Infectious Disease 1 Drug Cards

Front 1

Penicillin G

Back 1

Various Brands

Hint 1

Penicillins
Cell wall inhibitor
MOA: Bind transpeptidases (PBPs), block crosslinking of cells wall, activate autolyitc enzymes
Spectrum: Uncomplicated gram (+) cocci(Most Streptococcus species, S. viridans, S. pyogenes, Listeria monocytogenes (+), Clostridium perfringens (+, many resistant), Bacillis anthracis) ; uncomplicated N. gonorrhoeae, N. meningitidis and Haemophilus influenzae, Treponema Palladum, Borrelia Burgdorfi.
Resistant: Staph sp. and Strep pneumoniae
DOC for GAS
Cross BBB when meninges are inflamed; used as adjunct in bacterial meningitis
Gastric Juice destroys PenG; should be taken 1hr before or 2hrs after meals. T1/2 inc'd w/Probenacid
Mech of Resistance: Lack of porins, lack of appro. PBPs, mutations in genes of otherwise normal PBP's, homologous recombination (combo of sensitive and resistant genes)
Toxicity: hemolytic anemia, HSR's

Front 2

Penicillin V

Back 2

Veetids, Beepin, various others

Hint 2

Penicillins
Cell wall inhibitor
Spectrum: Uncomplicated gram (+) cocci(Most Streptococcus species, S. viridans, S. pyogenes, Listeria monocytogenes (+), Clostridium perfringens (+, many resistant), Bacillis anthracis) ; uncomplicated N. gonorrhoeae, N. meningitidis and Haemophilus influenzae, Treponema Palladum, Borrelia Burgdorfi.
Resistant: Staph sp. and Strep pneumoniae
DOC for GAS
Mech of Resistance: Lack of porins, lack of appro. PBPs, mutations in genes of otherwise normal PBP's, homologous recombination (combo of sensitive and resistant genes)

Front 3

Methicillin

Back 3

Various Brands

Hint 3

Semi-synthetic penicillinase-resistant penicillins
Cell wall inhibitor
Spectrum: B-lactamase expressing staph sp

Front 4

Nafcillin

Back 4

Nafcil, Unipen, Nalpen

Hint 4

Semi-synthetic penicillinase-resistant penicillins
Cell wall inhibitor
Spectrum: Methicillin sensitive b-lactamase expressing S. auerus and S. epidermidis.
Doses: Staphylococcal infections: 500 mg intravenously (IV) every 4 hours. For severe infections, 1 g every 4 hours is recommended. Levels should be checked and dosages adjusted accordingly in renal/hepatic dysfxn
AE: Vein irritation and extravasation, psuedo colitis, neurotoxic at large doses, HSR

Front 5

Oxacillin

Back 5

Bactocil

Hint 5

Semi-synthetic penicillinase-resistant penicillins
Cell wall inhibitor
Spectrum: No gram (–) coverage, used strictly in b-lactamase expressing staph infections, particularly S. aureus: Osteomyelitis – S. aureus
Bacteremia/Septicimia – S. aureus
Endocarditis – S. aureus and S. epidermidis
CNS infections - S. aureus
Dose: Staph infections: Mild to moderate infections: 250 to 500 mg IV every 4 to 6 hours. Severe infections: 1g IV every 4 to 6 hours.
AE: Psuedo colitis, neurotoxic at large doses, HSR

Front 6

Cloxacillin

Back 6

Cloxapen, Various others

Hint 6

Semi-synthetic penicillinase-resistant penicillins
Cell wall inhibitor
Spectrum: No gram (–) coverage, used strictly in b-lactamase expressing staph infections, particularly S. aureus: Osteomyelitis – S. aureus
Bacteremia/Septicimia – S. aureus
Endocarditis – S. aureus and S. epidermidis
CNS infections - S. aureus

Front 7

Dicloxacillin

Back 7

Diclocil, Various others

Hint 7

Semi-synthetic penicillinase-resistant penicillins
Cell wall inhibitor
Spectrum: No gram (–) coverage, used strictly in b-lactamase expressing staph infections, particularly S. aureus: Osteomyelitis – S. aureus
Bacteremia/Septicimia – S. aureus
Endocarditis – S. aureus and S. epidermidis
CNS infections - S. aureus

Front 8

Ampicillin

Back 8

Ominpen, Polycillin, Various others

Hint 8

Aminopenicillins- extended coverage agents
Cell wall inhibitor
Increased acid stability= >% oral F; excreted unchanged in the feces (70%)= diarrhea
Spectrum: Same as Pen G/V w/ addtional gram (-) coverage; Salmonella sp, Shigella sp (Most strains now resistant), Proteus mirabilis, E. coli
Indications: Respiratory: sinusitis, otitis media, bronchitis (S. pyogenes, S. pneumoniae (esp. amoxicillin), H. influenzae (amp-resistance growing). UTI: E. coli, Proteus mirabilis, Enterococcus sp. Meningitis: (In combos w/ other classes)Listeria monocytogenes. Others: Borrelia burgdorferi – Lyme disease

Front 9

Amoxicillin

Back 9

Amoxil, Trimox

Hint 9

Aminopenicillins- extended coverage agents
Cell wall inhibitor
95-100% absorbed--> less diarrhea
Spectrum: Same as Pen G/V w/ addtional gram (-) coverage; Salmonella sp, Shigella sp (Most strains now resistant), Proteus mirabilis, Escherichia coli; Enhanced H. Pylori coverage
Indications: Respiratory: sinusitis, otitis media, bronchitis (S. pyogenes, S. pneumoniae (esp. amoxicillin), H. influenzae (amp-resistance growing). UTI: E. coli, Proteus mirabilis, Enterococcus sp. Meningitis: (In combos w/ other classes)Listeria monocytogenes. Others: Borrelia burgdorferi – Lyme disease
AE: Diarrhea, N/V

Front 10

Bacampicillin

Back 10

Various

Hint 10

Aminopenicillins- extended coverage agents
Cell wall inhibitor
Ester prodrug of ampicillin--> increased absorption
Not really used

Front 11

Clavulanic Acid

Back 11

Augmentin (with amoxicillin)

Hint 11

β-lactamase inhibitors (polypharmacy only)
Cell wall Inhibitors
Mech leads to irreversible acylation of Ser-OH
"suicide substrate"

Front 12

Sulbactam

Back 12

Unasyn Injection (with ampicillin)

Hint 12

β-lactamase inhibitors (polypharmacy only)
Cell wall inhibitors

Front 13

Carbenicillin

Back 13

Geopen, Geocillin

Hint 13

Antipseudomonal penicillins: Carboxypenicillin
Cell wall inhibitors
Spectrum: Pseudomonas aeruginosa , Enterobacter sp., and certain Proteus sp.: P. mirabilis and P. vulgaris. Retain Gram + spectrum of Pen G but still ineffective against S. aureus
Used primarily in gram(–) UTI, RTI and osteomyelitis
Sensitive to b-lactamase

Front 14

Ticarcillin

Back 14

Ticar

Hint 14

Antipseudomonal penicillins
Cell wall inhibitors
Spectrum: Pseudomonas aeruginosa , Enterobacter sp., and certain Proteus sp.: P. mirabilis and P. vulgaris. Retain Gram + spectrum of Pen G but still ineffective against S. aureus
Used primarily in gram(–) UTI, RTI and osteomyelitis
Often dosed with tobramycin (T&T regimen)-->synergistic against pseudo; given as Na injection-->could lead to HTN
Sensitive to b-lactamase

