, Listeria, Actinomyces, Clostridium, etc.
Probenecid can block tubular secretion therefore extend the half-life of penicillins

Penicillin V is an acid stable version which can be administered orally.

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35
Q

Gram+ coccus:

Tx: natural penicillin

A

Streptococcus pneumoniae
Streptococcus pyrogenes
Streptococcus viridans group

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36
Q

Gram+ bacilli:

Tx: natural penicillin

A

Bacillus anthracis

Corynebacterium diphtheriae

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37
Q

Gram- cocci:

Tx: natural penicillin

A

Neisseria Gonorrhoeae

Neisseria meningitis

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38
Q

Gram- rods: anaerobic organisms

Tx: natural penicillin

A

Clostridium perfringens

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39
Q

Gram- rods: spirochetes

Tx: natural penicillin

A 
Treponema pallidum (syphillis)
Treponema pertenue (yaws)
40
Q

Syphillis

Tx: natural penicillin

A

A contagious venereal disease that progressively affects many tissues.
A single treatment with penicillin is curative for primary and secondary syphillis. No antibiotic resistance has been reported.

41
Q

Gonorrhea:
Tx: natural penicillin

A

Silver nitrates in the eyes prevent gonoccocal ophthalmia in newborns.
Penicillinase-producing strains are treated using ceftriaxone with spectinomycin as a backup.

42
Q

Pneumococcal pneumonia:

Tx: natural penicillin

A

Streptococcus pneumoniae is a major of bacterial pneumonia in all age groups.
Infection often occurs in an institutional setting in individuals who are ill from other causes.
Resistance to penicillin G has greatly increased worldwide due to mutations in one or more of the bacterial penicillin-binding proteins.

43
Q

ANTI-STAPHYLOCOCCAL PENICILLINS:
Semisynthetic penicillins effective against penicillinase producing Staphylococcus but not MRSA
Absorption increases on an empty stomach and they are highly protein bound.
These penicillins are not as effective against non-penicillinase producing organisms

A

Oxacillin
Dicloxacillin
Nafcillin
Methicillin

44
Q

Methicillin:

A

is not used clinically because of renal toxicity (interstitial nephritis)

45
Q

are mostly eliminated via biliary route

A

Nafcillin, Oxacillin and Dicloxacillin

46
Q

EXTENDED SPECTRUM PENICILLINS:
These penicillins have extended coverage to include gram negative organisms including E. Coli, H. Influenza, etc.
Often a beta lactamase inhibitor must be added for susceptibility

A

Amoxicillin

Ampicillin

47
Q

Category A drugs:

A

No human fetal risk or remote possibility of harm

48
Q

Category B drugs: no control studies show human risk; animal studies show potential toxicity

A 
Beta lactams
Beta lactams with inhibitors
Cephalosporins 
Aztreolam
Clindomyacin 
Erythromycin 
Azithromycin
Metronidazole 
Nitrofurantoin
Sulfanomides
49
Q

Category C drugs: animal fetal toxicity demonstrated; human risk undefined.

A 
Chloramphenicol 
Fluoroquinolones
Clarithromycin
Trimethoprim 
Vancomycin 
Gentamicin 
Trimethoprim-sulfa-methoxazole
50
Q

Category D drugs: human fetal risk present but benefits may outweighs risks

A 
Tetracycline 
Aminoglycosides (except gentomicin)
51
Q

Category X drugs:

A

Human fetal risk present but does not outweigh benefits; contraindicated in pregnancy

52
Q

ANTI-PSEUDOMONAL PENICILLINS:
These antibiotics can still be destroyed by penicillinase. They are often administered with beta lactamase inhibitors. These antibiotics are effective against Pseudomonas Aeruginosa. Usually combined with an aminoglycoside (synergy).

A

Mezlocillin
Carbenecillin
Ticarcillin
Piperacillin*

53
Q

Mechanisms of resistance to penicillins include:

A

Beta lactamase activity often acquired through plasmid transfer
Efflux pumps that decrease penetration of the antibiotic and prevent accumulation at the site of action
Altered PBPs that possess a lower affinity for beta lactam antibiotics. This is the mechanism of resistance for MRSA.

54
Q

SIDE EFFECTS of penicillin

A 
Hypersensitivity
Diarrhea
Interstitial Nephritis
Bone Marrow Suppression
Neurotoxicity (intrathecal)
Cation toxicity
55
Q

CEPHALOSPORINS

A

Contains beta-lactam ring
More resistant to penicillinase than penicillin
Ineffective against MRSA, Clostridium, Enterococci, and Listeria.

