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deck_3522262 Flashcards

1
Q

Penicillin G, V

A

Prototype β-lactam antibiotics (penicillinase-sensitive)

  • Penicilling G → Iv and IM form
  • Penicillin V → oral
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2
Q

Penicillin G, V mechanism

A

Bind penicillin-binding proteins (transpeptidases). Block transpeptidase cross-linking of peptidoglycan in cell wall. Activate autolytic enzymes.

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3
Q

Penicillin G,V clinical use

A

​Mostly used for gram-positive organisms

  • S. pneumoniae
  • S. pyogenes
  • Actinomyces Gram negative cocci
  • N. meningitidis Spirochetes
  • T. pallidum Bactericidal for gram-positive cocci, gram-positive rods, gram-negative cocci, and spirochetes.Penicillinase sensitive.
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4
Q

Penicilling G, V toxicity

A
  • Hypersensitivity reactions

* Hemolytic anemia

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5
Q

Penicillin G, V resistance

A

Penicillinase in bacteria (a type of β-lactamase) cleaves β-lactam ring.

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6
Q

Aminopenicillins

A
  • ​amoxicillin

* ampicllinPenicillinase-sensitive penicillins

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7
Q

Aminopenicillin mechanism

A
  • Same as penicillin → wider spectrum,
  • Penicillinase sensitive.
  • Also combine with clavulanic acid to protect against destruction by β-lactamase.(amoxicillin and ampicillin)Note that amoxicillin has greater oral bioavailability than ampicllin.
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8
Q

Aminopenicillin clinical use

A

Exteneded spectrum penicillin

  • H. influenzae (gram negative)
  • H. pylori (gram negative, oxidase positive, comma shaped)
  • E. coli (gram negative rod)
  • Listeria monocytogenes (gram positive rod)
  • Proteus mirabilis (gram negative rod)
  • Salmonella (gram negative rod)
  • Shigella (gram negative rod)
  • enterococci(gram positive cocci)
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9
Q

Aminopenicillin toxicity

A
  • hypersensitivity reactions
  • rash
  • pseudomembranous colitis (ie C. dif, a gram positive rod)
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10
Q

Aminopenicillin resistance

A

Penicillinase in bacteria (a type of β-lactamase) cleaves β-lactam ring.

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11
Q

Penicillinase-resistant penicillins

A
  • Dicloxacillin
  • Nafcillin
  • Oxacillin
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12
Q

Penicillinase resistant penicillins mechanism

A

(dicloxacillin, nafcillin, oxacillin)Same as penicillin → narrow spectrum.Penicillinase resistant because bulky R group blocks access of β-lactamase to β-lactam ring.

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13
Q

Penicillinase resistant penicillins clinical use

A

(dicloxacillin, nafcillin, oxacillin)S. aureus (except MRSA; resistant because of altered penicillin-binding protein target site).

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14
Q

Penicillinase resistant penicillins toxicity

A
  • Hypersensitivity reactions

* interstitial nephritis

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15
Q

Antipseudomonals

A
  • Piperacillin

* Ticarcillin

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16
Q

Antipseudomonal mechanism

A

(piperacillin, ticarcillin)Same as penicillin. Extended spectrum.

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17
Q

Antipseudomonal clinical use

A

(piperacillin, ticarcillin)Pseudomonas spp. and other gram-negative rods.Susceptible to penicillinase; use with β-lactamase inhibitors.

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18
Q

Antipseudomonal toxicity

A

(piperacillin, ticarcillin) Hypersensitivity reactions.

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19
Q

Beta lactamase inhibitors

A
  • Clavulanic Acid
  • Sulbactam
  • TazobactamOften added to penicillin antibiotics to protect the antibiotic from destruction by β-lactamase (penicillinase).
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20
Q

Cephalosporins (generations 1-4) mechanism

A

β-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal.Organisms typically not covered by cephalosporins are LAME:

  • Listeria
  • Atypicals (Chlamydia, Mycoplasma)
  • MRSA
  • EnterococciException: ceftaroline covers MRSA.
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21
Q

First generation cephalosporins

A
  • Cefazolin (IV)

* cephalexin (oral)

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22
Q

First generation cephalosporin clinical use

A

1st generation (cefazolin, cephalexin)—

  • gram-positive cocci gram-negative rods
  • Proteus mirabilis
  • E. coli
  • Klebsiella pneumoniae Cefazolin used prior to surgery to prevent S. aureus wound infections.
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23
Q