Front 15

Ticarcillin with Clavulanic Acid

Back 15

Timentin

Hint 15

Antipseudomonal penicillins
Cell wall inhibitors

Front 16

Mezlocillin

Back 16

Mezlin

Hint 16

Antipseudomonal penicillins
Cell wall inhibitor
Spectrum: Superior activity against Pseudomonas aeruginosa, Enterobacter sp., and Klebsiella sp
Preserves ampicillin gram + coverage, but have higher gram – potency
Used as injection with particular emphasis on gram( –): Klebsiella pneumoniae, Enterobacter sp. (UTI & RTI), P. vulgaris and P. mirabilis (UTI and wounds), P. aeruginosa (UTI, burns and wounds), Providencia rettgeri (UTI and GTI)
Morganella morganii (wide nosocomial range), Serratia marcescens (UTI and wounds)
Sensitive to b-lactamase

Front 17

Piperacillin

Back 17

Pipracil

Hint 17

Antipseudomonal penicillins: Ureidopenicillin
Cell wall inhibitor
Spectrum: Superior activity against Pseudomonas aeruginosa, Enterobacter sp., and Klebsiella sp
Preserved Gram + activity (Enterococci sp., Streptococcus pyogenes and pneumoniae)
Expanded Gram (–) activity (all previous)
Most active against Pseudomonas
Clostridium sp. (+)
Bacteroides fragilis and other sp. (-)
Sensitive to b-lactamase

Front 18

Piperacillin with tazobactam

Back 18

Zosyn

Hint 18

Antipseudomonal penicillins
Cell wall inhibitor
Broadest spectrum of any penicillin

Front 19

Cefazolin

Back 19

Ancef, Kefzol, Others
(parenteral)

Hint 19

1st generation Cephalosporins
Cell wall inhibitor
Longer t ½ than some of the other 1st generations
Allows for q6h versus q4h dosing (IV/IM only)
Sensitive to B-lactamase

Front 20

Cephalexin

Back 20

Keflex, Keftab
(Oral)

Hint 20

1st generation Cephalosporins
Cell wall inhibitor
Spectrum: Most gram + Cocci (Streptococci; Staphylococci), Limited gram (–) spectrum: E.coli, Klebsiella and P. vulgaris/mirabilis
Inactive against: MRSA, MRSE, L. monocytogenes
Mainly excreted by the kidneys, activity enhanced by Probenecid

Front 21

Cefadroxil

Back 21

Duricef
(Oral)

Hint 21

1st generation Cephalosporins
Cell wall inhibitor
"amoxicillin-like" R-grp-->excellent oral F
Spectrum: Most gram + Cocci (Streptococci; Staphylococci), Limited gram (–) spectrum: E.coli, Klebsiella and P. vulgaris/mirabilis
Inactive against: MRSA, MRSE, L. monocytogenes

Front 22

Cefuroxime

Back 22

Kefurox, Zinacef
(Parenteral)

Hint 22

2nd generation Cephalosporins
Cell wall inhibitor
Syn-oriented methoxyimino resist attack by b-lactamases
Spectrum: Penetrates into CSF, active against H. influenzae, N. meningitidis, and S. pneumoniae. Somewhat increased gram (–) activity E. coli, Klebsiella, Proteus. Particularly against Bacteroides fragilis

Front 23

Cefuroxime Axetil

Back 23

Ceftin
(Oral)

Hint 23

2nd generation Cephalosporins
Cell wall inhibitor
Syn-oriented methoxyimino resist attack by b-lactamases
Spectrum: Penetrates into CSF, active against H. influenzae, N. meningitidis, and S. pneumoniae. Somewhat increased gram (–) activity E. coli, Klebsiella, Proteus. Particularly against Bacteroides fragilis
Axetil ester prodrug – increases lipophilicity, oral absorption, T1/2

Front 24

Cefoxitin

Back 24

Mefoxin
(Parenteral)

Hint 24

2nd generation Cephalosporins
Cell wall inhibitor
Increased steric bulk yields resistance to b-lactamases
Somewhat increased gram (–) activity E. coli, Klebsiella, Proteus. More active than any other ceph against anaerobes, especially Bacterioides fragilis

Front 25

Cefotetan

Back 25

Cefotan
(Parenteral)

Hint 25

2nd generation Cephalosporins
Cell wall inhibitor
Resistant to many b-lactamases
Somewhat increased gram (–) activity E. coli, Klebsiella, Proteus. Similar anaerobic activity to cefoxitin, good B. fragilis activity

Front 26

Cefaclor

Back 26

Ceclor
(Oral)

Hint 26

2nd generation Cephalosporins
Cell wall inhibitor
Excellent oral absorption, stable to metabolism
Somewhat increased gram (–) activity
E. coli, Klebsiella, Proteus, H. influenzae
Particularly against Bacteroides fragilis
Less active at gram (–) than other 2nd gen but strong activity against H. influenzae

Front 27

Cefprozil

Back 27

Cefzil
(Oral)

Hint 27

2nd generation Cephalosporins
Cell wall inhibitor
Somewhat increased gram (–) activity
E. coli, Klebsiella, Proteus, H. influenzae
Particularly against Bacteroides fragilis
Less gram + coverage than other 1st or 2nd

Front 28

Loracarbef

Back 28

Lorabid
(Oral)

Hint 28

2nd generation Cephalosporins
Carbacephem
Cell wall inhibitor
Somewhat increased gram (–) activity
E. coli, Klebsiella, Proteus, H. influenzae
Particularly against Bacteroides fragilis
Less active at gram (–) than other 2nd gen but strong activity against H. influenzae
More chemically stable, so bid vs tid dosing

Front 29

Cefotaxime

Back 29

Claforan
(Parenteral)

Hint 29

3rd generation Cephalosporins
Cell wall inhibitor
Syn-methoxyimino group which protects from b-lactamases
Similar activity against gram (+) cocci to the 1st generation
Excellent gram (–) activity: Enterobacteriaceae, H. influenzae, E. coli, N. gonorrhoeae, N. meningitidis, Klebsiella sp, Serratia marcescens, Salmonella sp., Proteus sp.

Front 30

Ceftizoxime

Back 30

Cefizox
(Parenteral)

Hint 30

3rd generation Cephalosporins
Cell wall inhibitor
Syn-methoxyimino group which protects from b-lactamases
Similar activity against gram (+) cocci to the 1st generation
Excellent gram (–) activity: Enterobacteriaceae, H. influenzae, E. coli, N. gonorrhoeae, N. meningitidis, Klebsiella sp, Serratia marcescens, Salmonella sp., Proteus sp.

Front 31

Ceftriaxone

Back 31

Rocephin
(Parenteral)

Hint 31

3rd generation Cephalosporins
Cell wall inhibitor
Syn-methoxyimino group as well as a metabolically stable group in place of acyl ester--> aids in protection from b-lactamases
Similar activity against gram (+) cocci to the 1st generation
Excellent gram (–) activity: Enterobacteriaceae, H. influenzae, E. coli, N. gonorrhoeae, N. meningitidis, Klebsiella sp, Serratia marcescens, Salmonella sp., Proteus sp.
T ½ of about 8 hours is the outstanding feature
Often the agent of choice in pen-sensitive treatment of bacterial meningitis

Front 32

Cefixime

Back 32

Suprax
(Oral)

Hint 32

3rd generation Cephalosporins
Cell wall inhibitor
Syn-oximino acidic ether suppresses b-lactamase activity
Similar activity against gram (+) cocci to the 1st generation
Excellent gram (–) activity: Enterobacteriaceae, H. influenzae, E. coli, N. gonorrhoeae, N. meningitidis, Klebsiella sp, Serratia marcescens, Salmonella sp., Proteus sp.

