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Pharmacology > Antibiotic Charts > Flashcards

Antibiotic Charts Flashcards

1
Q

What is the MOA of penicillins?

A

inhibition of bacterial wall synthesis (stage 3)
-Bactericidal

*The primary mechanism of antibacterial action of the
penicillins involves inhibition of reactions involving transpeptidation

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2
Q

What is bactericidal vs bacteriostatic

A
  • cidal: organisms are killed

- static: organisms are prevented from growing

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3
Q

Describe the absorption of penicillins

A

-optimal absorption on an empty stomach

Pen G: IM/IV (poor oral)
Pen V: good oral
amox: good oral
Penicillinase-resistant: good oral (not methicillin or nafcillin)

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4
Q

Oral absorption of penicillins varies depending on __

A

acid stability

*use of insoluble salts to reduce absorption and extend duration of action

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5
Q

Describe the distribution of penicillins

A
  • Penetrate into tissue poorly

- can enter inflamed tissues or membranes more readily than normal

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6
Q

Describe the metabolism/excretion of penicillins

A
  • 90% Renal excretion

- excreted in breast milk

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7
Q

Common adverse reactions of penicillins

A

*Virtually non-toxic, except for hypersensitivity rxn

  1. anaphylaxis (type I, rare but life threatening)
  2. maculopapular or morbilliform skin rash
  3. Diarrhea (Amoxicillin-clavulanate > Ampicillin > Amoxicillin > Pen V)
  4. Seizures/convulsions or encephalopathy (high doses)
  5. “Salt effect” due to high doses of K+ or Na+ salts
  6.   Jarisch-Herxheimer reaction during syphilis treatment
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8
Q

Classes of penicillins

A
  1. Prototype: pen G (IV)
  2. Prototype/Acid-stable: pen V (PO)
  3. Penicillinase-Resistant: Methicillin, dicloxacillin
  4. Extended spectrum: amoxicillin, amox-clavulanate, ampicillin
  5. Anti-pseudomonal: Pip-taz, Ticarcillin-clavulante
  6. Beta-lactamase inhibitor: clavulanic acid, sulbactam
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9
Q

What is the spectrum coverage of prototype penicillins (penicillin G and V)

A

*Relatively narrow spectrum

  1. Cocci: gram + (Staph / Strep / Entero)
  2. Cocci: gram - (Neisseria, M. catarrhalis)
  3. Rods: gram +
  4. Anerobes (most but NOT Bacteroides)
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10
Q

What is Penicillin V commonly used to treat?

A

acute pharyngitis (S. pyogenes)

*or amoxicillin is used

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11
Q

What are penicillinase-resistant antibiotics?

A
  1. Oxacillin
  2. Dicloxacillin**
  3. Methicillin
  4. Nafcillin

*NOTE: All other PCN classes are penicillinase (β-lactamase) susceptible; unless combined w/β-lactamase inhibitor (amoxicillin-clavulanate [34] or piperacillin/tazobactam)

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12
Q

Describe the absorption of penicillinase-resistant antibiotics

(Oxacillin, Dicloxacillin, Methicillin, Nafcillin)

A

Good oral (NOT methicillin or nafcillin)

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13
Q

Describe the spectrum coverage of penicillinase-resistant antibiotics

A

*relatively narrow spectrum agents

penicillinase-producing S. aureus (MSSA**)

  • skin infections (NOT MRSA)
  • Gram + and gram - cocci

*No anerobes, no Gram negative rods

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14
Q

What is the clinical use of dicloxacillin?

A

MSSA

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15
Q

What are the extended spectrum penicillins?

A
  1. Amoxicillin
  2. amoxicillin-clavulanate
  3. ampicillin
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16
Q

Describe the absorption of extended spectrum penicillins

A
  • good oral
  • increased hydrophilicity (due to presence of amino (NH2) or carboxyl (COOH) groups) allowing penetration through porins out outer membrane of gram-neg. organisms
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17
Q

-increased hydrophilicity (due to presence of amino (NH2) or carboxyl (COOH) groups) allowing penetration through porins out outer membrane of gram-neg. organisms

A

extended spectrum penicillins

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18
Q

What is the spectrum of coverage for extended spectrum penicillins

A
  1. Rods: gram - (H. flu, E. coli, Proteus) gram neg bacilli
  2. Cocci: gram + (less than PenG/V)

*can be given w/ B-lactamase inhibitors to further extend their antimicrobial spectrum

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19
Q

Adverse reactions with extended spectrum penicillins

A
  1. diarrhea (less w/ amoxicillin)

2. superinfection (CDAD) possible

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20
Q

Clinical use of amoxicillin and ampicillin

A
  1. E. coli
  2. UTIs
  3. MSSA
  4. AOM
  5. acute pharyngitis
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21
Q

Examples of antipseudomonal pencillins

A

(Piperacillin / Ticarcillin ± β-lactamase inhibitor)

  1. Piperacillin-Tazobactam
  2. Ticarcillin-Clavulante
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22
Q

Describe the administration of antipseudomonal pencillins

A

IV (parenteral) only

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23
Q

Describe the spectrum coverage of antipseudomonal pencillins

A
  1. Pseudomonas aeruginosa
  2. Anaerobes including Bacteriodes fragilis
  3. Enterococci
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24
Q

What are the beta-lactamase inhibitors?

