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DD & BL Unit 2 > Antibiotics - Drug & Class Details > Flashcards

Antibiotics - Drug & Class Details Flashcards

1
Q

Penicillin G

A

MOA: Cell wall synthesis inhibition stage 3, bactericidal

PK: IM, IV (poor oral); renally excreted

Use limited to hospitalized patients with severe infections:

Gram positive cocci (Strep, entero)
C. perfringens

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2
Q

Penicillin V

A

MOA: Cell wall synthesis inhibition, stage 3; bactericidal

PK: Oral (acid stable); renally excreted

Gram positive cocci (Strep, Entero)
Anaerobes: C. perfringens

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3
Q

Dicloxacillin

A

Penicillinase-resistant Penicillin

MOA: Cell wall synthesis inhibition; bactericidal

PK: Oral administration; renal excretion

Spectrum/Uses:
Gram positive cocci (Strep, entero) + MSSA

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4
Q

Amoxicillin +/- Clavulanate

Ampicillin

A

Extended spectrum Penicillin

MOA: Cell wall synthesis inhibition; bactericidal; Increased hydrophilicity allows penetration through porins of gram negative OM; coupling to B-lactamase inhibitor allows activity against penicillinase-producing organisms

PK: Good Oral, Renally excreted

Spectrum:
Gram positive cocci (strep, entero) + MSSA
Gram negative rods (E. coli)
Anaerobes (C. perfringens, Bacteroides)

Adverse Reactions: Superinfection more likely, diarrhea (ampicillin > amoxicillin due to poorer oral absorption)

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5
Q

Piperacillin +/- Tazobactam

A

Antipseudomonal Penicillin

MOA: Cell wall synthesis inhibition; bactericidal; coupled to Beta lactamase inhibitor Tazobactam

PK: IV only

Spectrum:
Gram positive cocci (strep, entero) + MSSA
Gram negative rods (E. coli, K. pneumoniae, pseudomonas)
Anaerobes (C. perfringens, Bacteroides)

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6
Q

Cefazolin

A

1st Generation Cephalosporin

MOA: Cell wall synthesis inhibition, stage 3; bactericidal

PK: Oral absorption, renal elimination

Spectrum:
Gram positive cocci (Strep) + MSSA
Gram negative rods (E. coli, K. pneumoniae)

Adverse Reactions: Cross reactivity (1.5%) with penicillin hypersensitivity

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7
Q

Ceftriaxone

A

3rd generation Cephalosporin

MOA: Cell wall synthesis inhibition, stage 3; bactericidal

PK: IV, IM absorption with good CNS penetration

Spectrum:
Gram positive cocci (Strep) + MSSA
Gram negative cocci (N. gonorrhea)
Gram negative rods (E. coli, K. pneumoniae)

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8
Q

Vancomycin

A

MOA: Cell wall synthesis inhibition, stage 2; bactericidal

PK: Poor oral absorption - administered IV (except for GI C. diff); renal elimination

Gram positive cocci (Strep, entero) + MSSA + MRSA
Anaerobes (C. diff)

Adverse reactions: Infusion-related reactions (histamine flushing), nephrotoxicity, ototoxicity; Cp levels must be monitored. Pre-treat with diphenhydramine and acetaminophen.

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9
Q

Erythromycin

A

Macrolide class

MOA: Protein synthesis inhibition (50S); bacteriostatic

PK: Oral absorption; metabolized in liver and excreted in bile

Spectrum:
Gram positive cocci (Strep, Staph)
Gonorrhea
Atypicals (Mycoplasma, Chlamydia)

ARs: GI upset, DDI due to inhibition of P450 metabolism

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10
Q

Azithromycin

A

Macrolide class

MOA: Protein synthesis inhibition (50S); bacteriostatic

PK: Oral (empty stomach); biliary excretion

Spectrum:
Gram positive cocci (Strep, Staph)
Gonorrhea
Atypicals (Chlamydia, Mycoplasma)

ARs: GI disturbance (nausea, vomiting, diarrhea)

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11
Q

Clarithromycin

A

Macrolide class

MOA: Protein synthesis inhibition (50S); bacteriostatic

PK: Absorbed orally, metabolized to active compound that is renally eliminated

Spectrum:
Gram positive cocci (Strep, Staph)
Atypicals (Chlamydia, Mycoplasma)