Front 33

Cefdinir

Back 33

Omnicef
(Oral)

Hint 33

3rd generation Cephalosporins
Cell wall inhibitor
Similar activity against gram (+) cocci to the 1st generation
Excellent gram (–) activity: Enterobacteriaceae, H. influenzae, E. coli, N. gonorrhoeae, N. meningitidis, Klebsiella sp, Serratia marcescens, Salmonella sp., Proteus sp.
Chelates Fe and gives stool red appearance--> imp in Fe-supplemented formula fed babies-->looks like blood in stool

Front 34

Cefpodoxime proxetil

Back 34

Vantin
(Oral)

Hint 34

3rd generation Cephalosporins
Cell wall inhibitor
Prodrug
Similar activity against gram (+) cocci to the 1st generation
Excellent gram (–) activity: Enterobacteriaceae, H. influenzae, E. coli, N. gonorrhoeae, N. meningitidis, Klebsiella sp, Serratia marcescens, Salmonella sp., Proteus sp.

Front 35

Cefditoren

Back 35

Spectracef
(Oral)

Hint 35

3rd generation Cephalosporins
Cell wall inhibitor
Similar activity against gram (+) cocci to the 1st generation
Excellent gram (–) activity: Enterobacteriaceae, H. influenzae, E. coli, N. gonorrhoeae, N. meningitidis, Klebsiella sp, Serratia marcescens, Salmonella sp., Proteus sp.

Front 36

Ceftibuten

Back 36

Cedax
(Oral)

Hint 36

3rd generation Cephalosporins
Cell wall inhibitor
Similar activity against gram (+) cocci to the 1st generation
Excellent gram (–) activity: Enterobacteriaceae, H. influenzae, E. coli, N. gonorrhoeae, N. meningitidis, Klebsiella sp, Serratia marcescens, Salmonella sp., Proteus sp.

Front 37

Ceftazidime

Back 37

Fortaz
(Parenteral)

Hint 37

3rd generation Cephalosporins
Cell wall inhibitor
Excellent activity against Pseudomonas and other gram (–) organisms: Enterobacteriaceae, H. influenzae, E. coli, N. gonorrhoeae, N. meningitidis, Klebsiella sp, Serratia marcescens, Salmonella sp., Proteus sp.
Complex syn-side chain offers protection from chromosomal and plasmid b-lactamases –increases activity against otherwise resistant bugs
Weaker activity against gram + than other cephs

Front 38

Cefepime

Back 38

Maxipime
(Parenteral)

Hint 38

4th generation Cephalosporins
Cell wall inhibitor
Increased activity against otherwise resistant organisms-->Increased stability from hydrolysis by plasmid and chromosomally mediated b-lactamase
Distinguished by enhanced anti staphylococcal activity and broader gram (–) spectrum
Excellent activity for streptococci and MSSA
Active against many Enterobacteriaceae, H. influenzae, N. gonorrhoeae, N. meningitidis –penetrates into CSF
Comparable to Fortaz for P. aeruginosa

Front 39

Ceftaroline Fosamil

Back 39

Teflaro
(Parenteral)

Hint 39

5th generation Cephalosporins
Cell wall inhibitor
Coverage includes MRSA , VRSA and linezolid-resistant SA, Pseudomonas sp., Pen-Res Streptococcus pneumoniae (CAP) and other Streptococcus sp. Retains enterobactericiae activity
NOT active against ESBL expressing bugs

Front 40

Ceftobiprol

Back 40

Zevtera (Phase III)

Hint 40

5th generation Cephalosporins
Cell wall inhibitor

Front 41

Imipenem / cilastatin

Back 41

Primaxin

Hint 41

Carbapenems
Cell wall inhibitor
Binds a variety of PBPs--> broad spectrum: Streptococcus sp. (including Pen-resistant S. pneumoniae), Staphylococcus sp. (including b-lactamase producing; some MRSA strains), Enterococcus sp. (faecium, facials), Excellent against Enterobacteriaceae (Including Ceph-resistant), Excellent against anaerobes…Bacteroides fragilis, Clostridium sp., Psuedomonas sp., Proteus sp., Serratia sp., H. influenzae, N. meningitidis
Highly resistant to b-lactamases; Used for ESBL expressing bacteria

Front 42

Meropenem

Back 42

Merrem

Hint 42

Carbapenems
Cell wall inhibitor
More stable to dehydropeptidase I (not cleaved)
Broad spectrum: Streptococcus sp. (including Pen-resistant S. pneumoniae), Staphylococcus sp. (including b-lactamase producing; some MRSA strains), Enterococcus sp. (faecium, facials), Excellent against Enterobacteriaceae (Including Ceph-resistant), Excellent against anaerobes…Bacteroides fragilis, Clostridium sp., Psuedomonas sp., Proteus sp., Serratia sp., H. influenzae, N. meningitidis
Indicated for intra-abdominal infections caused by covered organisms and bacterial meningitis

Front 43

Aztreonam

Back 43

Azactam

Hint 43

Monolactams
Cell wall inhibitor
Spectrum devoted almost exclusively to gram (–) organisms (Gram + and anaerobes--> no effect)
Inactivates some b-lactamases
Excellent against: Enterobacteriaceae, P. aeruginosa, H. influenzae and N. gonorrhoeae

Front 44

Ertapenem

Back 44

Invanz

Hint 44

Carbapenems
Cell wall inhibitor
A synthetic carbapenem that is more stable to dehydropeptidase I
Different spectrum of activity: E. coli, Bacteroides fragilis, S. aureus (NOT MRSA), S. pyogenes
NO P. aeruginosa COVERAGE
Unique feature: Long t ½ due to extensive binding to serum proteins

Front 45

Doripenem

Back 45

Doribax

Hint 45

Carbapenems
Cell wall inhibitor
More stable to dehydropeptidase I (not cleaved)
Broad spectrum: Streptococcus sp. (including Pen-resistant S. pneumoniae), Staphylococcus sp. (including b-lactamase producing; some MRSA strains), Enterococcus sp. (faecium, facials), Excellent against Enterobacteriaceae (Including Ceph-resistant), Excellent against anaerobes…Bacteroides fragilis, Clostridium sp., Psuedomonas sp., Proteus sp., Serratia sp., H. influenzae, N. meningitidis
Indicated for intra-abdominal infections caused by covered organisms and complicated UTI, including pyelonephritis

Front 46

Vancomycin

Back 46

Vancocin

Hint 46

Lipoglycopeptides
Cell wall inhibitor
MOA: Recognizes terminal d-ala d-ala, prevents cleavage by transpeptidase.
Nephrotoxic--> must be monitored; Given slow IV infusion
Useful spectrum is restricted to gram + microorganisms, particularly gram + cocci
Staphylococcus aureus, including MRSA
Staphylococcus epidermidis, including MRSE
Enterococcus faecium and E. faecalis
Streptocococcus pyogenes and S. pneumoniae
Clostridium difficile (oral)--> only acceptible use for oral vanc
Clostridium tetani

Front 47

Telavancin

Back 47

Vibativ

Hint 47

Lipoglycopeptides
Cell wall inhibitor
MOA: Vanc-like inhibition of cell wall and FA tails sticks in membrane-->causes leakage--> cell lyse
More potent than vanc
Spectrum: limited to gram (+) organisms; MSSA and MRSA,
More activity than Vancomycin at VISA, Enterococcus sp. Some Vancomycin resistant Enterococci (VRE) (depending on isolate), Streptococcus sp. (including pen and multidrug resistant isolates), B. anthracis, Listeria sp., C. difficile
Approved for complicated skin and skin structure infections caused by susceptible organisms
Adverse effects: N/V/D, fetal risk, Nephrotoxicity, C. difficile associated diarrhea, QTc Prolongation, Coagulation Test Interference