A
  1. Clavulanic acid
  2. Sulbactam

*often given with antipseudomonal penicillins

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25
Q

Clavulanic acid + amoxicillin = ____

Sulbactam + ampicillin = ____

A

Augmentin

Unasyn

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26
Q

What is the clinical use of antipseudomonal pencillins (Pip-Taz)

A

Pip-Taz: pseudomonas/opportunistic infection, B. Fragilis (intraabdominal and brain abscess)

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27
Q

What is the MOA of cephalosporins?

A

Inhibits bacterial wall synthesis (stage 3)
-bactericidal

*similar to penicillins but:
-Broader spectrum of action vs gram-negative bacteria
-Less susceptibility to narrow spectrum β-lactamases
but ESBLs are emerging
- Less cross-reactivity in penicillin sensitive patients

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28
Q

What is the metabolism/excretion of cephalosporins

A

renal excretion (almost all except ceftriaxone)

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29
Q

Describe the distribution of cephalosporins

A
  • penetrate well into most tissues and fluids (including placenta) except brain and CSF
  • *Major feature of 3rd generations–> penetrate into CSF
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30
Q

What is the spectrum coverage of cephalosporins

A

extended spectrum

-NOT susceptible to penicillinase

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31
Q

What are adverse reactions of cephalosporins?

A
  1. hypersensitivity allergies (skin rash)
    * less severe than penicillins (increased risk w/ 1st generations)–> should not be given to pts w/ hx of immediate sensitivity to penicillin
  2. superinfection w/ 2nd and 3rd generation agents
  3. action to suppress flora can intensify effect of oral anicoagulants (warfarin)
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32
Q

What are 1st generation cephalosporins

A
  1. Cephalexin
  2. Cefazolin
  3. Cephradine
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33
Q

What are 2nd generation cephalosporins

A
  1. Cefaclor
  2. Cefuroxime
  3. Cefoxitin
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34
Q

What are 3rd generation cephalosporins

A
  1. Ceftriaxone
  2. Cefdinir
  3. Ceftazidime
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35
Q

What are 4th generation cephalosporins

A
  1. Cefepime
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36
Q

Describe the PK of 1st generation cephalosporins

A
  1. good oral

2. Cefazolin in IV/IM only

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37
Q

Describe the PK of 2nd generation cephalosporins

A
  1. good oral

2. Cefoxitin in IV/IM only

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38
Q

Describe the PK of 3rd generation cephalosporins

A
  1. good oral

2. good CNS penetration

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39
Q

Describe the spectrum coverage of 1st generation cephalosporins

A
  1. Cocci: gram + cocci
    * have greater activity against S. aureus (MSSA) than pen G
  2. Rods: gram − bacilli (Proteus, E. coli, Klebsiella)
  • Similar to amoxicillin
  • more stable then penicillins to many beta-lactamases
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40
Q

Describe the adverse reactions of 1st generation cephalosporins

A
  1. diarrhea

2. increased risk of cross-hypersensitivity w/ penicillins

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41
Q

Describe the spectrum coverage of 2nd generation cephalosporins

A
  1. Rods: GREATER activity against gram − (H. flu, Enterobacter)
  2. Anaerobes including bacterocides fragilis*
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42
Q

Describe DDI and adverse reactions of 2nd generation cephalosporins

A
  1. enhancement of warfarin anticoagulant activity

2. superinfection (CDAD) possible

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43
Q

Describe the spectrum coverage of 3rd generation cephalosporins

A
  1. Rods: expanded gram − (excellent against pneumococci)– more active against enteric gram neg than 2nd generation
  2. good gram + cocci for ceftriaxone
  3. moderate antipseudomonal (Ceftazidime)
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44
Q

Describe adverse reaction of 3rd generation cephalosporins

A
  1. superinfection (CDAD) possible
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45
Q

What antibiotics work best against N. gonorrhea and N. menigitis

A

3rd generation cephalosporins

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46
Q

Clinical uses of 1st generation cephalosporins

A

Gram pos. cocci:

  1. MSSA (strep. staph.)–> surgical prophylaxis
  2. skin infection

Gram neg. bacilli

  1. pneumonia
  2. UTI
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47
Q

Clinical uses of 2nd generation cephalosporins

A

Gram neg. bacilli

  1. pneumonia
  2. UTIs
  3. AOM
  4. sinusitis

Anaerobes:

  1. peritonitis
  2. diverticulitis
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48
Q