56
Q 
1st GEN. CEPHALOSPORINS:
Mostly Gram positive coverage
Used as prophylaxis for surgery
PEcK (Proteus, E. Coli, Klebsiella)
The spectrum and efficacy is similar to natural penicillins and staphylococcal penicillins
A

Cefazolin Cephalexin Cefadroxil
Cefalothin

57
Q

2nd GEN. CEPHALOSPORINS:
Adequate coverage for Hemophilus Influenza, Neisseria and Enterobacter species
Orally active medications
Do not cross the blood-brain barrier except Cefuroxime
HENPEcK

A 
Cefaclor
Cefoxitin
Cefuroxime
Cefprozil
Loracarbef
Cefotetan
Cefamandole
58
Q

3rd GEN. CEPHALOSPORIN:
These antibiotics cross the blood brain barrier so are effective against meningitis
Some are antipseudomonal: Ceftazidime and Cefoperazone
Less Gram positive coverage but extensive Gram negative coverage

A

Ceftibuten
Cefixime
Cefdinir
Cefotaxime

59
Q

4th GEN CEPHALOSPORINS:

Broader spectrum cephalosporins with anti-pseudomonal coverage as well as Gram positive coverage

A

Cefipime

Cefpirome

60
Q

5th Generation Cephalosporins:

A

Ceftaroline which is effective against MRSA as well as other Gram positive organisms and Gram negative organisms

61
Q

SIDE EFFECTS of cephalosporins

A

There is a 5-10% cross reactivity between allergies to penicillins and allergies to cephalosporins
Patients who have had SJS or TEN with penicillins should not be placed on cephalosporins or vice versa
Other side effects: diarrhea, alcohol intolerance, thrombocytopenia and other bleeding disorders

62
Q

CARBEPENEMS:
Carbepenems are synthetic beta lactam antibiotics
Broader spectrum – aerobes and anaerobes
Resistant to beta lactamase
Effective against many strains of Pseudomonas and Bacteroides
Other carbepenems are not susceptible to dipeptidase

A

Doripenem Ertapenem Imipenem

Meropenem

63
Q

Imipenem:

A

is broken down by enzymes in the brush border and kidneys (dipeptidase) which can be prevented by co-administering cilastatin.

64
Q

Ertapenem

A

is not effective against Pseudomonas and Imipenem should not be used as monotherapy against Pseudomonas Aeruginosa.

65
Q

Aztreonem

A

is a monobactam that is resistant to beta lactamase and is effective against Gram negative organisms including Pseudomonas

has no coverage of Gram positive organisms or anaerobes

66
Q

Side effects to Carbapenems:

A

Nausea and vomiting are the most common side effects, there can exist cross-reactivity to penicillin allergies, but this is much less common than with cephalosporins

Aztreonem has no cross reactivity with other beta lactam antibiotics

67
Q

BETA LACTAMASE INHIBITORS:
These drugs have NO antimicrobial activity on their own and cannot be used to treat infections
They are effective against penicillinase producing strains of organsims in conjunction with a bet lactam antibiotic, preventing the enzyme from destroying the antibiotic
Beta lactamase inhibitors are effective against plasmid encoded beta lactamases but ineffective against chromosomal beta lactamses produced by gram negative bacilli (Enterobacter, Acenitobacter, Citrobacter)

A

Clavulinic Acid Sulbactam Tazobactam

68
Q

VANCOMYCIN

A

Complex tricyclic glycopeptide that inhibits cell wall synthesis
Primarily effective against Gram positive organisms including MRSA (aerobes and anaerobes)
Ineffective against Gram negative organisms

69
Q

Vanco

A

Relatively large molecule (MW > 1500 daltons)
Resistant strains of enterococci have emerged
Due to alteration of target D-Ala-D-Ala to
D-Ala-D-lactate or D-Ala-D-Serine
Also S. Aureus has emerged with a plasmid that confers resistance to Vancomycin

70
Q

is poorly absorbed afte oral administration and has to be given parenterally for systemic effects.
Can be given orally for C. Difficile pseudo-membranous colitis
30% protein bound, large Vd and penetrates into the CNS when meningitis is present.
Eliminated 90% unchanged by the kidneys

A

Vancomycin

71
Q

Vancomycin has to be monitored due to many adverse effects:

A

Red man syndrome from histamine release leading to hypersensitivity and anaphylaxis
Nephrotoxicity
Ototoxicity
Plasma Peak and Trough levels must be monitored for potential toxicity
Pre-treatment with antihistamines may be necessary
Other side effects: Fever, Chills and Phlebitis

72
Q

DAPTOMYCIN

A

Cyclic lipopeptide antibiotic effective in treating MRSA or VRE
Induces rapid depolarization of the bacterial membrane and inhibiting DNA, RNA and protein synthesis. This effect is bactericidal and concentration dependent
Daptomycin is only effective against Gram positive organisms
Daptomycin is inactivated by pulmonary surfactants and should never be used in treating pneumonias and left-sided endocarditis

73
Q

Side Effects of DAPTOMYCIN

A

headache, myalgia, elevated CPK, elevated LFTs, insomnia, constipation, nephrotoxicity if used with other agents that can cause this. Also, use with caution in the presence of HMG-CoA reductase inhibitors.
Pharmacokinetics: > 90% protein-bound
No significant drug-drug interactions and is excreted 80% unchanged in the urine

74
Q

TELEVANCIN

A

Semisynthetic lipoglycopeptide derivative of Vancomycin effective against MRSA and other resistant Gram positive organisms
Inhibitor of bacterial cell wall synthesis and causes disruption of bacterial cell membrane
Effective against MRSA, Streptococcus, VSE

75
Q

Side effects of TELEVANCIN

A

metallic taste, headache, nausea, vomiting, insomnia, foamy urine, long QT interval, contraindicated in pregnancy, can interfere with coagulation tests.

76
Q

TEICOPLANIN

A

Glycopeptide antibiotic that inhibits cell wall synthesis. Mechanism of action is similar to Vancomycin
Binds to D-Ala-D-Ala terminus of cell wall precursor units and prevents assembly. Effective only for Gram positive organisms, including MRSA, Listeria, Corynebacterium, Clostridium and anaerobic Gram positive cocci.
Alteration of cell wall targets will create resistance to Teicoplanin

77
Q

Side Effects of TEICOPLANIN

A

rash, hypersensitivity, fever, neutropenia and ototoxicity

Highly protein bound (90%) and a t½ = 100 hours
Elimination is renal
Dosage adjustment necessary for renal insufficiency

78
Q

List of TETRACYCLINES

A 
Tetracycline
Doxycycline
Minocycline
Demeclocycline
Tigecycline (Glycylcycline)
79
Q

List of AMINOGLYCOSIDE

A 
Netilmicin
Kanamycin
Tobramycin
Gentamycin
Streptomycin
Amikacin
Neomycin
Paromomycin
80
Q

List of MACROLIDES

A

Erythromycin
Clarithromycin
Azithromycin
Telithromycin

81
Q

OTHER protein synthesis inhibitors

A 
Clindamycin
Chloramphenicol
Linezolid
Quinupristin/Dalfopristin
Spectinomycin
82
Q

TETRACYCLINES

A

Bacteriostatic antibiotics
Inhibit protein synthesis by binding to 30S subunit
Broad spectrum aerobes, anaerobes, Gram positive, Gram negative
Effective against Rickettsia, Mycoplasma, Chlamydia, Legionella, etc.Ureaplasma, Borrelia, Treponema, etc.
Resistance is widespread
Many side effects

83
Q

Absorption of tetracycline

A

Variable absorption via oral administration:
Doxycycline > Minocycline > Tetracycline
Absorption is decreased with dairy products or antacids
Large volume of distribution
Metabolized by the liver and excreted by kidneys and entero-hepatic circulation

84
Q

Indication for tetracycline

A 
Rickettsial Infections
Mycoplasma Pneumoniae
Chlamydial infections
Often used in STD treatment to ensure eradication of Chlamydia
Anthrax
Brucellosis
Tularemia
Cholera
Borrelia
Gram Positive Cocci including MRSA and Strep
85
Q

SIDE EFFECTS of tetracyclines

A 
GI Irritation which can improve with foods
Pseudomembranous Colitis
Photosensitivity
Hepatic Toxicity
Renal Toxicity (except Doxycycline)
Vestibular problems such as vertigo, dizziness
Effects on Teeth and Bone
Hypersensitivity Reactions
Pseudotumor Cerebri
Contraindicated in Pregnancy
86
Q