Front 48

Bacitracin

Back 48

Various

Hint 48

Cyclic polypeptide
Cell wall inhibitor
Nephrotoxicity limits to topical use
MOA: Inhibits late-stage cell wall synthesis, interferes with lipid carrier of PG building blocks.Thereby inhibiting the NAM and NAG to be transported out to PG layer
Spectrum: Broad Gram + activity, but some gram - :Neisseria sp. (-), H. influenzae (-), Clostridium difficile (+)

Front 49

Polymyxin B

Back 49

Various

Hint 49

Cell membrane disruptor
MOA: Alters cytoplasmic membrane permeability by binding to negatively charged sites-->Allows leakage of cytosolic components, Fatty acid portion dissolves in hydrophobic region of membrane and disrupts membrane integrity
Binds and inactivates endotoxin (LPS) in 1:1 ratio
Being used more and more as a aerosol for ventilator associa’d pneumonia

Front 50

Polymyxin E, aka Colistin

Back 50

Colymycin M

Hint 50

Cell membrane disruptor
Most gram (-), particularly P. aeruginosa
Serious Considerations include: Renal toxicity, variable CNS effects, Neuromuscular blockade
Very toxic, only used in special cases

Front 51

Daptomycin

Back 51

Cubicin

Hint 51

Cell Membrane Disruptors
MOA: Directly binds the membrane and causes depolarization and loss of membrane potential-->Does NOT cause rupture, but slow leakage of K-->no endotoxin released due to lysis--> No immune storm
Spectrum: Gram positive activity only; Enterococci sp. (including VRE), Staphylococci aureus (including MRSA, some VISA/VRSA), Streptococci sp.
Indicated for skin/skin structure infections caused by above agents and indicated for right-sided endocarditis caused by above agents-->inactivated by lung surfactants**--> cant be used for pneumonia or left-sided endocar

Front 52

Streptomycin

Back 52

Various

Hint 52

Aminoglycosides
Protein-Synthesis Inhibitors
MOA: Enters through porin channels and cross cell membrane via active, aerobic pumps. Irreversibly binds to a single domain on the 30S ribosomal subunit. 1) Blocks initiation of protein synthesis 2) Blocks further translation and elicits premature termination 3) Incorporation of the incorrect aa
Spectrum: primarily aerobic gram(-) esp. mycobacterium tuberculosis (in combo with another agent) and Yersinia pestis with limited gram(+) coverage: Streptococcus sp., Enterococcus sp. (In combo with CWI , Vancomycin and AG), Excellent synergism with b-lactams for gram + infections but resistance is emerging (enzymatic alterations)
Used in TB, more serious sepsis, bone, endocarditis, RTI, skin/burn infections, bubonic and pneumonic plague
AE: nephrotoxicity, ototoxicity (may be irreversible), NM blockade (do not use in myasthenia gravis)

Front 53

Gentamicin

Back 53

Garamycin

Hint 53

Aminoglycosides
Protein-Synthesis Inhibitors
MOA: Enters through porin channels and cross cell membrane via active, aerobic pumps. Irreversibly binds to the A-site on the 16S subunit (of the 30S) ribosomal subunit. 1) Blocks initiation of protein synthesis 2) Blocks further translation and elicits premature termination 3) Incorporation of the incorrect aa
Spectrum: primarily aerobic gram(-) esp. P. aeruginosa, Enterobacter sp., Klebsiella sp., Serratia sp., and Y. pestis with limited gram(+) coverage: Enterococcus sp. (In combo with CWI , Vancomycin and AG), and Listeria monocytogenes (gram +). Typically never used alone in any gram + infection, but excellent synergist! Incompatible with b-lactam antibiotics if given in the same compartment.
Used in more serious sepsis, bone, endocarditis, RTI, skin/burn infections, bubonic and pneumonic plague
AE: nephrotoxicity, ototoxicity (may be irreversible), NM blockade (do not use in myasthenia gravis)

Front 54

Tobramycin

Back 54

Nebcin, Tobrex

Hint 54

Aminoglycosides
Protein-Synthesis Inhibitors
MOA: Enters through porin channels and cross cell membrane via active, aerobic pumps. Irreversibly binds to the A-site on the 16S subunit (of the 30S) ribosomal subunit. 1) Blocks initiation of protein synthesis 2) Blocks further translation and elicits premature termination 3) Incorporation of the incorrect aa
Spectrum: primarily aerobic gram(-) Superior activity against P. aeruginosa, esp. when used with antipseudomonal b-lactam (T&T regimen). Not as effective with Pen in treatment of Enterococci or other gram (+)
Used in more serious sepsis, bone, endocarditis, RTI, and skin/burn infections
AE: nephrotoxicity, ototoxicity (may be irreversible), NM blockade (do not use in myasthenia gravis)

Front 55

Amikacin

Back 55

Amikin

Hint 55

Aminoglycosides
Protein-Synthesis Inhibitors
MOA: Enters through porin channels and cross cell membrane via active, aerobic pumps. Irreversibly binds to the A-site on the 16S subunit (of the 30S) ribosomal subunit. 1) Blocks initiation of protein synthesis 2) Blocks further translation and elicits premature termination 3) Incorporation of the incorrect aa.
Large side chain protects from enzymatic attack
Broadest spectrum of all AGs; for use in resistance-incident settings-->Preferred agent in initial treatment of nosocomial gram (–) bacillary infections: Enterobacter sp., H. influenzae , P. mirabilis, E. coli, K. pneumoniae, Serratia marcescens, P. aeruginosa, Mycobacterium tuberculosis, Mycobacterium avium (MAC-M. avium complex) DOC by some for MAC/AIDS. Including gentamicin and tobramycin resistant species
AE: nephrotoxicity, ototoxicity (may be irreversible), NM blockade (do not use in myasthenia gravis)

Front 56

Neomycin

Back 56

Mycifradin, Neosporin, Various others

Hint 56

Aminoglycosides
Protein-Synthesis Inhibitors
MOA: Enters through porin channels and cross cell membrane via active, aerobic pumps. Irreversibly binds to the A-site on the 16S subunit (of the 30S) ribosomal subunit. 1) Blocks initiation of protein synthesis 2) Blocks further translation and elicits premature termination 3) Incorporation of the incorrect aa.
Broad spectrum includes gram(-): E. coli, Enterobacter sp., K. pneumoniae, P. vulgaris and gram(+):S. aureus (MSSA), E. faecalis. P. aeruginosa is resistant
Highly toxic if used systemically, oral use for surgical preparation. Used topically for S. aureus

Front 57

Tetracycline

Back 57

Sumycin, others

Hint 57

Tetracyclines
Protein-Synthesis Inhibitors
MOA: Reversibly binds to A site at 16S (of the 30S) ribosomal subunit (static). Passively diffuse through outer membrane and taken in by active aerobic pump
Pregnancy Cat D.
Spectrum: Primarily effective against: Rickettsia sp. (Rickettsia rickettsii –RMSF), Chlamydia sp., N. gonorrhoeae (used if PCN allergy), C. difficile, Combo treatment in resistant H. Pylori, in place of clarithromycin (+bismuth, metronidazole, PPI). Gram + cocci :Some S. aureus are sensitive so can be used IF susceptibility is confirmed eg, CA-MSSA, CA-MRSA (exception)
AE's: Pregnancy: Renal/Hepatic effects, Ca+2 effects, Hepatic toxicity: Inc’s BUN, Superinfections: Candida albicans and Clostridium difficile, sun sensitivity