Clinical uses of 3rd generation cephalosporins

A

Gram + cocci
1. pneumonia

Gram - cocci

  1. gonorrhea
  2. meningitis

Gram - bacilli

  1. UTIs
  2. pneumonia
  3. mengitis
  4. sepsis
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49
Q

A major distinction between 1st and 3rd generation cephalosporins is:
A. 3rd generation agents have less activity against Pseudomonas
B.  3rd generation agents have increased activity against chlamydia
C.  1st generation agents have increased penetration into the CNS
D.  3rd generation agents have increased activity against resistant gram-negative organisms
E.  1st generation agents have greater activity against methicillin-resistant Staphylococcus aureus

A

D. 3rd generation agents have increased activity against resistant gram-negative organisms

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50
Q

Amoxicillin (extended-spectrum penicillin) shares all of the following properties with cephalexin (1st C ) EXCEPT:
A.  Inhibition of cell wall synthesis
B.  Bactericidal action
C.  Elimination primarily by the kidneys
D.  Beta-lactam ring in structure
E.  High susceptibility to bacterial beta-lactamases

A

E.  High susceptibility to bacterial beta-lactamases

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51
Q

Select the FALSE statement concerning inhibitors of cell wall synthesis:
A.  Second generation cephalosporins have good-to excellent activity against anaerobic organisms.
B.  The concentration of penicillin G in the CSF is higher when administered to patients with meningococcal meningitis than it is when given to normal, uninfected patients.
C.  First generation cephalosporins have greater activity against Pseudomonal infections than third generation cephalosporins.
D.  First generation cephalosporins (e.g., cefazolin) should not be given to patients with a Type I anaphylactic reaction to amoxicillin.

A

C.  First generation cephalosporins have greater activity against Pseudomonal infections than third generation cephalosporins.

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52
Q

Describe the MOA of vancomycin

A

Inhibits bacterial wall synthesis (stage 2)–> blocks linear polymerization
-Bactericidal

*tricyclic glycopeptides acts by inhibiting cell wall synthesis at site different from pencillin

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53
Q

Describe the administration and elimination/metabolism of vancomycin

A
  • poor oral absorption except for GI tract indications

- renal excretion

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54
Q

Describe the spectrum coverage of vancomycin

A
  • narrow spectrum
    1. gram + cocci: MRSA, staph. strep., enterococci
    2. Anerobes: C. difficile
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55
Q

Describe the adverse reactions of vancomycin

A
  1. infusion related: chills/fever/rash (red man syndrome)
  2. ototoxicity
  3. renal toxicity
  4. routine monitoring of Cp levels
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56
Q

Describe the clinical uses of vancomycin

A

Gram + cocci: (MRSA)

  1. severe skin infection
  2. soft tissue infection

Anaerobes
1. pseudomembranous colitis (C. difficile)

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57
Q

What is the MOA of carbapenems

A

inhibition of bacterial wall synthesis (stage 3)

-Bactericidal

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58
Q

Describe the MOA of macrolides

A

Protein synthesis inhibition (50S)– blocks translocation of peptidyl tRNA from acceptor to donor site on ribosome– prevents elongation
-Bacteriostatic

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59
Q

What type of antibiotics are protein synthesis inhibitors?

A
  1. Macrolides
  2. Tetracyclines
  3. Clindamycin
  4. Aminoglycosides
  5. SMX-TMP–> inhibitor of intermediary metabolism
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60
Q

describe the absorption of macrolides

A
  • good oral (also IV)
  • concentrates in lungs

Eryth: absorption varies depending on salt form
Clarith: can be taken w/o meals
Azi: should be taken on empty stomach

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61
Q

Describe the metabolism/excretion of Erythromycin

A
  • QID

- Metabolized in liver and excreted in bile

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62
Q

Describe the metabolism/excretion of Azithromycin

A
  • QD

- not metabolized–> biliary excretion

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63
Q

Describe the metabolism/excretion of Clarithromycin

A
  • BID

- metabolism to active compound that is renally eliminated

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64
Q

Describe the distribution of macrolids

A
  1. distributed widely, also fetus

2. Azi-Clarith. accumulates in lungs, skin, sputum

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65
Q

The primary mechanism of resistance of gram-positive organisms to macrolide antibiotics is:
A.  Decreased activity of uptake mechanisms
B.  Decreased permeability of drug through cytoplasmic membrane
C.  Synthesis of drug-inactivating acetyltransferases
D.  Synthesis of esterases that hydrolyze the lactone ring
E.  Methylation of drug binding sites on the 50S ribosomal subunit

A

E.  Methylation of drug binding sites on the 50S ribosomal subunit

66
Q

Describe the spectrum coverage of macrolides

A
  • Extended spectrum:
    1. Gram positive cocci (strep. pneumoniae, pyogenes)
    2. gram neg. cocci (M. catarrhalis)
    3. Rods gram neg. bacilli (Legionella, Bordetella, H. pylori)
    4. Atypical: mycoplasma/chlamydia pneumonia
67
Q

