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Multisystems I > Pharmacology-Antibiotics > Flashcards

Pharmacology-Antibiotics Flashcards

1
Q

6 categories of antibiotics that target bacteria and note host cells

A

1) Cell Wall Biosynthesis (our cells don’t have a cell wall and we don’t have D amino acids) #2) Membrane Potential #3) Cell Membrane Disruption #4) Protein Synthesis #5) Nucleic Acid Biosynthesis #6) DNA Replication or Transcription

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2
Q

MIC

A

Lowest concentration that inhibits bacterial growth after 24 hrs in vitro

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3
Q

Post-antibiotic effect

A

Suppression of bacterial growth continues even when antibiotic concentration is below MIC due to residual concentration in bacteria or in plasma.

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4
Q

Superinfection

A

2nd opportunistic infection after antibiotic therapy often due to loss of normal flora

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5
Q

What is the LADME process?

A

Liberation of drug -> Absorption of drug -> Distribution of drug to other tissues -> Metabolism of drug -> Excretion of drug

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6
Q

What is the one-compartment model?

A

Drugs rapidly equilibrate in a linear time course to all body tissues.

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7
Q

What is the two-compartment model?

A

Distribution phase: movement of drug into tissue compartment. Elimination phase: the predominant process.

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8
Q

Antibiotic that binds the least protein in plasma and is therefore the most active in plasma?

A

Amoxicillin.

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9
Q

3 kinetic patterns of antibiotic action

A

1) Concentration-dependent killing of microbes 2) Time-dependent killing of microbes 3) Area of curve killing of microbes

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10
Q

What are the inhibitors of bacterial cell wall synthesis?

A

Beta lactams: penicillins, cephalosporins, monolactams and carbapenems. Note that all classes have the beta lactam ring (in red). Glycopeptides: vancomycin and telcoplanin.

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11
Q

How do beta lactam antibiotics work?

A

The look like D-Ala-D-Ala, COVALENTLY bind the bacterial transpeptidase enzyme and inhibit cell wall synthesis.

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12
Q

What are the penicillin binding proteins?

A

Though transpeptidase is the classic target, proteins required for bacterial shape, formation of septum and D-Ala carboxypeptidases are also targeted.

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13
Q

How have bacteria gained resistance to the beta lactam antibiotics?

A

1) Penicillinases and 2) Amidases

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14
Q

4 classes within the penicillin group of beta lactam antibiotics? What is each group tailored to?

A

Penicillin G & V (Gram +), Penicillinase-resistant penicillin, extended range penicillin (covers more gram -) and antipseudomonal penicillin (for pseudomonas)

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15
Q

Which penicillin can only be given IV or IM? Which can be given orally? Which has a longer half life?

A

Penicillin G is not acid stable and must be given IM or IV, it has a short half life (10-15 min). Penicillin V is modified to be acid stable and can be given orally and has a slightly longer half life.

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16
Q

How can you improve the half life of penicillin G given IM?

A

Combine it with procaine or benzathine (bases) that decrease penicillin solubility. This slows the release of penicillin from the injection site and prolongs the half life.

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17
Q

What organisms are penicillin V and G largely effective against?

A

Pneumococcus, streptococcus and peptococcus, gram + bacteria.

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18
Q

What drugs fall into the penicillinase-resistant penicillins of the beta lactam antibiotics? What organisms are these used to treat?

A

Nafcillin, cloxacillin, methicillin and oxacillin. These are used against Staph aureus and Staph epidermidis organisms that developed a penicillinase to open up the beta lactam ring. They are also useful against all microbes that normal penicillin clears.

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19
Q

How long is the half life of the penicillinase-resistant drug cloxacillin, the extended range penicillin amoxicillin?

A

~4 hours, it is orally available.

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20
Q

What drugs fall into the class of extended range penicillins of the beta lactam antibiotics? What microbes are these used to treat?

A

Ampicillin and amoxicillin. These are active against gram negative E. coli, P. mirabilis, H. influenzae, Salmonella, Shigella, Neisseria.