Front 58

Oxytetracycline

Back 58

Terramycin, others

Hint 58

Tetracyclines
Protein-Synthesis Inhibitors
MOA: Reversibly binds to A site at 16S (of the 30S) ribosomal subunit (static). Passively diffuse through outer membrane and taken in by active aerobic pump
Pregnancy Cat D.
Spectrum/Indications: Low dose oral or topical therapy for acne vulgaris – Propionibacteria sp. (esp., P. acnes), Lyme Disease – Borrelia burgdorferi, Rickettsial Infections (Rickettsia sp., gram - ) - i.e, Rocky Mountain Spotted Fever, Chlamydia (gram -) Chlamydia trachomatis: STD, UT symptoms, Common co-infection with N. gonorrhoeae, Chlamydia pneumoniae( pneumonia, bronchitis, sinusitus), Cholera – Vibrio cholerae (gram -), Clostridium sp. – Gangrene (perfringens), Tetanus (tetani) , Colitis (difficile), Add-on for treatment of Y. pestis or B. anthracis. Gram (+) cocci :Some S. aureus are sensitive so can be used IF susceptibility is confirmed eg, CA-MSSA, CA-MRSA (exception)
AE's: Pregnancy: Renal/Hepatic effects, Ca+2 effects, Hepatic toxicity: Inc’s BUN, Superinfections: Candida albicans and Clostridium difficile, sun sensitivity

Front 59

Minocycline

Back 59

Minocin, others

Hint 59

Tetracyclines
Protein-Synthesis Inhibitors
MOA: Reversibly binds to A site at 16S (of the 30S) ribosomal subunit (static). Passively diffuse through outer membrane and taken in by active aerobic pump
Pregnancy Cat D.
Excellent oral F; food dec's absorption to 80%;Higher lipophilicity provides mechanism which damages bug membranes and causes leakage -> high doses can penetrate into mammalian cells
Spectrum/Indications: Low dose oral or topical therapy for acne vulgaris – Propionibacteria sp. (esp., P. acnes), Lyme Disease – Borrelia burgdorferi, Rickettsial Infections (Rickettsia sp., gram - ) - i.e, Rocky Mountain Spotted Fever, Chlamydia (gram -) Chlamydia trachomatis: STD, UT symptoms, Common co-infection with N. gonorrhoeae, Chlamydia pneumoniae( pneumonia, bronchitis, sinusitus), Cholera – Vibrio cholerae (gram -), Clostridium sp. – Gangrene (perfringens), Tetanus (tetani) , Colitis (difficile), Add-on for treatment of Y. pestis or B. anthracis.Gram + cocci :Some S. aureus are sensitive so can be used IF susceptibility is confirmed eg, CA-MSSA, CA-MRSA (exception)
AE's: Pregnancy: Renal/Hepatic effects, Ca+2 effects, Hepatic toxicity: Inc’s BUN, Superinfections: Candida albicans and Clostridium difficile, sun sensitivity

Front 60

Doxycycline

Back 60

Vibramycin, others

Hint 60

Tetracyclines
Protein-Synthesis Inhibitors
MOA: Reversibly binds to A site at 16S (of the 30S) ribosomal subunit (static). Passively diffuse through outer membrane and taken in by active aerobic pump
Pregnancy Cat D.
Most stable TET and 100% orally absorbed; longest t1/2, allows qd dosing
Spectrum: Same TET spectrum; Excellent activity against Treponema pallidum and N. gonorrhoeae (resistance increasing), Gram + cocci :Some S. aureus are sensitive so can be used IF susceptibility is confirmed eg, CA-MSSA, CA-MRSA (exception). DOC for RMSF
AE's: Pregnancy: Renal/Hepatic effects, Ca+2 effects, Hepatic toxicity: Inc’s BUN, Superinfections: Candida albicans and Clostridium difficile, sun sensitivity

Front 61

Tigecycline

Back 61

Tygacil

Hint 61

Glycylcycline
Extended Spectrum Tetracycline
Protein-Synthesis Inhibitors
MOA: Reversibly binds to A site at 16S (of the 30S) ribosomal subunit (static). Passively diffuse through outer membrane and taken in by active aerobic pump
Pregnancy Cat D.
Binds ribosomes more effectively than TET-->Overcomes (for now) the resistance due to Efflux pumps and Ribosomal protection
Spectrum: All TET-sensitive orgs; E. coli, K. pneuomoniae, Bacteroides fragilis, Staphylococci (MSSA), Enterococcus sp., Ehrlichiosis/Rickettsia
AE's: Pregnancy: Renal/Hepatic effects, Ca+2 effects, Hepatic toxicity: Inc’s BUN, Superinfections: Candida albicans and Clostridium difficile, sun sensitivity

Front 62

Erythromycin

Back 62

E-Mycin, others

Hint 62

Macrolide
Protein-Synthesis Inhibitor
MOA: Blocks the P-site of the 23S (of the 50S) ribosomal subunit-->results in shortened proteins.
Food reduces absorption to nearly nothing
Spectrum: Primarily for URTI and LRTI by gram + organisms: S. Pyogenes, S. pneumoniae, S. viridans (endocarditis prophylaxis), S. agalactiae (GBS), S. aureus (Meth-Sens), Clostridium perfringens, Listeria monocytogenes, Chlamydia trachomitis (PID, STD), B. anthracis. Some modest effect against gram(-) : H. influenzae, N. gonorrhoeae, L. pneumophilia(DOC) (Legionella; GI, CNS infection)
AE: GI cramping
Drug-Drug interactions: Involve competition for oxidative metabolism by CYP450-3A4

Front 63

Erythromycin estolate

Back 63

Ilosone, others

Hint 63

Macrolide
Protein-Synthesis Inhibitor
Ester Prodrug allows for more favorable dosing, hides taste-->good for peds
MOA: Blocks the P-site of the 23S (of the 50S) ribosomal subunit-->results in shortened proteins.
Spectrum: Primarily for URTI and LRTI by gram + organisms: S. Pyogenes, S. pneumoniae, S. viridans (endocarditis prophylaxis), S. agalactiae (GBS), S. aureus (Meth-Sens), Clostridium perfringens, Listeria monocytogenes, Chlamydia trachomitis (PID, STD), B. anthracis. Some modest effect against gram(-) : H. influenzae, N. gonorrhoeae, L. pneumophilia (Legionella; GI, CNS infection)
AE: GI cramping
Drug-Drug interactions: Involve competition for oxidative metabolism by CYP450-3A4

Front 64

Erythromycin ethylsuccinate

Back 64

E.E.S, others

Hint 64

Macrolide
Protein-Synthesis Inhibitor
Ester Prodrug allows for more favorable dosing, hides taste-->good for peds
MOA: Blocks the P-site of the 23S (of the 50S) ribosomal subunit-->results in shortened proteins.
Spectrum: Primarily for URTI and LRTI by gram + organisms: S. Pyogenes, S. pneumoniae, S. viridans (endocarditis prophylaxis), S. agalactiae (GBS), S. aureus (Meth-Sens), Clostridium perfringens, Listeria monocytogenes, Chlamydia trachomitis (PID, STD), B. anthracis. Some modest effect against gram(-) : H. influenzae, N. gonorrhoeae, L. pneumophilia (Legionella; GI, CNS infection)
AE: GI cramping
Drug-Drug interactions: Involve competition for oxidative metabolism by CYP450-3A4

Front 65

Clarithromycin

Back 65

Biaxin

Hint 65

Macrolide
Protein-Synthesis Inhibitor
6-position –OH changed to –OCH3 leads to increased lipophilicity and decreases formation of the ketal-->dec cramps
MOA: Blocks the P-site of the 23S (of the 50S) ribosomal subunit-->results in shortened proteins.
Spectrum: Excellent activity at: Chlamydia pneumoniae, Mycobacterium avium complex, Legionella sp., H. pylori, Borrelia burgdorferi (Advanced Lyme), Mycoplasma pneumoniae, extraordinary potency at H. Influenzae
AE: GI cramping
Drug-Drug interactions: Involve competition for oxidative metabolism by CYP450-3A4