Describe DDI and adverse reactions of macrolides

A
  1. GI disturbances (N/V, diarrhea, gut stimulation- esp. Erythro.)
  2. prolong QT interval
  3. hepatotoxicity
  4. DDI: due to inhibition of P450 metabolism (NOT azithro)
68
Q

What is the MOA of tetracyclines

A

Protein synthesis inhibition (30S)–> prevent access of aminoacyl tRNA to mRNA site – block addition AAs
-Bacteriostatic

69
Q

What are examples of tetracyclines

A
  1. Tetracycline
  2. Doxycycline
  3. Minocycline
70
Q

If the patient with CAP were prescribed erythromycin you should advise her to:
A.  Avoid exposure to sunlight
B.  Avoid taking supplemental iron tablets
C.  Decrease her intake of caffeinated beverages
D.  Have her serum creatinine checked before starting therapy
E.  Temporarily stop the antihistamine

A

C.  Decrease her intake of caffeinated beverages

71
Q

When are carbapenems typically used

A

wide spectrum (reserved for multidrug resistant organisms)

72
Q

Describe the administration and elimination of tetracyclines

A

Tetracycline: PO, renal excretion

Doxycycline: PO, biliary (NON-RENAL EXCRETION)

**best given on an empty stomach

73
Q

Describe the spectrum of tetracyclins

A
  • BROAD spectrum but many gram +/- now resistant
    1. Gram positive Cocci: strep, staph, MRSA w/ Doxy
    2. Gram neg. cocci: N. gonorrhea
    3. anaerobes
    4. ATYPICALS: chlamydia, mycoplasma, Ricketssia, spirochetes
74
Q

Describe the adverse reactions with tetracyclines

A
  1. GI upset
  2. Photosensitivity/sunburn
  3. yeast overgrowth/superinfection
  4. Depression of bone growth
  5. permanent discoloration of teeth
  6. cannot use in less 8y/o and preg
  7. Cannot take w/ diary products, antacids, or iron supplments–> ineractions w/ metal irons in stomach
  8. hepatotoxicity
75
Q

DDI w/ tetracyclines

A
  1. cannot take w/ antacids/iron supplements (metal ions): decrease bioavailability by forming insoluble salts
  2. increased metabolism of doxy w/ phenytoin, barbiturates, and carbamazepine
  3. oral anticoagulants: increased anticoag. effect
76
Q

What is the MOA of Clindamycin

A

protein synthesis inhibition (50S)- preventing translocation of peptidyl tRNA

*bacteriostatic BUT can be bacteriocidal against certain organisms at higher concentrations

77
Q

Describe the absorption, distribution, and elimination of clindamycin

A
  • good PO (also IV)
  • penetrates into bone
  • Hepatobiliary elimination and excreted in breast milk
78
Q

Describe the spectrum coverage of clindamycin

A

*narrow spectrum

  1. gram positive cocci: staph, streph, MRSA, MSSA
  2. Anaerobes: Bacteroides fragilis

**DO NOT USE FOR C. DIFF

79
Q

What are the adverse reactions of clindamycin

A
  1. Pseudomembranous colitis if used w/ C. difficile
  2. severe diarrhea
  3. rare: neutropenia
80
Q

What is the clinical use of Clindamycin

A
  1. **treat of severe anaerobic infections like:
  2. intraabdominal and brain abscess
  3. acne (topically)
  4. pneumonia
  5. MSSA: osteomylitis
  6. MRSA: skin infection
81
Q

What are the clinical uses of tetracyclines

A 
1. acne (tetra and mino)
Doxy:
2. Ricketssia
3. Lyme disease
4. Chlamydia
5. Q fever
6. Cat scratch fever
7. RMSF
8. PID
9. MRSA
82
Q

What is the MOA of aminoglycosides

A
  • protein synthesis inhibition (30S)

- bacteriocidal

83
Q

What are examples of aminoglycosides

A
  1. Tobramycin
  2. Gentamycin
  3. Neomycin
  4. Streptomycin
84
Q

Describe the absorption and distribution of AGs

A
  • poor oral absorption (IV/IM*) QD
  • *NOT GOOD for CNS penetration
  • distributed in extracellular fluid
  • accumulates in kidney and inner ear
85
Q

Describe the elimination of AGs

A

renal excretion

86
Q

___ have a concentration-dependent killing and a postantibiotic effect

A

Aminoglycosides

87
Q

what does it mean to say AGs have concentration-dependent killing and a postantibiotic effect