Second generation cephalosporin clinical use

A

2nd generation (cefoxitin, cefaclor, cefuroxime)—

  • gram-positive cocci
  • Haemophilus influenzae
  • Enterobacter aerogenes
  • Neisseria spp.
  • Proteus mirabilis
  • E. coli
  • Klebsiella pneumoniae
  • Serratia marcescens
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24
Q

Second generation cephalosporins

A
  • cefoxitin (IV)
  • cefaclor
  • cefuroxime
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25
Q

Third generation cephalosporins

A
  • ceftriaxone
  • cefoxatime
  • ceftazidime
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26
Q

Third generation cephalosporin clinical use

A

3rd generation (ceftriaxone, cefotaxime,ceftazidime)—serious gram-negative infectionsresistant to other β-lactams.Ceftriaxone—meningitis, gonorrhea, disseminated Lyme disease (borrelia).Ceftazidime—Pseudomonas

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27
Q

Fourth generation cephalosporins

A

cefepime

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28
Q

Fourth generation cephalosporin clinical use

A

4th generation (cefepime)—gram-negativeorganismswith ↑activity against Pseudomonasand gram-positive organisms.

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29
Q

Fifth generation cephalosporins

A

Ceftaroline

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30
Q

Fifth generation cephalosporin clinical use

A

5th generation (ceftaroline)— broadgram-positive and gram-negative organism coverage, including MRSA.Does not cover Pseudomonas.

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31
Q

Cephalosporin toxicity

A
  • hypersensitivity reactions
  • autoimmune hemolytic anemia
  • disulfiram-like reaction
  • vitamin K deficiency
  • Exhibit cross-reactivity with penicillins, ↑nephrotoxicity of aminoglycosides.
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32
Q

Cephalosporin resistance

A

Structural change in penicillin-binding proteins (transpeptidases).

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33
Q

Carbapenems

A
  • imipenem
  • meropenem
  • ertapenem (limited Pseudomonas coverage)
  • doripenem
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34
Q

Carbapenem mechanism

A

Imipenem is a broad-spectrum, β-lactamase– resistant carbapenem. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to ↑inactivation of drug in renal tubules.

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35
Q

Carbapenem clnical use

A

(imipenem, meropenem, ertapenem, doripenem)

  • ​Gram-positive cocci
  • Gram-negative rods
  • AnaerobesWide spectrum, but significant side effects limit use to life-threatening infections or after other drugs have failed.Meropenem has a ↓risk of seizures and is stable to dehydropeptidase I.
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36
Q

Carbapenem toxicity

A
  • GI distress
  • skin rash,
  • CNS toxicity (seizures) at high plasma levels
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37
Q

Monobactams

A

Aztreonam

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38
Q

Monobactam mechanism

A

Prevents peptidoglycan cross-linking by binding to penicillin- binding protein 3.

  • Less susceptible to β-lactamases.
  • Synergistic with aminoglycosides.
  • No cross-allergenicity with penicillins.
39
Q

Monobactam clinical use

A

Gram-negative rods only—no activity against gram-positives or anaerobes.For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.

40
Q

Monobactam toxicity

A

Usually nontoxic; occasional GI upset.

41
Q

Glycopeptides

A
  • Bacitracin

* Vancomycin

42
Q

Vancomycin mechanism

A

Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors.Bactericidal. Not susceptible to β-lactamases.

43
Q

Vancomycin clinical use

A

Gram-positive bugs only—serious, multidrug-resistant organisms, including

  • MRSA
  • S. epidermidis
  • sensitive Enteroccocus species
  • Clostridium difficile (oral dose for pseudomembranous colitis)
44
Q

Vancomycin toxicity

A

Well tolerated in general—but NOT trouble free.

  • Nephrotoxicity
  • Ototoxicity
  • Thrombophlebitis
  • diffuse flushing—red man syndrome (can largely prevent by pretreatment with antihistamines and slow infusion rate)
45
Q

Vancomycin resistance

A

Occurs in bacteria via amino acid modification of D-ala D-ala to D-ala D-lac.

46
Q

Aminoglycosides

A
  • Gentamicin
  • Neomycin
  • Amikaein
  • Tobramycin
  • Streptomycin
47
Q

Aminoglycoside mechanism

A

Bactericidal.Irreversible inhibition of initiation complex through binding of the 30S subunit. Can cause misreading of mRNA. Also block translocation.Require O2 for uptake; therefore ineffective against anaerobes.