Front 66

Azithromycin

Back 66

Zithromax, Z-PAK

Hint 66

Macrolide
Protein-Synthesis Inhibitor
MOA: Blocks the P-site of the 23S (of the 50S) ribosomal subunit-->results in shortened proteins.
Far more lipophillic-->excellent penetration into tissue, LONG t1/2-->loading agent
Spectrum: similar to Biaxin, enhanced H. influenzae (otitis media) penetration, syngergistic with cephs against: N. gonorrhoeae, Mycoplasma pneumoniae
Decreased CYP450-3A4 inhibition compared to others

Front 67

Fidaxomicin

Back 67

Dificid
(C. difficile ONLY)

Hint 67

Macrolide
Indirect Protein-Synthesis Inhibitor
MOA: Inhibits bacterial RNA polymerase-->decreases RNA synthesis--> decrease protein synthesis
Spectrum: In vitro activity is primarily directed against Clostridium sp, particularly C. difficile: Approved for C. difficile associated diarrhea in > 18 yo; Oral formulation has same effectiveness of vancomycin with lower risk of recurrence
Poorly absorbed so minimal systemic ADRs

Front 68

Telithromycin

Back 68

Ketek

Hint 68

Ketolide
Macrolide
Protein-Synthesis Inhibitor
MOA: Blocks the P-site of the 23S (of the 50S) ribosomal subunit-->results in shortened proteins.
Spectrum: S. aureus (Meth sensitive only), S. Pneumoniae ***MDRI***, Chlamydia pneumoniae, H. Influenzae, Mycoplasma pneumoniae
**Now only indicated for community acquired pneumonia of mild to moderate severity**
CYP450-3A substrate
BBW due to problematic SE’s: severe liver damage (esp w/ 3A4 co-admin i.e. statin), spontaneous fainting, visual disturbances (including loss)

Front 69

Clindamycin

Back 69

Cleocin

Hint 69

Lincosamide
Protein-Synthesis Inhibitor
MOA: Binds to the 50S ribosomal subunit, at a site overlapping the macrolide site
Spectrum:Esp. P. acnes, S. pyogenes, S. viridans, S. pneumoniae, S. agalactiae (GBS), S. aureus (Meth-sens), Bacteroides fragilis, Clostridium perfringens and tetani. also used to treat pneumocystis pneumonia (P. jirovecii)
Potent cause of C. difficile overgrowth

Front 70

Lincomycin

Back 70

Lincocin

Hint 70

Lincosamide
Protein-Synthesis Inhibitor
MOA: Binds to the 50S ribosomal subunit, at a site overlapping the macrolide site
Spectrum:Esp. P. acnes, S. pyogenes, S. viridans, S. pneumoniae, S. agalactiae (GBS), S. aureus (Meth-sens), Bacteroides fragilis, Clostridium perfringens and tetani
Potent cause of C. difficile overgrowth

Front 71

Linezolid

Back 71

Zyvox

Hint 71

Oxazolidinone (New, first in class)
Protein-Synthesis Inhibitor
MOA: Binds to the P site at interface of complex and dissociates 30S from the rest of the complex. Inhibits the binding of initiating tRNA-fMET to the 70S ribosome, thus preventing formation of the initiating ternary complex (tRNA, 30S, 50S)
Spectrum: Strictly gram + spectrum: MRSA and VISA-VRSA!!!, Staphylococcus sp., Streptococcus sp, Enterococcus sp. Including VRE, Listeria monocytogenes, Mycobacterium tuberculosis (acid fast)
AE: serotonin syndrome

Front 72

Quinupristin/Dalfopristin

Back 72

Synercid

Hint 72

Straptogramins
Protein-Synthesis Inhibitor
MOA: Quin: Binds at the same site as macrolides (P site at 23S subunit)--> peptide formation can't occur. Dalf: binds A-site on 23S; synergizes binding of Quin
Approved in US for treatment of MDR- or Vancomycin-resistant Enterococcus faecium (NOT useful for E. faecalis). Also approved for complicated skin/skin structure infections caused by MSSA or S. pyogenes. Used IV only
Main side effects are infusion mediated (pain, myalgia, arthralgia)
Both are potent inhibitors of CYP3A4
Concomitant administration with other CYP3A4 substrates can cause toxicity and result in hypertension: Antihistamines (clemastine), Anticonvulsants (fosphenytoin, felbamate), Macrolides, some Fluoroquinolones, Antidepressants (SSRIs, TCAs, SNRIs), Antipsycotics, Azole antifungals

Front 73

Chloramphenicol

Back 73

Chloromycetin

Hint 73

Protein-Synthesis Inhibitor
MOA: Binds to the 23S RNA of the 50S subunit, near the macrolide/clindamycin site-->Inhibits binding of the tRNA to the A-site, inhibiting peptide bond formation
Spectrum: Broad (covers everything). Crosses BBB effectively= last resort for B. meningitis
Highly toxic: Inhibits mitochondrial protein synthesis in mammalian cells, aplastic anemia, thrombocytopenia, and leukopenia. Bone marrow toxicity limits use

Front 74

Sulfanilamide

Back 74

Various

Hint 74

Sulfonomide
MOA: Mimics PABA= antimetabolite-->inhibits dihydropteroate synthase--> no THF. Secondary mech: bacteria uses sulfa as substrate and make false metabolite-->conjugation can’t occur. Ionized form is the active bacterial species
Spectrum: Covers everything
AE: Crystaluria & hypersensitivity

Front 75

Sulfadiazine/Sulfamerazine/Sulfamethazine

Back 75

Triple Sulfa, various

Hint 75

Sulfonomide
MOA: Mimics PABA= antimetabolite-->inhibits dihydropteroate synthase--> no THF. Secondary mech: bacteria uses sulfa as substrate and make false metabolite-->conjugation can’t occur. Ionized form is the active bacterial species. Often dosed with Na-bicarb to increase clearance
Created to further alleviate the formation of crystals b/c each has a distinct pKa range
Spectrum: Covers everything, Used for UTI (E. coli; K. pneumoniae; Salmonella sp., Shigella sp.)
AE: Crystaluria & hypersensitivity

Front 76

Silver-Sulfadiazine

Back 76

Silvadene

Hint 76

Sulfonomide
MOA: Mimics PABA= antimetabolite-->inhibits dihydropteroate synthase--> no THF. Secondary mech: bacteria uses sulfa as substrate and make false metabolite-->conjugation can’t occur. Ionized form is the active bacterial species.
Spectrum: Highly effective against many gram – and gram + organisms (Inhibits growth of nearly all bacteria and fungi, in vitro) Topical use--> Agent of choice for non-life threatening burns

Front 77

Sulfisoxazole

Back 77

Gantrisin

Hint 77

Sulfonomide
MOA: Mimics PABA= antimetabolite-->inhibits dihydropteroate synthase--> no THF. Secondary mech: bacteria uses sulfa as substrate and make false metabolite-->conjugation can’t occur. Ionized form is the active bacterial species.
Spectrum: Good activity in UTI as well as otitis media: E.coli, Salmonella sp., Shigella sp., Klebsiella sp., Proteus sp., H. influenzae
AE: Crystaluria & hypersensitivity

Front 78

Sulfisoxazole/Phenazopyridine

Back 78

Azo-Gantrisin

Hint 78

Sulfonomide
MOA: Mimics PABA= antimetabolite-->inhibits dihydropteroate synthase--> no THF. Secondary mech: bacteria uses sulfa as substrate and make false metabolite-->conjugation can’t occur. Ionized form is the active bacterial species. Phenazopyridine has local analgesic properties in the UT (Decreased irritation and discomfort on urination)
Spectrum: Good activity in UTI as well as otitis media: E.coli, Salmonella sp., Shigella sp., Klebsiella sp., Proteus sp., H. influenzae
AE: discolored urine, crystaluria, and hypersensitivity

Front 79

Sulfisoxazole Acetyl

Back 79

(component of) Pediazole w/E.E.S.