A

concentration-dependent killing: increasing concentration s kill increasing proportion of bacteria at faster rates

a postantibiotic effect:bactericidal effect persists beyond plasma half-life

88
Q

Describe the spectrum coverage of aminoglycosides

A
  • narrow spectrum

1. Gram neg aerobes: E. coli, Pseudomonas**

89
Q

What are clinical uses of AGs

A
  • *Declining use due to toxicity
  • commonly used w/ PCN for broad spectrum empiric coverage
  1. Bowel sterilization presurgery (Neomycin)
  2. Tuberculosis (Streptomycin)
  3. Pseudomonas infections
  4. E. coli/UTI
90
Q

AGs are being replaced by

A
  1. FQ
  2. antipseudomonal PCNs
  3. 3rd generation cephalosporins
91
Q

Adverse Reactions of AGs

A
  1. vestibular and auditory toxicity (8th CN damage)
  2. nephrotoxicity
  3. routine monitoring of Cp levels** ( VERY TOXIC)
  4. skin rash
  5. neuromuscular block: resp. arrest
92
Q

DDI w/ AGs

A
  1. Synergy: enhanced AG entry brought about by β- lactam damage to the cell wall
  2. inhibitory effects: irreversible binding of AGs to certain PCNs can result in AG inactivation (both in vitro and in vivo)
93
Q

How is in vitro and in vivo inactivation w/ AG avoided?

A
  • In vitro inactivation is avoided by administering each drug individually
  • in vivo inactivation may be minimized by the timing of drug administration (β-lactam first)
94
Q

Select the TRUE statement regarding the pharmacologic actions of macrolide antibiotics:
A.  Erythromycin use is associated with less GI upset than clarithromycin.
B.  Possess bactericidal action via irreversible inhibition of protein synthesis.
C.  Erythromycin can elevate plasma levels of co-administered drugs metabolized by CYP450.
D.  Erythromycin has a longer half-life and requires less frequent administration than clarithromycin.
E.  Macrolides are more effective than metronidazole against anaerobic infections.

A

C.  Erythromycin can elevate plasma levels of co-administered drugs metabolized by CYP450.

95
Q

A 26-year-old woman was treated for gonorrhea at a neighborhood clinic. She was treated with a single IM dose of ceftriaxone and given a prescription for oral
doxycycline (100 mg bid x 7d). Two weeks later she returned to the clinic with a mucopurulent cervicitis. On
questioning she admitted not having the prescription filled. The best course of action at this point would be to:
A.  Delay drug treatment until the infecting organism is identified
B.  Rewrite the original prescription for oral doxycycline
C.  Treat her in the clinic with a single oral dose of amoxicillin
D.  Treat her in the clinic with a single oral dose of azithromycin
E.  Write a prescription for oral erythromycin for 7 days

A

D.  Treat her in the clinic with a single oral dose of azithromycin

96
Q

A 5-year-old kindergarten student presents with headache, fever, and cough of 2 days duration. Sputum is scant and nonpurulent and a Gram stain reveals many white cells but no organisms. Since this patient appears to have atypical (mycoplasmal) pneumonia, you should initiate treatment with:
A.  Azithromycin (Zithromax®)
B.  Doxycycline
C.  Cephalexin (Keflex®, a 1st generation cephalosporin)
D.  Chloramphenicol
E.  Either A or B

A

A.  Azithromycin (Zithromax®)

97
Q

Doxycycline is:
A.  Bactericidal
B.  Excreted mainly in the urine
C.  Eliminated rapidly and is dosed 4 times a day
D.  More effective than tetracycline against H. pylori
E.  Recommended therapy for community-acquired pneumonia

A

E.  Recommended therapy for community-acquired pneumonia

98
Q

A patient is being discharged from the hospital on a 3-week course of clindamycin. Which of the following potential adverse effects should be discussed with her?
A.  Nephrotoxicity
B.  Drug interactions due to enzyme induction
C.  C. difficile diarrhea
D.  Skin rash
E.  Ototoxicity

A

C.  C. difficile diarrhea

99
Q

Regarding the mechanism of action of aminoglycosides, the drugs:
A.  Are bacteriostatic
B.  Bind irreversibly to the 30S ribosomal subunit
C.  Cause misreading of the code on the mRNA template
D.  Inhibit peptidyl transferase
E.  Cause breakup of polysomes

A

B.  Bind irreversibly to the 30S ribosomal subunit

C.  Cause misreading of the code on the mRNA template

E.  Cause breakup of polysomes

100
Q

All of the following statements about the clinical uses of the aminoglycosides are accurate EXCEPT:
A.  They are effective in the treatment of Pseudomonal infections
B.  Owing to their polar nature, aminoglycosides are not absorbed after oral administration
C.  MRSA are usually sensitive to aminoglycosides
D.  Antibacterial action is concentration-dependent
E.  Ototoxicity due to aminoglycosides includes vestibular function and is often irreversible
F.   The earliest sign of aminoglycoside-induced nephrotoxicity is an increased blood creatinine

A

C.  MRSA are usually sensitive to aminoglycosides

101
Q 
A 30-year-old pregnant female has cellulitis caused by MRSA. Which of the following would be the most appropriate option for outpatient therapy? 
A.  Amoxicillin-clavulanate
B.  Ceftaroline 
C.  Clindamycin 
D.  Doxycycline 
E.  Minocycline 
F.   Vancomycin
A

C.  Clindamycin

102
Q

What is the MOA of Chloramphenicol?