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21
Q

What drug falls into the class of anti-pseudomonal penicillins of the beta lactam antibiotics? What microbes is it used to treat?

A

Ticarcillin. It is used to treat Pseudomonas, Enterobacter, Proteus, H. influenzae and E. coli.

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22
Q

What drug is a ureidopenicillin derivative used to treat gram positive cocci, Pseudomonas and Klebsiella?

A

Piperacillin

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23
Q

What is the half-life of ticarcillin?

A

It drops rapidly from time of administration and is almost eliminated at 6 hours because it is given IV.

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24
Q

The cephalosporins add increased diversity to the beta lactam class because you can substitute at what positions?

A

7 on beta lactam ring = change in bacterial spectrum. 3 on dihydrothiazine ring = change in pharmacokinetics.

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25
Q

How does bacterial coverage change as you move from the 1st to the 4th generation cephalosporins?

A

1st = increased gram + coverage. 4th = increased gram - coverage.

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26
Q

What drugs fall into the class of 1st generation cephalosporins of the beta lactam antibiotics? What microbes are they used to treat?

A

Cefazolin (IV/IM), cephalexin (oral), cephradine (oral, IV, IM), cefadroxil (oral). These are used for gram positive streptococci and staph aureus.

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27
Q

What 1st generation cephalosporin is often used prophylactically for surgery? What are the 2nd generation cephalosporins used for in surgical prophylaxis?

A

Cefazolin is used for normal flora, it has a longer half life of 2 hours than its counterparts. 2nd generations are used for prophylaxis against intestinal microbes.

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28
Q

What drugs fall into the class of 2nd generation cephalosporins of the beta lactam antibiotics? What microbes are they used to treat?

A

Cefotetan, cefoxitin (B. fragilis), cefuroximine, cefaclor (H. influenzae), locarbef. These are less active against gram + but more active against gram -. Also note that these drugs have some beta-lactamase resistance.

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29
Q

Which 2nd generation cephalosporin is able to penetrate the CNS?

A

Cefuroximine

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30
Q

What drugs fall into the class of 3rd generation cephalosporins of the beta lactam antibiotics? What microbes are they used to treat?

A

Ceftriaxone (N. meningitides w/ 8 hr half life), cefotaxime (highly resistant to gram - beta lactamases) ceftazidime and cefoperazone (last 2 good against drug-resistant pseudomonas). Ceftaroline has good gram + coverage and is used for MRSA. This class is good for Klebsiella, Enterobacter and Proteus.

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31
Q

What tissues are affected by the 3rd generation cephalosporins?

A

CNS, lung, bone and urinary tract

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32
Q

What drug falls into the class of 4th generation cephalosporins of the beta lactam antibiotics? What microbes is it effective against?

A

Cefepime. It can access the CNS, is resistant to chromosomal-encoded beta-lactamases and kills lots of gram negative bacteria (esp. Haemophilus influenzae).

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33
Q

Cephalosporin class typically used for pneumonias

A
  1. Class 2 are used for some respiratory infections.
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34
Q

What drugs fall into the class of carbapenems of the beta lactam antibiotics? What microbes are they used against?

A

Imipenem (E. coli, S. aureus, Klebsiella, Enterobacter and H. influenzae), Meropenem (longer 1/2 life b/c not hydrolyzed by renal tubule dipeptidase and has reduced nephrotoxicity), Ertapenem (longer 1/2 life) and Doripenem (no nephrotoxicity, contraindicated w/valproate). All of these are resistant to beta-lactamases and broad spectrum antibiotics.

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35
Q

What drug falls into the class of monobactams of the beta lactam antibiotics? What microbes is it effective against?

A

Aztreonam. It is good against gram negative aerobes like Klebsiella, H. influenzae, Pseudomonas, Enterobacter, Citrbacter and P. mirabilis. Note that is is poorly active against gram +, crosses the placenta, has low allergenicity with penicillin and is safe for pregnancy.