Hint 79

Sulfonomide
MOA: Mimics PABA= antimetabolite-->inhibits dihydropteroate synthase--> no THF. Secondary mech: bacteria uses sulfa as substrate and make false metabolite-->conjugation can’t occur. Ionized form is the active bacterial species. Acetyl grp grants tastlessness--> imp in Peds
Spectrum: Good activity for otitis media
AE: Crystaluria & hypersensitivity

Front 80

Sulfamethoxazole

Back 80

Gantanol, others

Hint 80

Sulfonomide
MOA: Mimics PABA= antimetabolite-->inhibits dihydropteroate synthase--> no THF. Secondary mech: bacteria uses sulfa as substrate and make false metabolite-->conjugation can’t occur. Ionized form is the active bacterial species.
Spectrum: Broad, covers everything including Toxoplasma gondii (protozoa), does NOT cover MRSA alone. Most used sulfa
AE: Crystaluria & hypersensitivity

Front 81

Sulfacetamide

Back 81

Isoptocetamide, others

Hint 81

Sulfonomide
MOA: Mimics PABA= antimetabolite-->inhibits dihydropteroate synthase--> no THF. Secondary mech: bacteria uses sulfa as substrate and make false metabolite-->conjugation can’t occur. Ionized form is the active bacterial species. 90x aqueous solubility
Spectrum: used extensively in ophthalmic infection

Front 82

Trimethoprim

Back 82

Trimpex

Hint 82

Sulfonomide
MOA: Prevents the reduction of DHF to THF by blocking DHFR
AE: Dec urinary K excretion--> hyperkalemia; caution w/ACEs, ARBs, and K-sparring diuretics

Front 83

Sulfamethoxazole/Trimethoprim

Back 83

Bactrim, Septra, others

Hint 83

Sulfonomide
MOA: Mimics PABA= antimetabolite-->inhibits dihydropteroate synthase--> no THF. Secondary mech: bacteria uses sulfa as substrate and make false metabolite-->conjugation can’t occur. Ionized form is the active bacterial species. (Trimethoprim)Prevents the reduction of DHF to THF by blocking DHFR. The two drugs are acting on sequential steps in folate production in bacteria--> synergistic and leads to greater antimicrobial effect.
Spectrum: Very wide spectrum, including MRSA, Toxoplasma gondii and Pneumocystis jirivecii (protozoal)
AE: Crystaluria, hypersensitivity, (trimethoprim) dec urinary K excretion--> hyperkalemia; caution w/ACEs, ARBs, and K-sparring diuretics

Front 84

Nalidixic acid

Back 84

Negram

Hint 84

1st generation quinolone
MOA: Bind to and inhibit the actions of: DNA gyrase (gram -)= Inhibits supercoiling and tension relaxation & TOPO IV (gram +)= Inhibits decatenation, stimulates scission.
Spectrum: Extensively used in gram (–) UTI: E. coli, M. morganii, Proteus sp., Providencia rettgeri. Lack of activity against P. aeruginosa, gram + organisms, intracellular organisms (like UPEC)
Poor serum and tissue concentrations-->Not valuable for systemic infections-->Limited to use as UT disinfectants against susceptible bugs
AE: photosensitivity, arthropathy (Joint pain, swelling, rupture of load bearing tendons (esp Achilles)), pregnancy-acidosis effect (NOT used in1st trimester), Crystaluria (rare, if urine is too basic), chelation with cations

Front 85

Norfloxacin

Back 85

Noroxin

Hint 85

2nd generation Flouroquinolones
MOA: Bind to and inhibit the actions of: DNA gyrase (gram -)= Inhibits supercoiling and tension relaxation & TOPO IV (gram +)= Inhibits decatenation, stimulates scission.
Spectrum: Mostly gram (-), some gram (+)- Staphylococcus sp. (MSSA), P. aeruginosa, E. coli, M. morganii, Proteus sp., Providencia rettgeri, Salmonella sp., Shigella sp., Enterobacter sp., Neisseria sp.
AE: Proconvulsant, photosensitivity, arthropathy (Joint pain, swelling, rupture of load bearing tendons (esp Achilles)), pregnancy-acidosis effect (NOT used in1st trimester), Crystaluria (rare, if urine is too basic), chelation with cations

Front 86

Ciprofloxacin

Back 86

Cipro

Hint 86

2nd generation fluoroquinolone
MOA: Bind to and inhibit the actions of: DNA gyrase (gram -)= Inhibits supercoiling and tension relaxation & TOPO IV (gram +)= Inhibits decatenation, stimulates scission.
Spectrum: similar to norfloxacin but greater potency at P. Aeruginosa. Includes: Legionella sp., Rickettsia rickettsii, Bacillus anthracis, K. pneumoniae, H. influenzae, Neisseria sp., Enterococcus sp., Streptococcus sp., V. cholera. Crosses CSF--> used prophylactically for bacterial meningitis
AE: proconvulsant, photosensitivity, arthropathy (Joint pain, swelling, rupture of load bearing tendons (esp Achilles)), pregnancy-acidosis effect (NOT used in1st trimester), Crystaluria (rare, if urine is too basic), chelation with cations

Front 87

Ofloxacin

Back 87

Floxin

Hint 87

Quinolones
2nd generation Flouroquinolones
MOA: Bind to and inhibit the actions of: DNA gyrase (gram -)= Inhibits supercoiling and tension relaxation & TOPO IV (gram +)= Inhibits decatenation, stimulates scission.
AE: proconvulsant, photosensitivity, arthropathy (Joint pain, swelling, rupture of load bearing tendons (esp Achilles)), pregnancy-acidosis effect (NOT used in1st trimester), crystaluria (rare, if urine is too basic), chelation with cations

Front 88

Levofloxacin

Back 88

Levaquin, Iquix, Others

Hint 88

2nd generation flouroquinolone
Active S enantiomar of Ofloxacin
MOA: Bind to and inhibit the actions of: DNA gyrase (gram -)= Inhibits supercoiling and tension relaxation & TOPO IV (gram +)= Inhibits decatenation, stimulates scission.
Spectrum: same as Cipro, but more effective against gram (+): Staphylococcus sp. (Not MRSA or MRSE), Streptococcus sp. (Including MDR - S. pneumoniae), Enterococcus sp., Mycobacterium pneumoniae, H. influenzae, Chlamydia sp.
AE: Levo- alleviates seizure potential, photosensitivity, arthropathy (Joint pain, swelling, rupture of load bearing tendons (esp Achilles)), pregnancy-acidosis effect (NOT used in1st trimester), crystaluria (rare, if urine is too basic), chelation with cations

Front 89

Gatifloxacin Ophthalmic Solution

Back 89

Zymar

Hint 89

3rd generation flouroquinolones
MOA: Bind to and inhibit the actions of: DNA gyrase (gram -)= Inhibits supercoiling and tension relaxation & TOPO IV (gram +)= Inhibits decatenation, stimulates scission.
Spectrum: Better gram(+) coverage, active against S. pneumoniae and atypical organisms