ARs: GI disturbance, DDI due to inhibition of CYP450

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12
Q

Tetracycline

A

Tetracycline class

MOA: Protein synthesis inhibition; bacteriostatic

PK: oral administration, renal excretion

Spectrum - Broad (but high resistance)
Gram positive cocci (Strep, Staph + MSSA + MRSA)
Gram negative rods (E. coli, K. pneumoniae,)
Other Gram negatives (V. cholera, H. pylori)
Spirochetes (Borrelia burgdorferi)
Atypical (Mycoplasma, Chlamydia)

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13
Q

Doxycycline

A

Tetracycline class

MOA: Protein synthesis inhibition; bacteriostatic

PK: Oral administration, biliary excretion; choice for patients with renal disease

Spectrum - Broad (but high resistance)
Gram positive cocci (Strep, Staph + MSSA + MRSA)
Gram negative rods (E. coli, K. pneumoniae)
Atypicals (Mycoplasma, Chlamydia)

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14
Q

Clindamycin

A

Lincomycin class

MOA: Binds to ribosome preventing translocation of peptidyl tRNA; bacteriostatic

PK: Oral absorption, penetrates most tissues well (especially bone) but not CSF; metabolized by the liver and excreted through the bile

Spectrum:
Gram positive cocci (Strep, Staph + MSSA + MRSA)
Anaerobes (C. perfringens, Bacteroides)
Choice in CA-MRSA

ARs: Selection of C. diff overgrowth leading to pseudomembranous colitis; nausea, diarrhea

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15
Q

Ciprofloxacin

A

Fluoroquinolone Class, 2nd generation

MOA: Preferential inhibition of DNA gyrase; bactericidal

PK: Oral absorption, primarily renal excretion

Spectrum:
Gram negative rods (E. coli, K. pneumoniae, Pseudomonas)
Atypical (Chlamydia, Mycoplasma)

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16
Q

Levofloxacin

A

Fluoroquinolone Class, 3rd generation; “respiratory quinolone”

MOA: Inhibition of both DNA gyrase and Topoisomerase IV; bactericidal

PK: Oral absorption, primarily renal excretion

Spectrum
Gram positive cocci (Strep)
Gram negative rods (E. coli, K. pneumoniae, pseudomonas)
Atypical (Chlamydia, Mycoplasma)

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17
Q

Moxifloxacin

A

Fluoroquinolone Class, 4th generation, “respiratory quinolone)

MOA: Preferential inhibition of Topoisomerase IV; bactericidal

PK: Primarily hepatic excretion (20% renal)

Spectrum
Gram positive cocci (Strep)
Gram negative rods (E. coli, K. pneumoniae)
Atypicals (Chlamydia, Gonorrhea)

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18
Q

Nitrofurantoin

A

MOA: Reduced in cell to intermediates that damage bacterial DNA; bactericidal

PK: Rapid, complete GI absorption followed by rapid excretion via kidneys (contraindicated in renal impairment); not used for systemic infections because effective Cp cannot be obtained with safe doses

Spectrum:
Gram negative rods (E. coli, K. pneumoniae)

ARs: GI upset, occasional hypersensitivity, neuropathies

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19
Q

Metronidazole

A

MOA: Reduced intracellularly to active form, a highly reactive radical anion that interferes with DNA function; bactericidal

PK: Oral absorption, distribution includes CSF and bone; hepatic metabolism

Spectrum:
Anaerobes (C. diff, Bacteroides, H. pylori)
Protozoa (trichomoniasis, amebiasis, giardiasis)

ARs: Antabuse-like reaction (via inhibition of aldehyde dehydrogenase), GI upset, candidal superinfections

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20
Q

Penicillins - Adverse Reactions & Toxicity

A

Type I: Immediate hypersensitivity mediated by IgE & Mast cells (0.05%)

Maculopapular rash most common (1-4%), Diarrhea,

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21
Q

Penicillins - Mechanisms of Resistance

A

Production of penicillinase enzyme via plasmid transfer

Alterations of penicillin-binding proteins (responsible for MRSA)