48
Q

Aminoglycoside clinical use

A

Severe gram-negative rod infections. Synergistic with β-lactam antibiotics.Neomycin for bowel surgery.

49
Q

Aminoglycoside toxicity

A
  • Nephrotoxicity
  • Neuromuscular blockade
  • Ototoxicity (especially when used with loop diuretics)
  • Teratogen.
50
Q

Aminoglycoside resistance

A

Bacterial transferase enzymes inactivate the drug by

  • acetylation
  • phosphorylation
  • or adenylation
51
Q

Tetracyclines

A
  • Tetracycline
  • Doxycycline
  • Minocycline
52
Q

Tetracycline mechanism

A

Bacteriostatic.Bind to 30S and prevent attachment of aminoacyl-tRNA.Limited CNS penetration. Doxycycline is fecally eliminated and can be used in patients with renal failure.Do not take tetracyclines with

  • milk (Ca2+),
  • antacids (Ca2+ or Mg2+),
  • or iron-containing preparationsbecause divalent cations inhibit drugs’ absorption in the gut.
53
Q

Tetracycline clinical use

A
  • Borrelia burgdorferi
  • M. pneumoniaeDrugs’ ability to accumulate intracellularly makes them very effective against Rickettsia and Chlamydia. Also used to treat acne.
54
Q

Tetracycline toxicity

A
  • GI distress
  • discoloration of teeth
  • inhibition of bone growth in children
  • photosensitivity
  • Contraindicated in pregnancy.
55
Q

Tetracycline resistance

A

↓ uptake or ↑efflux out of bacterial cells by plasmid-encoded transport pumps.

56
Q

Chloramphenicol mechanism

A

Blocks peptidyltransferase at 50S ribosomal subunit. Bacteriostatic.

57
Q

Chloramphenicol clinical use

A

Meningitis

  • Haemophilus influenzae
  • Neisseria meningitidis
  • Streptococcus pneumoniaeRocky Mountain spotted fever
  • Rickettsia rickettsiiLimited use owing to toxicities but often still used in developing countries because of low cost.
58
Q

Chloramphenicol toxicity

A
  • Anemia (dose dependent)
  • aplastic anemia (dose independent)
  • gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase).
59
Q

Chloramphenicol mechanism of resistance

A

Plasmid-encoded acetyltransferase inactivates the drug.

60
Q

Lincosamide

A

Clindamycin

61
Q

Clindamycin mechanism

A

Blocks peptide transfer (translocation) at 50S ribosomal subunit. Bacteriostatic.

62
Q

Clindamycin clinical use

A

Anaerobic infections (e.g.,

  • Bacteroides spp.
  • Clostridium perfringensin
  • aspiration pneumonia
  • lung abscesses
  • oral infections.Also effective against invasive group A streptococcal infection (strep pyogenes).[Treats anaerobic infections above the diaphragm vs. metronidazole (anaerobic infections below diaphragm)]
63
Q

Clindamycin Toxicity

A
  • Pseudomembranous colitis (C. difficile overgrowth)
  • fever
  • diarrhea
64
Q

Oxazolidinones

65
Q

Oxazolidinones mechanism

A

Inhibit protein synthesis by binding to 50S subunit and preventing formation of the initiation complex.

66
Q

Oxazolidinones clinical use

A

Gram-positive species including MRSA and VRE

67
Q

Oxazolidinones toxicity

A
  • Bone marrow suppression (especially thrombocytopenia)
  • peripheral neuropathy
  • serotonin syndrome
68
Q

Oxazolidinones resistance

A

Point mutation of ribsomal RNA.

69
Q

Macrolides

A
  • Azithromycine
  • Clarithomycin
  • Erythromycin
70
Q

Macrolide mechanism

A

(Azithromycin, clarithromycin, erythromycin)Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S ribosomal subunit. Bacteriostatic.