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36
Q

Adverse effects of penicillin

A

Allergy (when PCN binds with host proteins), vitamin K deficiency and hemolytic anemia, seizures in renal failure patients and nephritis

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37
Q

Types of penicillin allergies

A

Immediate anaphylaxis (IgE mediated), delayed non-uticarial rash (not itchy), idiopathic (patients with mono) and non-allergic (nausea + diarrhea)

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38
Q

What beta-lactams can patients take who get a delayed, non-uticarial rash from PCN?

A

Cephalosporins

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39
Q

Adverse effects of carbenicillin/ticarcillin?

A

Cross allergenicity w/PCN, Na overload (salt in compound), hypokalemia, platelet dysfunction (loss of vitamin K)

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40
Q

Adverse effects of cephalosporins

A

Thrombophlebitis in older patients (Vit K def), cross allergenicity w/PCN, diarrheal superinfection, hemolytic anemia (vit K def) and nephrotoxicity.

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41
Q

Why shouldn’t patients drink alcohol when taking 2nd generations cephalosporins?

A

Inhibition of aldehyde dehydrogenase in ethanol metabolism results in build up of toxic acetaldehyde intermediate.

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42
Q

Most beta lactams are weak organic acids and are cleared by renal organ anion transports. Which beta lactams are the exception to this rule?

A

Penicillinase resistant beta lactams: nafcillin and oxacillin. Some cephalosporins (ceftriaxone and cefoperazone)

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43
Q

What is augmentin?

A

Amoxicillin (beta lactam) + clavulonate (beta lactamase inhibitor) overcomes beta lactam resistance in some bacteria.

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44
Q

Why does augmentin not work in MRSA patients?

A

Although clavulonate in augmentin overcomes the beta-lactamase, there is also decreased affinity of penicillin binding proteins. Note that MRSA is also resistant to cephalosporin

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45
Q

Why might gram negative bacteria have a particular advantage in become resistant to beta lactam antibiotics?

A

They have an outer membrane through which the beta lactams must travel. The drug must pass through porins that can mutate and prevent the beta-lactams from gaining access to the cell wall. They also have efflux pumps that pump the drug out of the bacteria’s cytoplasm.

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46
Q

How do vancomycin and telcoplanin work?

A

Inhibition of the transglycosylase step by binding D-Ala-D-Ala and sterically inhibiting it from interacting with the enzyme.

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47
Q

What organisms are vancomycin and telcoplanin useful for?

A

Gram positives only (most effective against staph, strep and MRSA in pneumonia, it can also reach the CNS if meninges are inflamed), this is because they are large molecules that cannot fit through the gram negative outer membrane porin channels.

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48
Q

When do you use oral vancomycin?

A

C. difficile colitis

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49
Q

How is vancomycin eliminated?

A

Renally

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50
Q

Adverse effects of vancomycin?

A

Red Man Syndrome exfoliative dermatitis (directly causes mast cell degranulation and histamine release, NOT AN ALLERGIC REACTION). Nephrotoxicity. Ototoxicity.

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51
Q

How to treat red man syndrome caused by vancomycin

A

Antihistamines and slow IV infusion

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52
Q

Why might teicoplanin be a better option if someone had a bad reaction to vancomycin in the past?

A

Less histamine release, less nephrotoxicity and no ototoxicity.

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53
Q

What antibiotics are involved in inhibition of the cell membrane potential?

A

Lipopeptides: daptomycin

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54
Q

How does IV daptomycin work?

A

Binds to cell membrane, forms a channel, K+ leaks out and membrane depolarizes.

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55
Q

What bugs does daptomycin work against?

A

Gram + aerobes and anaerobes, especially those resistant to vancomycin, methicillin and linezolid.

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56
Q

What drugs are involved in disruption of bacterial membranes? What bugs are they effective against?

A

IV polymyxins. Good against gram negatives (including acinetobacter from Iraq).

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57
Q

Adverse effects of polymyxins

A

Nephrotoxicity and neurotoxicity

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58
Q

Mammalian ribosome vs. bacteria ribosome

A

Mammalian = 80S, bacteria = 70S

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59
Q

How does protein synthesis normally occur in bacteria?