Inability to penetrate into bacterial cell

Escape or Persisters - metabolically inactive organisms (“L forms”) that can survive in a hypertonic environment

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22
Q

Penicillins - Pharmacokinetics

A

Absorption: varies depending on acid stability
Pen G: IV or IM (poor oral)
Pen V, Amoxicillin, and Dicloxacillin: Good oral
Piperacillin: IV only

Distribution: strong acid, largely ionized at physiological pH; penetrates tissues poorly but enters inflamed tissues more easily

Metabolism/Excretion: Excreted as active drug via the kidney; also excreted into breast milk

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23
Q

Cephalosporins - Pharmacokinetics

A

Absorption: Oral, IV / IM

Distribution: Penetrate well into most tissues and fluids, including placenta; only 3rd gen penetrates into CSF

Metabolism-Excretion: Kidneys, requires renal dosing

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24
Q

Cephalosporins - Adverse Reactions

A

Hypersensitivity

Cross-hypersensitivity with Penicillins <1% - increased risk with 1st gen

Superinfection - increased risk with 2nd and 3rd gen

Alterations of normal gut flora may decrease synthesis of Vitamin K and intensify the anticoagulant effect of Warfarin

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25
Q

Vancomycin - Pharmacokinetics

A

Administered IV (poor oral absorption)

Excreted by kidneys; half life is extended in renal failure

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26
Q

Vancomyosin - Adverse Reactions

A

Ototoxicity, chills, fever, rash, renal toxicity

Routine monitoring of Cp levels required with infusion

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27
Q

B-lactamase Inhibitors

A

i.e. Clavulanic acid and Tazobactam

Resemble B-lactam molecules; they are potent, irreversible inhibitors of B-lactamase; they are coupled to a penicillins to extend the antibacterial spectrum against resistant organisms that exhibit B-lactamase activity

Clavulanic acid + Amoxicillin

Tazobactam + Piperacillin

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28
Q

Cefazolin

A

1st Generation Cephalosporin

MOA: Cell wall synthesis inhibition; bactericidal

PK: IV / IM

Spectrum:
Cocci: gram + (Strep, Staph, non MRSA)
Bacilli: gram - (Proteus, diarrhea E. coli, Klebsiella)

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29
Q

Aminoglycosides

A

MOA: Actively transported into cells (O2-dependent), binds irreversibly to bacterial ribosome, blocking initiation of translation; bacteriocidal

PK: IV/IM (poor oral) absorption; distribution is limited to extracellular fluid (excluded from CNS) but accumulates in renal cortex and inner ear; renal elimination - 1x/daily dosing possible due to concentration-dependent killing and post-antibiotic effect

Spectrum:
Gram negative rods (E. coli, K. pneumoniae, Pseudomonas)

ARs: Very toxic! 8th nerve damage, renal toxicity

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30
Q

Macrolides - Adverse Reactions & Toxicity

A

GI upset (worse with erythromycin due to direct sitmulation of gut motility)

Hepatotoxicity

Prolonged QT interval

DDIs due to inhibition of CYP450 (erythromycin and clarithromycin only)

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31
Q

Macrolides - Mechanism of Action

A

Macrolides bind to the 23S ribosomal RNA of the 50S subunit, preventing chain elongation and inhibiting protein synthesis

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32
Q

Tetracyclines - MOA and Resistance

A

MOA: Binds to ribosomal A site, preventing access of aminoacyl-tRNAs to the ribosomal active site; bacteriostatic

Resistance: Decreased influx, increased efflux, alterations to the ribosome that prevent tetracycline binding

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33
Q

Tetracyclines - Adverse Reactions & Toxicity

A

Inhibition of bone growth & discoloration of teeth (avoid use < 8 years old)

GI disturbance

DDIs with metal ions (antacids, iron) in stomach

Photosensitivity

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34
Q

Fluoroquinolones - MOA in Gram negative vs. Gram positive

A

Fluoroquinolones target DNA Gyrase and DNA Topoisomerase IV causing release of lethal, double-stranded DNA breaks

DNA gyrase is more susceptible to inhibition in Gram negative bacteria; Ciprofloxacin preferentially targets DNA gyrase and is more active against gram negative bacteria