71
Q

Macrolide clinical use

A

Atypical pneumonias

  • Mycoplasma
  • Chlamydia
  • Legionella STIs
  • Chlamydia gram-positive cocci
  • streptococcal infections in patients allergic to penicillin
  • B. pertussis
72
Q

Macrolide toxicity

A
  • Gastrointestinal motility issues
  • Arrhythmia caused by prolonged QT interval
  • acute cholestatic hepatitis
  • rash
  • eosinophilia.
  • Increases serum concentration of theophyllines, oral anticoagulants.
  • Clarithromycin and erythromycin inhibit cytochrome P-450.
73
Q

Macrolide resistance

A

Methylation of 23S rRNA-binding site prevents binding of drug

74
Q

Floroquinolones

A
  • Ciprofloxacin
  • norfloxacin
  • levofloxacin
  • ofloxacin
  • moxifloxacin
  • gemifloxacin
  • enoxacin
75
Q

Floroquinolone mechanism

A

Inhibit prokaryotic enzymes topoisomeraseII (DNA gyrase) andtopoisomerase IV.Bactericidal. Must not be taken with antacids.

76
Q

Floroquinolone clinical use

A
  • Gram-negative rods of urinary and GI tracts (including Pseudomonas)
  • Neisseria
  • some gram-positive organisms
77
Q

Floroquinolone toxicity

A
  • GI upset
  • superinfections
  • skin rashes
  • headache
  • dizziness
  • Less commonly, can cause leg cramps and myalgias.
  • Contraindicated in pregnant women, nursing mothers, and children < 18 years old due to possible damage to cartilage.
  • Some may prolong QT interval.
  • May cause tendonitis or tendon rupture in people > 60 years old and in patients taking prednisone.
78
Q

Floroquinolone resistance

A
  • Chromosome-encoded mutation in DNA gyrase
  • plasmid-mediated resistance
  • efflux pumps
79
Q

Lipopeptide

A

Daptomycin

80
Q

Daptomycin mechanism

A

Lipopeptide that dirsupts cell membcane of gram-positive cocci.

81
Q

Daptomycin clinical use

A

S. aureus skin infections (especially MRSA) bacteremia endocarditis VRE(vancomycin resistant eneterococcus)Not used for pneumonia (avidly binds to and is inactivated by surfactant).

82
Q

Daptomycin toxicity

A

Myopathy rhabdomyolysis

83
Q

Nitroimidazole

A

Metronidazole

84
Q

Metronidazole mechanism

A

Forms toxic free radical metabolites in the bacterial cell that damage DNA.Bactericidal, antiprotozoal.

85
Q

Metronidazole clinical use

A

Treats

  • Giardia
  • Entamoeba
  • Trichomonas
  • Gardnerella vaginalis Anaerobes
  • Bacteroides
  • C. difficile Used with a proton pump inhibitor and clarithromycin for “triple therapy” against H. Pylori.Treats anaerobic infection below the diaphragmvs. clindamycin (anaerobic infections above diaphragm).
86
Q

Metronidazole toxicity

A

Disulfiram-like reaction with alcohol

  • severe flushing
  • tachycardia
  • hypotension
  • headache
  • metallic taste
87
Q

Sulfonamides

A

​Sulfamethoxazole (SMX) (short acting) Sulfisoxazole (topical) Sulfadiazine (short acting)

88
Q

Sulfonamide mechanism

A

Inhibit folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase.Bacteriostatic (bactericidal when combined with trimethoprim).(Dapsone, used to treat lepromatous leprosy, is a closely related drug that also inhibits folate synthesis.)

89
Q

Sulfonamide clinical use

A
  • Gram-positives
  • gram-negatives
  • Nocardia
  • Chlamydia
  • Triple sulfas or SMX for simple UTI
90
Q

Sulfonamide toxicity

A
  • Hypersensitivity reactions
  • hemolysis if G6PD deficient
  • nephrotoxicity (tubulointerstitial nephritis)
  • photosensitivity
  • kernicterus in infants
  • displace other drugs from albumin (e.g., warfarin)
91
Q

Sulfonamide resistance

A

Altered enzyme (bacterial dihydropteroate synthase), ↓uptake, or ↑PABA synthesis.

92
Q

Trimethoprim mechanism

A

Inhibits bacterial dihydrofolate reductase.Bacteriostatic.

93
Q

Trimethoprim clinical use

A

Used in combination with sulfonamides (trimethoprim-sulfamethoxazole [TMP- SMX]), causing sequential block of folate synthesis.Combination used for

  • UTIs
  • Shigella
  • Salmonella
  • Pneumocystis jirovecii pneumonia treatment and prophylaxis
  • toxoplasmosis prophylaxis
94
Q

Trimethoprim toxicity

A
  • Megaloblastic anemia
  • leukopenia
  • granulocytopenia(May alleviate with supplemental folinic acid)

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