A

Initiation factors send 30S to mRNA start codon -> Start codon lines up with 30S “P” site -> EF-T brings tRNA to start codon -> Initiation factors bring in 50S to form the initiation complex -> tRNA binds mRNA at A site -> peptidyl transferase forms a peptide bond between 2 amino acids -> tRNA leaves and translocase shifts ribose down to next codon with assistance of EF-G, which blocks binding to the A site while translocation is occurring.

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60
Q

What drugs are involved in inhibiting the 50S subunit in bacterial protein synthesis?

A

Oxazoladinones, macrolides, ketolides, lincosamines, streptogramins and chloramphenicol.

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61
Q

How do linezolid and posizolid work?

A

They are oxazoladinones, which means they bind to the 50s subunit and prevent formation of the 70s initiation complex.

62
Q

What bugs are oxazoladinones good for treating?

A

Gram + broad spectrum, MRSA, VRE, VISA, PRPN and multi-drug resistant strains.

63
Q

How are oxazoladinones taken and excreted?

A

Taken orally, excreted renally

64
Q

Side effects of oxazoladinones?

A

Enhances effects with adrenergics b/c it inhibits MAO. Nausea, vomiting. Rare myelosuppression.

65
Q

What drugs are involved in inhibiting the 30S subunit in bacterial protein synthesis?

A

Tetracyclines, glycylcylines and aminoglycosides. Tetracyclines and glycylcylines bind 30s and prevent binding of tRNA. Aminoglycosides freeze the initiation complex which causes misreading of mRNA and premature termination

66
Q

Why are tetracyclines active against bacteria and not host mitochondria?

A

The drug diffuses across gram negative porin channels in the outer membrane and is actively transported through the inner membrane into the cell. Mammalian cells lack the active transport system into the cytoplasm.

67
Q

What conditions are tetracyclines used to treat?

A

Broad spectrum gram positive, rickettsial disease (Rocky Mountain spotted fever) and spirochete disease (Lyme disease)

68
Q

What medication could a patient take that will render tetracyclines inactive?

A

Antacids. They require an acidic environment to be absorbed.

69
Q

Adverse effects of tetracyclines

A

Teeth and bone abnormalities due to deposition in bone. This is why the drug is never used in children < 8 years old.

70
Q

What are the mechanisms of resistance cells have against tetracycline?

A

Efflux pumps, ribosome protecting proteins (Tet-O forces dissociation of tetracycline) and enzymatic inactivation.

71
Q

What bugs are glycylcyclines good for?

A

Broad spectrum against gram +/- and anaerobes/aerobes.

72
Q

What patients are ideal for administration of glycylcyclines?

A

Renal failure or mild to moderate hepatic failure. This is because it is not extensively metabolized and the kidney is not the main metabolizer.

73
Q

Adverse effects of glycylcyclines

A

Nausea, diarrhea, interaction w/warfarin and OCPs.

74
Q

Mechanisms of resistance to glycylcyclines

A

Not susceptible to efflux pump or TetO like tetracycline is; however, it is susceptible to mono-oxygenase Tet(X) inactivation by oxidation and AcrAB transport system.

75
Q

What drugs fall into the class of aminoglycosides?

A

Streptomycin, gentamicin, neomycin, kanamycin and spectinomycin.

76
Q

What bugs are amino glycosides effective against?

A

Broad spectrum gram - bacteria. Note that it passively diffuses through porin channels in the outer membrane and is actively pumped into the bacteria by the inner membrane. This makes it inactive against anaerobes that do not have active transport.

77
Q

What drugs are synergistic with aminoglycosides?

A

Beta lactams

78
Q

What tissues do aminoglycosides affect and how is it administered?

A

It is poorly absorbed so it must be given IV. It does not affect the lungs or eye and only crosses the BBB during active inflammation.

79
Q

How are aminoglycosides excreted?