DNA topoisomerase is more susceptible to inhibition in Gram positive bacteria; Levofloxacin and Moxifloxacin target Topoisomerase and so are effective against gram positive bacteria

35
Q

Tetracyclines - Pharmacokinetics

A

Oral absorption BUT impaired by milk products, metal cations, and iron salts

Distribution - good penetration into tissues, including placenta

Elimination - concentrated in liver, secreted into bile; tetracycline is excreted into urine (doxy and mino are not)

36
Q

Fluoroquinolones - Pharmacokinetics

A

Oral absorption

Good penetration into most tissues including high urinary levels

Primarily renal excretion

37
Q

Fluoroquinolones - Adverse Reactions

A

Overall very well tolerated but rarely GI upset, dizziness, headache

Black Box Warning: increased risk of tendon rupture and potential for arthropathies

DDIs with Theophylline and caffeine due to FQ inhibition of metabolism

DDIs with antacids containing metal cations; reduced oral absorption of FQ

38
Q

Community- vs. Hospital-acquired pneumonia

A

CAP: Strep pneumo is a normal flora in the oropharynx that can become micro-aspirated into the lungs, causing infection; treated with B-lactam + macrolide or respiratory fluoroquinolone (i.e. Ceftriaxone + Azithromycin)

HAP: Occurs as a result of colonization with gram negative rods that occurs in over 40% of patients by day 5 of a hospital stay; treated with Vancomycin + Pip-Tazo

39
Q

B - Lactams Mechanism of Action (Penicillins) & Cephalosporins

A

B-lactams irreversibly bind to and inactivate Penicillin Binding Proteins (PBPs) in the susceptible organism which carry out the transpeptidase (cross-linking) reaction necessary for peptidoglycan synthesis in the cell wall

40
Q

B-lactamase

A

B-lactamases are enzymes that inhibit B-lactam antibiotics by hydrolyzing the B-lactam ring; they can be encoded by chromosomal or plasmid genes and are found in both gram positive and gram negative bacteria; generally associated with gram negative enterics (E. coli, Enterobacter, Klebsiella)

41
Q

Methicillin Resistant Staph Aureus

A

MRSA contains an exogenous piece of DNA called staphylococcal chromosome cassette (SCCmec) containing the gene MecA which codes for PBP2a; PBP2a has low affinity for methicillin-type antibiotics

(Remember, MRSA also contains the plasma-encoded narrow spectrum B-lactamase that confers resistance to Penicillin & Ampicillin)

42
Q

Vancomycin - Mechanism of Action

A

Vancomycin binds to the terminal D-ala-D-ala portion of the five member peptide chain of the peptidoglycan precursor molecule which hangs off of MurNAc; it physically blocks the ability of the PBPs to put the precursor molecule into the growing peptidoglycan, thereby blocking both transglycosylase AND transpeptidase activity (stage 2 synthesis inhibitor)

43
Q

Mechanism of Vancomycin-Resistant Enterococci (VRE)

A

VRE expresses a plasmid-encoded VanA gene, which codes for an enzyme that results in synthesis of precursor peptidoglycan molecules with peptide chains terminating as D-ala-D-lactate; this modified peptidoglycan precursor binds Vancomycin with reduced affinity

Most VRE isolates are E. faecium; VRE is rarer in E. faecalis

*Also VERY RARELY seen in staph (VRSA)

44
Q

Mechanism of Vancomycin-intermediate S. aureus (VISA)

A

VISA expresses an unusually thick peptidoglycan cell wall that is less completely cross-linked and therefore contains free D-ala-D-ala tails which can bind Vancomycin, “absorbing” it into the wall and preventing its binding to peptidoglycan precursor molecules and inhibition of peptidoglycan synthesis

45
Q

Respiratory Fluoroquinolones

A

Levofloxacin and Moxifloxacin are respiratory fluoroquinolones because they preferentially target Topoisomerase IV in Gram positive organisms common in respiratory infections

Ciprofloxacin is NOT a respiratory fluoroquinolone because it preferentially targets DNA gyrase in gram negative organisms that are less frequently found in respiratory infections

46
Q

Mechanism of Fluoroquinolone resistance

A

Fluoroquinolone resistance occurs as a result of the accumulation of point mutations in the region GyrA of DNA gyrase or ParC of topoisomerase IV; these regions are called the quinolone-resistance-determining region (QRDR); these mutations reduce the affinity of the enzyme-DNA complex for the quinolone