Resistance to Tetracyclines

A

Resistance to Tetracyclines is emerging. Several mechanism of resistance:
Active efflux of the drug from the cytoplasm via a Mg++ dependent pathway
Enzymatic inactivation of the drug
Alterations in ribosome binding sites – production of proteins that displace drug from ribosomal binding sites
Cross resistance is very common among the tertracyclines
Tigecycline has activity against MRSA and other resistant strains of microorganisms but no effect against Pseudomonas or Proteus strains

87
Q

AMINOGLYCOSIDES

A

Most effective against aerobic Gram negative bacilli. They are bactericidal.
Synergistic effects with beta lactams
Very toxic which limits usefulness
Mechanism of Action – diffuse through porins and bind to 30S subunit causing misreading of codon. Also premature termination of translation and impaired assembly of polysomes.
Some aminoglycosides also bind to the 50S subunit

88
Q

Indications for aminoglycosides

A

Aminoglycosides are rarely if ever used as single agents
They are most effective against aerobic gram negative bacilli: Pseudomonas, Proteus
Enterococcus are highly resistant to all aminoglycosides
Streptomycin is used primarily for Mycobacterium species and many enteric organisms are resistant to Streptomycin
Endocarditis, pneumonia, tularemia, UTIs

89
Q

Resistance to Aminoglycosides

A

Bacteria may acquire resistance to aminoglycosides by failure to allow penetration of the drug intracellularly
Also low affinity of the drug for bacterial ribosomes
Drug inactivation by modification: acetylation, phosphorylation or adenylation
Amikacin is least modified of the aminoglycosides therefore little resistance develops in comparison to other aminoglycosides

90
Q

SIDE EFFECTS of Aminoglycosides

A

Aminoglycosides are particularly toxic and require monitoring of drug levels via peaks and troughs.
Ototoxicity – vestibular and cochlear. Aminoglycoside administration in pregnancy will cause the newborn deafness. Neomycin, Kanamycin, Amikacin are more apt to cause hearing loss. Gentamycin and Streptomycin are more apt to cause vestibular problems. These are effects are dose dependent.
These effects may be permanent.
Co-administration of loop diuretics can worsen the damage
Nephrotoxicity – Effects of aminoglycosides on proximal tubular cells can interfere with calcium-mediate transport and damage the kidney. Some of these effects may be irreversible.

91
Q

Nephrotoxicity

A

The most nephrotoxic agents are Gentamycin, Tobramycin and Neomycin.
Nephrotoxicity is always preceded by a rise in plasma creatinine
Vancomycin, ACEI, Amphotericin, Cisplatin and cyclosporine can worsen the nephrotoxicity

92
Q

Other side effects of Aminoglycosides

A

Neuromuscular blockade – Aminoglycosides can potentiate neuromuscular blockers and other anesthetic agents. This will also be seen in patient who have Myasthenia Gravis.
Neuromuscular blockade can be reversed by the administration of calcium gluconate or neostigmine.
This effect is most likely to be seen with intrapleural or intraperitoneal administration of aminoglycosides
Mechanism of action is decreased release of Acetylcholine and decreased sensitivity of muscarinic receptors
Streptomycin can cause optic neuritis and scotomas.
Aminoglycosides do not cause pseudomembranous colitis or allergic reactions

93
Q

MACROLIDES

A

Bacteriostatic antibiotic that is concentration dependent
Drug of choice for patients allergic to Penicillins
Indications:
Mycoplasma Infections
Legionnaire’s Disease
Chlamydial Infections
Hemophilus Influenza
Heliobacter Pylori
Diphtheria
Pertussis
Effective against Gram positive bacilli such as Clostridium

94
Q

Erythromycin and Clarithromycin inhibit CYP3A4 and can cause drug-drug interactions with substrates such as

A

carbamazepine, theophylline, antihistamines, coumadin, valproic acid, benzodiazepines, etc.

95
Q

Food inhibits absorption of Erythromycin and Azithromycin but increases absorption of

A

Clarithromycin

96
Q

Side effects of Macrolides

A

GI upset and hypermotility – binds motilin in GI tract
Cholestatic Jaundice
Ototoxicity
Hepatotoxicity
Long QT Syndrome
Drug-drug interactions
Allergic Reactions: fever, eosinophilia, rash, etc.

97
Q

CLINDAMYCIN

A

Bacteriostatic inhibitor of protein synthesis that binds to the 50S subunit
Shows greater efficacy against anaerobic organisms
Streptococci and MSSA are sensitive but aerobic Gram negative bacilli are resistant

Pharm (8 decks)

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