A

Renally

80
Q

Adverse effects of aminoglycosides

A

Nephrotoxicity, ototoxicity, neuromuscular blockade (decreased ACh release and AChR sensitivity).

81
Q

How might you negate the neuromuscular blockade risk in a patient taking aminoglycosides?

A

Neostigmine (AChE inhibitor negates the decrease in ACh caused by aminoglycosides)

82
Q

Why does resistance to aminoglycosides occur frequently?

A

There are many open sites on the molecule available for enzymatic modification.

83
Q

How does chloramphenicol work?

A

It inhibits peptidyl transferase on the 50s subunit so polymerization of amino acids cannot occur during protein synthesis.

84
Q

What bugs are affected by chloramphenicol?

A

95% of gram negative strains, however this is used as a last resort and in foreign countries for typhoid fever, bacterial meningitis etc.

85
Q

How is chloramphenicol excreted?

A

Liver inactivation and renal excretion. This is why you have to reduce the dose in patients with liver failure.

86
Q

Adverse effects of chloramphenicol

A

Idiosyncratic aplastic anemic that may be irreversible, mammalian mitochondria inhibition, gray baby syndrome

87
Q

How do bugs become resistant to chloramphenicol?

A

Decreased membrane permeability and acetyl transferase activity. This is especially prevalent in Salmonella and Shigella.

88
Q

What do the letters stand for in the “MLS” group? How do these drugs work?

A

Macrolides, Lincosamides and Streptogramins. Theywork by inhibiting translocation of the 50s subunit.

89
Q

Macrolide drugs

A

Erythromycin, clarithromycin and azithromycin

90
Q

What bugs are macrolides effective against?

A

Gram + bacteria, especially strep (azithromycin is drug of choice for sinusitis and mild pneumonia).

91
Q

How are macrolides excreted?

A

Biliary

92
Q

What are adverse effects of macrolides?

A

Their metabolites inhibit CYP3A4 and thus have lots of drug-drug interactions (verapamil, lipitor, digoxin, metoprolol, rifampin, phenytoin, theophyline etc). Cholestatic hepatitis, prolonged QT w/V-tach, transient auditory impairment.

93
Q

Drug of choice for pregnant women with gram + bacterial infections

A

Azithromycin. Note that erythromycin is contraindicated later in pregnancy because of risk of cholestatic jaundice.

94
Q

How do bugs become resistant to macrolides?

A

Efflux pumps, MLSB determinant is a methylase that modifies the ribosome RNA so macrolides can’t bind, esterase hydrolysis

95
Q

Lincosamide drug is effective against what bugs?

A

Clindamycin is good for B. fragilis, Peptococcus and most clostridium, otherwise it is a broad-spectrum antibiotic.

96
Q

How is clindamycin excreted?

A

Renally and biliary

97
Q

What drugs should you never use in combination with clindamycin?

A

Macrolides and chloramphenicol. These binding sites are near those of clindamycin and can cause competitive inhibition of one another.

98
Q

Adverse effects of clindamycin

A

Inhibition of neuromuscular transmission, pseudomembranous colitis (C. Diff), skin rash in immunosuppressed patients.

99
Q

How do bugs become resistant to clindamycin?

A

MLSB determinant methylation of ribosomal RNA. Note that ATP-dependent efflux pumps render macrolides ineffective, but NOT clindamycin.

100
Q

Drugs that fall in the class of streptogramins? How do they work?

A

Dalfopristin (A) and quinupristin (B). Dalfopristin works by inducing a conformational change in 50S that increases binding of quinupristin. Quinupristin then inhibits 50S translocation. The combination of the 2 is called synercid.

101
Q

What bugs are streptogramins effective against?

A

Gram + cocci, VR E. faecium and skin staph/strep infections.

102
Q

How do you administer streptogramins?

A

IV in 5% dextrose over 1 hour

103
Q

Adverse effects of streptogramins?

A

Inhibition of CYP3A4. Arthralgias and myalgias due to metabolite accumulation.

104
Q

How do bugs become resistant to streptogramins?

A

Efflux pumps, MLSB ribosomal RNA methylation, lactonases and acetyl transferases.