47
Q

Macrolides - Resistance

A
  1. The erm gene, usually found on plasmids, encodes an enzyme that dimethylates the 23S ribosomal RNA, preventing macrolide (and clindamycin) binding

erm can be inducible or constitutive; microbes are resistant to Macrolides under inducible or constitutive conditions but resistant to clindamycin only under inducible conditions

  1. Macrolide-specific efflux pump
48
Q

D test

A

When an isolate is found to be macrolide resistant, the D test distinguishes between efflux- and erm-mediated resistance

Disks of erythromycin and clindamycin are placed on a plate spread with the test pathogen; if the pathogen expresses inducible erm then erythromycin will induce resistance to clindamycin and the zone of inhibition for clindamycin will be blunted, forming a “D” shape of colony growth; if the efflux system is present no blunting will occur

49
Q

Which antimicrobials are effective vs. MRSA?

A

Vancomycin
Clindamycin
Macrolides

50
Q

Which antimicrobials are effective vs. Pseudomonas?

A 
Pip/Tazo
Aminoglycosides 
Aztreonam
Ciprofloxacin
Levofloxacin
51
Q

Which antimicrobials are effective vs. Atypical organisms (Mycoplasma, Chlamydia)?

A

Macrolides
Tetracyclines
Fluoroquinolones (all)
SMX / TMP

52
Q

Which antimicrobials are effective vs. C. diff?

A

Vancomycin

Metronidazole

53
Q

1st generation Cephalosporins (2)

A

Cephalexin

Cephazolin

54
Q

Second generation Cephalosporins (2)

A

Ceflacor

Cefuroxime

55
Q

Third generation Cephalosporins (4)

A

Ceftriaxone
Ceftazidime
Cefdinir
Cefepime

56
Q

Carbapenem Agents (2)

A

Imipenem / Cilastatin

Ertapenem

57
Q

Carbapenem - Mechanism & Pharmacokinetics

A

Structurally related to B-lactams but are B-lactamase resistant; cell wall synthesis inhibitor (Stage 3)

IV/IM administration only
Penetrates CSF
Renal excretion

58
Q

Carbapenems - Spectrum

A

Gram positive cocci (except MRSA)
Gram negative rods (including Pseudomonas)
Anaerobic (including Bacteroides; not C.diff)

59
Q

Carbapenems - Adverse Reactions

A

Nausea, vomiting, diarrhea
Skin rash
Rarely seizures - usually in patients with a history of CNS and renal disease

60
Q

Cilastatin

A

Inhibits dihydroreductase in the kidney, which prevents Imipenem from being prematurely inactivated

61
Q

Aztreonam - Mechanism & Pharmacokinetics

A

Monobactam class; synthetic B-lactam ring that is resistant to B-lactamases

Administered IV/IM only
Penetrates CSF
Renal elimination

62
Q

Aztreonam - Spectrum

A

Gram negative, aerobic bacteria ONLY

Synergistic use with aminoglycosides vs. Pseudomonas

63
Q

Chloramphenicol - Mechanism, Pharmacokinetics

A

Protein synthesis inhibitor; binds 50S bacterial ribosome; bacteriostatic

Oral absorption with good distribution to the CNS
Hepatic elimination

64
Q

Gray baby syndrome

A

Toxic complication of chloramphenicol

Occurs in infants 2-9 days after therapy initiated with vomiting, abnormal respiration, cyanosis, and vasomotor collapse

40% mortality rate

65
Q

Chloramphenicol - Spectrum and Toxicity

A

Wide spectrum BUT not used in the US due to toxicity

Gram positive cocci (except MRSA) 
Gram negative cocci (Gonorrhea) 
Gram negative rods (except Pseudomonas) 
Anaerobes (except C. diff) 
Atypicals

Poor selectivity for bacterial ribosome; also inhibits ribosomes in mammalian bone marrow. Causes aplastic anemia / myelosuppression, requiring CBC monitoring every 2-3 days; also causes Gray Baby syndrome