A
  • protein synthesis inhibition (50S)

- bacteriostatic

103
Q

Describe the absorption and distribution of chloramphenicol

A
  • good PO (also IV)

- distributes to CNS/ CSF

104
Q

Describe the elimination/metabolism of chloramphenicol

A
  • metabolized by glucuronidation –> in fetus and neonate immature liver cannot conjugate this (toxic)
  • excreted in breast milk (avoid in preg. )
105
Q

Describe the spectrum of chloramphenicol

A

Broad spectrum but potential toxicity limits use in US

  1. Gram +
  2. Gram neg. (H. flu, Neisseria meningitis)
  3. Anaerobes (Bacteroides Fragilis**)
  4. Atypical (Rickettsia)
106
Q

What are adverse reactions of chloramphenicol

A
  1. bone marrow toxicity (avoid if leukopenic, aplastic and hemolytic anemic, or thrombocytopenic)
  2. Gray baby syndrome
  3. GI upset
107
Q

What is the MOA of Linezolid

A
  • protein synthesis inhibition (50S)

- bacteriostatic (-cidal for strep)

108
Q

Describe the absorption and elimination of Linezolid

A
  • excellent PO, also used IV

- eliminated by non-enzymatic oxidation (50%) plus renal (30%)

109
Q

Describe the spectrum of linezolid

A
  1. excellent gram positive (staph-MRSA, strep, entero-VRE)
    * reserve for use as alternative for MDR
110
Q

Describe the clinical use of Linezolid

A
  • Reserve for use as alternative for MDR and life-threatening conditions
    1. endocarditis (VRE)
    2. MRSA
    3. pneumonia
111
Q

What are the adverse effects of Linezolid

A
  • well tolerated
    1. Minor: diarrhea, HA, rash
    2. thrombocytopenia
    3. MAO inhibitor→serotonin sydnrome
112
Q

What is the MOA of Fluoroquinolones

A
  • inhibition of DNA gyrase

- bactericial

113
Q

Describe the absorption of Fluoroquinolones

A

good oral (also IV)

114
Q

What are examples of Fluoroquinolones

A
  • Ciprofloxacin (2nd generation)
  • Levofloxacin (3rd generation-respiratory)
  • Moxifloxacin (4th generation-respiratory)
115
Q

Describe the elimination of the Fluoroquinolones

A
  1. Cipro: primarily renal
  2. levo: primarily renal
  3. moxi: primarily hepatic (20% renal)
116
Q

What is spectrum coverage for Ciprofloxacin

A
  1. EXCELLENT gram neg: (Psuedomonas, H. influ
  2. atypicals

*NOT used for Gram positive (ie. CAP)

117
Q

What is the spectrum coverage for Levofloxacin?

A
  1. EXCELLENT gram positive: (s. pygoenes, and s. pneumoniae)– respiratory
118
Q

What is the spectrum coverage for Moxifloxacin?

A
  1. BEST gram positive (s. pygoenes, and s. pneumoniae), Anaerobic and Atypical
    * NOT gram neg. aerobes
119
Q

What are adverse reactions of FQ

A
  • well tolerated
    1. Superinfection
    2. some GI upset
    3. DDI w/ Theophylline and antacids
    4. CI in preg. and less than 18 y/o due to risk of tendon rupture/articular cartilage/ arthalgia–> may exacerbate myasthenia gravis
    5. prolong QT
120
Q

What are clinical uses of Cipro

A
  1. UTI
  2. pyelo
  3. gastroenteritis
121
Q

What are clinical uses of Levo

A
  • respiratory dz
    1. CAP
    2. UTI/pyelo
122
Q

What are clinical uses of Moxifloxcin

A
  1. resp. dzs
123
Q

what are DDI w/ FQ

A
  1. theophylline increased toxicity due to inhibition of metabolism
  2. antacids reduce oral absorption of cipro.
124
Q

Describe the MOA of Nitrofurantoin

A
  • reduced in cell to intermediates that damage bacterial DNA

- Bacericidal

125
Q

Describe the absorption and elimination of nitrofurantoin

A
  • rapid and complete GI absorption but rapid excretio via kidneys
  • thus acts as urinary antiseptic
126
Q

Describe the spectrum of nitrofurantoin

A
  1. E. coli
  2. enterococci

1st line agent in UTIs if TMP-SMX resistant E. Coli

127
Q

Adverse effets of nitrofurantoin

A
  1. GI upset (macrocrystalline forms are better tolerated)
  2. hypersensitivity pneumonitis
  3. chronic pulmonary fibrosis
  4. Category B in preg. BUT don’t use in 3rd trimester due to risk of hemolytic anemia in newborn*
128
Q

Clinical use of Nitrofurantoin

A
  1. 1st line agent in UTIs if TMP-SMX resistant E. Coli
  2. urinary antiseptic

**Cystitis/ uncomplicated UTIs

129
Q

What is the MOA of metronidzaole (Flagyl)

A
  • Prodrug reduced intracellularly to active form
  • interference w/ DNA fxn
  • bactericidal
130
Q

Describe the absorption and elimination of metronidazole

A
  1. good oral bioavilability

2. hepatic metabolism

131
Q

What is the spectrum coverage of Metronidazole?