105
Q

How does nitrofurantoin work?

A

Inhibition of ribosomal proteins, DNA damage, binding of bacterial proteins.

106
Q

What is nitrofurantoin used for?

A

UTI from E. coli, staph aureus and E. faecalis. This is because bactericidal concentrations are only reached when the drug is concentrated in the urine in the bladder.

107
Q

Adverse effects of nitrofurantoin

A

Neuropathy, hemolytic anemia in G6PD.

108
Q

When is nitrofurantoin safe in pregnancy?

A

1st 2 trimesters

109
Q

How do antibiotics target DNA biosynthesis without harming mammalian cells? What are the types of antibiotics that do this?

A

Bacteria have enzymes to synthesize folic acid and mammalians do not. Sulfonamides and benzylpyrimidines do this.

110
Q

Drugs to know in the sulfonamide antibiotic class

A

Sulfisoxazole and sulfamethoxazole

111
Q

What bugs are sulfonamides used to treat?

A

Broad spectrum against UTIs, meningitis and pneumocystic pneumonia

112
Q

What tissues do sulfonamides find to treat infections?

A

Broad distribution to include the CNS.

113
Q

What drug interactions occur in patients who take sulfonamides?

A

Potentiation of anticoagulants, sulfonylureas, hydantoin anti seizure drugs. Hypersensitivity reactions (to include Stevens-Johnson syndrome with high incidence in patients with HIV), crystalluria (from high [drug] that precipitates) and pancytopenia.

114
Q

What is responsible for the hypersensitivity reaction (Stevens-Johnson syndrome) in patients with HIV who take sulfamethoxazole?

A

Covalent binding of macromolecules in the drug elimination phase. The drug-protein complex serves as the antigen that triggers the IgE and/or autoantibody response. In patients with HIV this process is exacerbated because acetylation is slow and HIV proteins (TAT) affect drug metabolism, allowing for more time to form that antigen.

115
Q

How do bugs become resistant to sulfonamides?

A

Increased PABA production (sulfonamides competitively inhibit dihydropteroate synthase), dihydropteroate synthase become resistant, decreased bacterial permeability and efflux pumps.

116
Q

Drug to know in the benzylpyrimidine class of antibiotics? How does it work?

A

Trimethoprim. It inhibits dihydrofolate reductase.

117
Q

What bugs are covered by trimethoprim?

A

Broad spectrum against gram + and gram -. Note that this TMP-SMX can access the prostate and is not safe in pregnancy.

118
Q

Adverse effects of trimethoprim

A

Pancytopenia in patients with folate deficiency, skin hypersensitivity and permanent damage in patients with renal disease.

119
Q

How do bacteria become resistant to trimethoprim?

A

Increased production of dihydrofolate reductase, reduced permeability and efflux pumps.

120
Q

What happens when you combine trimethoprim with sulfamethoxazole (TMP-SMX)?

A

Two bacteriostatic drugs become bactericidal

121
Q

What drugs are involved in inhibition of DNA replication or transcription?

A

Fluoroquinolone (inhibit DNA gyrase and topoisomerase, note bacteria don’t have a gyrase and mammalian topoisomerase is only inhibited at high concentrations), nitroimidazoles (metronidazole), rifamycins (rifampin and rifaximin)

122
Q

Bugs affected by fluoroquinolone

A

DNA gyrase inhibition covers gram -, topoisomerase inhibition covers gram + bacteria.

123
Q

Drug you need to know that falls in the fluoroquinolone class

A

Ciprofloxacin

124
Q

Adverse interactions of fluoroquinolones

A

Absorption blocked by dairy and antacids, increases theophylline levels and can cause seizures & cardiorespiratory failure, cartilage damage in fetus and nursing babies, retinal detachment.

125
Q

How do bugs become resistant to fluoroquinolones?

A

Decreased permeability, efflux pumps, decreased affinity of DNA gyrase or acquisition of a new DNA topoisomerase IV.

126
Q

What bugs are susceptible to treatment with nitroimidazoles?