66
Q

Streptogramins - Combo agent mechanisms & pharmacokinetics

A

Quinupristin / Dalfopristin (30:70)

Quinupristin binds to 50S ribosome (same sate as Macrolides) to inhibit peptide elongation

Dalfopristin binds at a nearby site on the 50S ribosome, inducing a conformational change that enhances Quinupristin binding

IV Administration only

67
Q

Streptogramins - Spectrum

A

Gram positive cocci (including MRSA and VRE)

Use held in reserve for life-threatening infections only

68
Q

Streptogramins - Adverse Effects

A

Irritation at infusion site
Arthralgias / myalgias
Nausea, diarrhea
Rash

69
Q

Linezolid - Mechanism & Pharmacokinetics

A

Oxazolidinone class; binds to 50S ribosome at a different site than other agents, so no cross-resistance with other protein synthesis inhibitors

Inhibits early formation of 70S ribosome complex; bacteriostatic

Administered oral or IV
Renally excreted but no dosage adjustment necessary in mild renal impairment

70
Q

Linezolid - Spectrum & Uses

A

Gram positive cocci (including MRSA and VRE)

71
Q

Linezolid - Adverse Effects / Toxicity

A

Well tolerated with minor side effects - diarrhea, headache, nausea

Rarely, thrombocytopenia

Inhibits MAO - risk of hypertensive response with co-administration of sympathomimetics or foods high in tyramine; serotonin syndrome if given with SSRIs

72
Q

Sulfamethoxazole / Trimethoprim - Mechanism

A

Sulfamethoxazole inhibits dihydropteroate synthetase

Trimethoprim inhibits dihydrofolate reductase

In combination, these two agents inhibit two sequential steps in the enzymatic conversion of PABA to tetrahydrofolic acid, necessary for synthesis of DNA and certain AAs

Bacteriostatic with delayed onset of action

73
Q

SMX / TMP - Pharmacokinetics & Adverse Effects

A

Good oral absorption with distribution into CSF

Hepatic acetylation to an inactive compound which can be toxic due to low solubility, causing renal crystalluria; Na-HCO3 alkalinizes the urine and decreases crystal formation

74
Q

SMX / TMP - Spectrum and Uses

A

Gram positive cocci including MRSA
Gram negative cocci (Gonorrhea)
Gram negative rods (including pseudomonas)
Atypical

75
Q

SMX / TMP - Adverse Effects

A

Sensitization - fever, rashes
Rarely - agranulocytosis, aplastic anemia, Stevens-Johnson Syndrome
Renal damage via crystalluria
Hemolytic anemia in patients with G6PD deficiency

Displaces bilirubin from albumin binding sites in infants, causing kernicterus

76
Q

Polymixins

A

Cell membrane disrupter; interacts with membrane phospholipids to lyse cells with detergent-like action; bactericidal

Active against gram negative only; used for pseudmonas meningitis after other agents have failed

Highly nephrotoxic

77
Q

Daptomycin

A

Binds to bacterial cell membrane causing rapid depolarization which inhibits protein, DNA, and RNA synthesis resulting in cell death (bactericidal)

Spectrum similar to Vancomycin; active against MRSA, including Vancomycin-resistant MRSA

IV administration
Renal elimination

78
Q

Treatment of uncomplicated Gonorrhea

A

Ceftriaxone - 250mg IM

Azithromycin (1g oral) OR Doxycycline (100mg 2x/day for 7 days) - empirical coverage of Chlamydia

79
Q

Treatment of ocular Chlamydia in infants

A

1% silver nitrate OR 1% tetracycline OR 0.5% Erythromycin topical to eyes at time of birth

80
Q

Treatment of pregnant women with Gonorrhea

A

3rd Generation Cephalosporins

81
Q

Treatment of uncomplicated Chlamydia

A

Azithromycin - 1g oral

OR

Tetracycline - 100mg BID x 7 days

82
Q

Prevention of neonatal transmission of Chlamydia

A

Erythromycin or amoxicillin to treat the mother

83
Q

Treatment of neonatal inclusion conjunctivitis (chlamydial)

A

Erythromycin (oral)

84
Q

Treatment of syphilis

A

Penicillin is first line

Azithromycin for patients who are penicillin allergic

DD & BL Unit 2 (7 decks)

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