A
  1. anerobes (C. diff, B. fragillis)

2. Protazoa (Giardia, trichomonias, amebias)

132
Q

Adverse effects of Metronidazole

A
  1. GI upset
  2. HA
  3. Candidal superinfection (furry tongue)
  4. inhibits aldehyde dehydrogenase and produces Antabuse-like effect) w/ alcohol is consumed w/in 3 days ((Disulfiram-like rxn))
133
Q

Clinical uses of metronidazole

A
  1. pseudomembranous colitis (c. diff)
  2. intraabdominal and brain abscess
  3. giardia
  4. gastritis/PUD
134
Q

What is the MOA of sulfamthoxazole Trimethoprim

A
  • inhibition of folate synthesis
  • interference w/ DNA synthesis
  • bacteriostatic if either used alone
  • *Bactericidal in combo (SMX/TMP)
135
Q 
Which antibacterial drug target is also present in humans? 
A.  70S ribosome 
B.  DNA gyrase 
C.  50S ribosomal subunit 
D.  Dihydropteroate synthesis 
E.  Dihydrofolate reductase
A

E.  Dihydrofolate reductase

136
Q

Describe the absorption and elimination of SMX/TMP

A
  • good oral (also IV)
  • best to take on an empty stomach
  • hepatic/renal elimination
  • excreted unchanged by kidney–> take w/ plenty of fluids (can be toxic bc of low solubility)
137
Q

Describe the spectrum of SMX/TMP

A
  • broad spectrum
    1. Gram positive: stap, strep, MRSA*
  • NOT ACTIVE AGAINST GAS
    2. Gram neg cocci: (Moraxella catarrhalis)
    3. Gram neg bacilli: (Klebsiella, proteus, entero, Pseudomonas**)
    4. Atypical (chlamydia, pneumocystis carinii)
138
Q

What is the 1st and 2nd best PO coverage for MRSA

A
  1. Linezolid

2. Bactrim (SMX/TMP)

139
Q

What are adverse reactions of SMX/TMP

A
  1. hypersensitivity skin reactions
  2. Steven Johnson Syndrome
  3. leukopneia, hemolytic anemia
  4. GI upset
  5. Hepatitis
  6. kernicterus in neonates
  7. renal crystalluria (rarely) via decreased H20 solubility of metabolites
  8. Avoid in pregnancy and infants
140
Q

Clinical uses of SMX/TMP

A
  1. UTI
  2. AOM
  3. ABECB
  4. MRSA

*PCP drug of choice

141
Q 
Which of the following treatments for urinary tract infections acts via a bacteriostatic action? 
A.  Sulfamethoxazole 
B.  Sulfamethoxazole-trimethoprim 
C.  Nitrofurantoin 
D.  Ciprofloxacin - uFQ 
E.  Levofloxacin - urFQ 
F.   Cephalexin - 1st C 
G.  Amoxicillin - ePCN
A

A.  Sulfamethoxazole

142
Q

What antibiotics treat strep. pneumo and strep. pyogenes

A
  1. Penicillins
  2. Cephalosporins
  3. Vancomycin
  4. Macrolides
  5. TCNs
  6. Clindamycin
  7. (Moxifloxacin*)

**NOT SMX-TMP, AGs, cipro, DNA inhibitors

143
Q

What antibiotics best treat MSSA

A
  1. Dicloxacillin
  2. Amox/clav
  3. pip/taz
  4. cephalosporins
  5. (protein synthesis inhibitors)
  6. (SMX-TMP)
144
Q

What antibiotics best treat MRSA

A
  1. Vancomycin
  2. TCNs
  3. Clindamycin
  4. SMX-TMP
145
Q

What antibiotics best treat N. gonhorrhea

A
  1. Ceftriaxone (3rd gen)
146
Q

What antibiotics best treat E. coli

A
  1. Amox/ampicillin
  2. amox/clav
  3. pip/taz
  4. SMX-TMP
  5. AGs
  6. Nitrofurantoin
  7. (Ciprofloxacin)
  8. (levofloxacin)
  9. 3rd gen cephalosporins
147
Q

What antibiotics best treat gram negative rods

A
  1. Amox/ampicillin
  2. amox/clav
  3. pip/taz
  4. SMX-TMP
  5. AGs
  6. Nitrofurantoin
  7. (Ciprofloxacin)
  8. (levofloxacin)
  9. (cephalosporins
148
Q