A

Anaerobic bacteria (bacteroides, clostridium, eubacterium, peptococcus and peptostreptococcus) and protozoa. Specifically those involved in GI infection, vaginitis.

127
Q

How do nitroimidazoles work?

A

Radical-mediated DNA damage from metabolites after 1st pass through liver.

128
Q

What drug interactions should you be aware of when giving nitroimidazoles?

A

Barbiturates induce liver enzymes and decrease its half life. Metronidazole interferes with alcohol metabolism.

129
Q

How do bugs become resistant to nitroimidazoles?

A

nim genes

130
Q

How do rifamycins work?

A

They inhibit RNA synthesis by covalently binding the bacterial DNA-dependent RNA polymerase (which is different from eukaryotic cells)

131
Q

What bugs are rifamycins effective against?

A

Breast spectrum, typically used for Neisseria, Mycobacteria and prophylaxis for H. influenzae or meningococcal meningitis

132
Q

Adverse effects from rifamycins?

A

Red-orange tears, sweat, urine and feces. Induces liver enzymes and has lots of drug drug interaction (anticoagulants, OCPs and corticosteroids)

133
Q

How do bugs become resistant to rifamycins?

A

Decreased affinity of RNA polymerase for drug

134
Q

What drug is used for traveler’s diarrhea?

A

Rifamixin is used against E. coli, Shigella, Salmonella and enteropathogens.

135
Q

Antibiotic combinations to avoid

A

MLS and ketolides: these compete for the same site on bacterial enzymes. Aminoglycosides and tetracyclines: both use porin channels and inhibit cell permeability of the other antibiotic.

136
Q

Synergistic antibiotic combos

A

Sulfonamides + trimethoprim (inhibit different steps of DNA synthesis pathway). Streptogramins A and B (binding of one enhances binding of the other). Beta lactams and aminoglycosides (uptake of one enhances uptake of the other). Beta lactamase inhibitors and beta lactams (evades resistance enzymes)

137
Q

Drugs that are rendered ineffective by decreases in bacterial permeability

A

Aminoglycosides, chloramphenicol, sulfonamides, trimethoprim, fluoroquinolones and tetracyclines.

138
Q

Drugs that are rendered ineffective by active efflux pumps

A

Sulfonamides, tetracyclines, macrolides, streptogramin A and glycylcyclines

139
Q

How are penicillins enzymatically inactivated by bacterial resistance enzymes? Aminoglycosides? Chloramphenicol? Macrolides? Streptogramin A? Streptogramin B?

A

PCN = beta-lactamases. Aminoglycosides: group transferases. Chloramphenicol: acetyltransferase. Macrolides: esterases and hydrolysis. Streptogramin A: acetyltransferase. Streptogramin B: lactonases.

140
Q

How do bugs become resistant to MLS antibiotics?

A

Methylation of ribosomal binding site.

141
Q

How do bugs become resistant to tetracycline?

A

Ribosomal protection protein decreases drug binding

142
Q

3 ways to limit development of antibiotic resistance

A

Limit use in animal food, reduce unnecessary prescribing and use specific drugs instead of broad spectrum drugs.

143
Q

Beta lactam adverse effect

A

Allergy

144
Q

Glycopeptide (vancomycin) adverse effect

A

Red Man syndrome

145
Q

Aminoglycocides (streptomycin) adverse effect

A

Curare-like neuromuscular blockade

146
Q

Chloramphenicol adverse effect

A

Gray baby syndrome

147
Q

Ketolide adverse effect

A

Fatal liver toxicity

148
Q

Polymyxin adverse effect

A

Renal toxicity

149
Q

Sulfonamide adverse effect

A

Stevens-Johnson Syndrome

150
Q

Tx for MRSA

A

TMP/SMX, doxycycline or clindamycin are 1st line. Linezolid can be used in failure of 1st line drugs or in patients with allergies. Rifampin may be added for recurrent infection. Vancomycin for hospitalized patients with systemic infection.

Multisystems I (36 decks)

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