What antibiotics best treat pseudomonas

A
  1. Pip/taz
  2. Ceftazidimine (3rd gen. ceph)
  3. AGs
  4. (Ciprofloxacin)
  5. (levofloxacin)
149
Q

What antibiotics best treat c. diff

A
  1. Vancomycin

2. Metronidazole (DNA inhibitor)

150
Q

What antibiotics best treat most anaerobes

A
  1. penicillin
  2. cephalosporins
  3. moxifloxacin
  4. metronidazole
151
Q

What antibiotics best treat B. fragiliis

A
  1. PIP/taz
  2. Clindamycin
  3. Metronidazole
152
Q

What antibiotics best treat atypicals (chlamydia and mycoplasma)

A
  1. Macrolides
  2. TCNs
  3. Fluoroquinolones
  4. SMX-TMP– chlamydia only
153
Q 
Which drug inhibits the hepatic metabolism of co- administered drugs?
A.  Azithromycin 
B.  Doxycycline 
C.  Erythromycin 
D.  Amoxicillin 
E.  Tobramycin - AG 
F.   Ceftriaxone
A

C.  Erythromycin

154
Q

Which of the following drugs is INcorrectly matched with the mechanism of resistance to the organism?
A.  Amoxicillin –> decreased entry into Pseudomonas
B.  Azithromycin –> altered target in S. pneumoniae
C.  Penicillins —> altered target in S. pneumoniae
D.  Dicloxacillin –> altered target in MRSA
E.  Ceftriaxone –> enzymatic inactivation by MSSA
F.   Piperacillin –> enzymatic inactivation by MSSA

A

E.  Ceftriaxone –> enzymatic inactivation by MSSA

155
Q

A 24-year-old pregnant woman (24 weeks gestation) presents to the urgent care clinic with fever, urinary frequency and urgency. She is diagnosed with a urinary tract infection (UTI). Based on potential harm to the fetus, which of the following medications should generally be AVOIDED in treating her UTI?
A.  Nitrofurantoin
B.  Amoxicillin - ePCN C.  Cephalexin - 1st C
D.  Ampicillin
E.  Trimethoprim-sulfamethoxazole (weigh benefit risk)

A

E.  Trimethoprim-sulfamethoxazole (weigh benefit risk)

156
Q

Amoxicillin (a penicillin) and cephalexin (a cephalosporin) share all of the following properties EXCEPT:
A.  Inhibit cell wall synthesis
B.  Activity against gram negative organisms
C.  Elimination primarily by the kidneys
D.  Contain beta-lactam ring in structure
E.  Inactivation by penicillinase (NSBL)

A

E.  Inactivation by penicillinase (NSBL)

*if augmentin and cephalexin all share the same properties

157
Q

Vancomycin:
A.  Is bacteriostatic
B.  Binds to penicillin-binding proteins
C.  Is active against MRSA
D.  Has advantage of oral bioavailability
E.  Requires dosage reduction in renal impairment
F.   Is inactivated by beta-lactamases
G.  Acts at stage 2 of bacterial cell wall synthesis

A

C.  Is active against MRSA

E.  Requires dosage reduction in renal impairment

G.  Acts at stage 2 of bacterial cell wall synthesis

158
Q

Azithromycin and clarithromycin have very similar spectra of antimicrobial activity. Advantages of azithromycin include:
A.  Does not inhibit drug metabolizing enzymes
B.  Eradicates mycoplasmal infections in a single dose
C.  Is active against methicillin-resistant strains of staphylococci
D.  Is metabolized to an active metabolite
E.  Greater duration of activity

A

A.  Does not inhibit drug metabolizing enzymes

B.  Eradicates mycoplasmal infections in a single dose

E.  Greater duration of activity

159
Q 
Consumption of ethanol together with this drug causes nausea, vomiting, abdominal cramps, flushing, and headache in some patients. 
A.  Amoxicillin 
B.  Nitrofurantoin 
C.  Metronidazole 
D.  Doxycycline
E.  Erythromycin
A

C.  Metronidazole

160
Q

A 25-year-old male, otherwise healthy, comes to your office with symptoms of nasal congestion, clear rhinorrhea, and headache of 4 days duration. He reports that he was treated with penicillin V for strep throat as a 10 year-old
with no adverse responses. Six weeks ago he received a single IM dose of ceftriaxone for a gonococcal infection. Current clinical guidelines suggest that a reasonable initial course of action should be treatment with:
A.  Azithromycin
B.  High dose amoxicillin
C.  Amoxicillin plus clavulanate
D.  Oral 3rd generation cephalosporin (Cefdinir-Omnicef®)
E.  Ibuprofen as needed for pain and saline nasal lavage

A

E.  Ibuprofen as needed for pain and saline nasal lavage

Pharmacology (31 decks)

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