Front 90

Moxifloxacin

Back 90

Avelox

Hint 90

4th generation flouroquinolones
MOA: Bind to and inhibit the actions of: DNA gyrase (gram -)= Inhibits supercoiling and tension relaxation & TOPO IV (gram +)= Inhibits decatenation, stimulates scission.
Spectrum: Less effective against UTI due to elimination (metabolized before it gets to the kidneys). Better activity against: Intracellular bacteria, Anaerobes (Bacteroides fragilis). Excellent activity at Streptococcus pneumoniae and other gram (+).Loss of activity at some gram (–) species
AE: QT prolongation, photosensitivity, arthropathy (Joint pain, swelling, rupture of load bearing tendons (esp Achilles)), pregnancy-acidosis effect (NOT used in1st trimester), crystaluria (rare, if urine is too basic), chelation with cations

Front 91

Gemifloxacin

Back 91

Factive

Hint 91

4th generation flouroquinolones
MOA: Bind to and inhibit the actions of: DNA gyrase (gram -)= Inhibits supercoiling and tension relaxation & TOPO IV (gram +)= Inhibits decatenation, stimulates scission.
Spectrum: Excellent coverage of gram + organisms including: Streptococcus pneumoniae (including MDR), Streptococcus pyogenes, MSSA, Anaerobes (Bacteroides fragilis), and the gram (–)'s that the other FQs target. Distinguished by having the most potent gram + effect of the FQs, and having the lowest level of resistance of the FQs
AE: QT prolongation, photosensitivity, arthropathy (Joint pain, swelling, rupture of load bearing tendons (esp Achilles)), pregnancy-acidosis effect (NOT used in1st trimester), crystaluria (rare, if urine is too basic), chelation with cations

Front 92

Besifloxacin

Back 92

Besivance Ophthalmic Solution

Hint 92

Quinolones
MOA: Bind to and inhibit the actions of: DNA gyrase (gram -)= Inhibits supercoiling and tension relaxation & TOPO IV (gram +)= Inhibits decatenation, stimulates scission.

Front 93

Methenamine and Hippuric Acid

Back 93

Hiprex

Hint 93

Urinary tract antiseptic
MOA: Decomposes in water to generate: ammonia and formaldehyde. Less formaldehyde is formed in more basic pH-->Hippuric acid acidifies urine to get more formaldehyde formation.
Never used alone to treat UTI
Spectrum: nearly all bacteria are sensitive, Proteus sp. are resistant (has a urease makes urine more basic)

Front 94

Nitrofurantoin

Back 94

Furadantin (powder), Macrodantin (macrocrystals), Macrobid (macrocrystals w/ gelatinous polymer)

Hint 94

Miscellaneous UTI Agent
MOA: Bacteria metabolize this agent into a reactive intermediates that covalently binds to bacterial DNA, RNA, and protein.
Spectrum: E.coli and Enterococci sp. Only
The three forms are not interchangeable or substitutable for each other
AE: Furdantin- N/V, colors urine. Macrodantin slows absorption and alleviates N/V

Front 95

Quinine

Back 95

Various

Hint 95

Antiparasitic Agent
Acts primarily as a blood merozoiticide for all Plasmodium sp., Gametocidal for P. vivax and & P. malariae
Hypothesized MOAs: DNA intercalation, Interference with Hb digestion, Interference with protozoal DHFR
Toxic, rarely drug of choice

Front 96

Quinidine

Back 96

Various

Hint 96

Antiparasitic Agent
Acts primarily as a blood merozoiticide for all Plasmodium sp., Gametocidal for P. vivax and & P. malariae
Hypothesized MOAs: DNA intercalation, Interference with Hb digestion, Interference with protozoal DHFR
Toxic, rarely drug of choice (more toxic and potent than quinine)

Front 97

Metronidazole

Back 97

Flagyl

Hint 97

Antiparasitic Agent
MOA: Metabolized by sensitive species (usually anaerobes) into hydroxyamine + ROS + RNS
Spectrum: Excellent activity against Trichomonas vaginalis (DOC), Entamoeba histolyctica (DOC), Giardia lamblia (DOC), Toxoplasma gondii (useful, but so is sulfa/trimeth), Clostridium difficile (non-recurrent) – DOC, H. pylori (In combination), All anaerobic cocci and bacilli (Bacteroides sp.)
AE: Contraindicated in 1st trimester**, antabuse effect- contraindicated w/alcohol

Front 98

Diloxanide Furoate

Back 98

Furomide

Hint 98

Antiparasitic Agent
Only available in the US through the CDC
Directly amebicidal (Entamoeba histolyctica ), often used with metronidazole in ameobiosis that is difficult to treat

Front 99

Atovaquone

Back 99

Mepron

Hint 99

Antiparasitic Agent
MOA: Inhibits the Pneumocystis oxidative metabolism processes--> inhibits ability to produce ATP
Used to treat pneumocystis pneumonia and toxoplasma gondii (not approved)

Front 100

Chloroquine
Hydroxychloroquine

Back 100

Aralen
Plaquenil

Hint 100

Antiparasitic Agent
MOA: Inc's pH of lysozyme--> parasite unable to breakdown Hgb for use as energy.
Usually DOC for Malaria
Excellent activity at all Plasmodium sp.
Particularly useful in suppressing recurrent attacks by P. vivax and P. ovale. Hydroxy- resistance prevalent in P. falciparum. Also, has activity against Entamoeba histolytica

Front 101

Mefloquine

Back 101

Lariam

Hint 101

Antiparasitic Agent
Highly effective suppressive and prophylactic agent
Advantage: Active against Chloroquine-resistant Plasmodium sp.
High SE profile: Seizures, suicidal tendencies, GI upset, Bradycardia

Front 102

Pyrimethamine

Back 102

Daraprim

Hint 102

Antiparasitic Agent
MOA: Extremely high affinity for Plasmodium DHFR-->Reduces THF synthesis in Plasmodium-->Results in deficiencies in proteins, purines, thymadine
Effective for treatment and prevention of chloroquine-resistance malaria

Front 103

Nitazoxanide

Back 103

Alinia

Hint 103

Antiparasitic agent
Limited to Giardiasis only (investigational for C. difficle

Front 104

Tinidazole

Back 104

Tindamax

Hint 104

Antiparasitic agent
MOA: similar to metronidazole-->creation of RNS induces DNA damage.
Approved for:
Trichomoniasis and bacterial vaginosis: in non-pregnant, adult women, Giardiasis: in patients age 3 and older, Amebiasis: in patients age 3 and older

Front 105

Trimetrexate

Back 105

Neutrexin

Hint 105

Antiparasitic agent
DHFR inhibitor
Used with Folinic acid (Leucovorin®) to treat pneumocystis pneumonia

Front 106

Atovaquone and Proguanil

Back 106

Malarone

Hint 106

Antiparasitic
MOA: Atovaquone – Selective inhibitor of parasitic mitochondrial electron transport. Proguanil – Metabolized to cycloguanil--> selective DHFR inhibitor in parasites
Active against the erythrocytic and exoerythrocytic stages of Plasmodium sp.
Indications: Prophylaxis of P. falciparum malaria, including in areas where chloroquine resistance has been reported, Treatment of acute, uncomplicated P. falciparum malaria
DI: Concurrent use with tetracyclines, metoclopramide, rifamfin/rifabutin reduces plasma concentrations

Front 107

Paramomycin

Back 107

Humatin

Hint 107

Antiparasitic

Front 108

γ-benzene hexachloride or Lindane

Back 108

Kwell

Hint 108

Anti-ectoparasitics
Treatment of lice and scabies
MOA: CNS stimulation due to GABA-R inhibition (highly lipophilic, absorbed through exoskeleton)
SE: CNS toxicity (dizziness, clumsiness, confusion), Potential for toxicity in children and those <110 lbs -->2nd line treatment

Front 109

Pyrethryins

Back 109

A-200, RID

Hint 109

Anti-ectoparasitics
MOA: Bind to voltage dependant Na channel-->blocks arm, leaves in open formation-->constant Na influx-->contractility= paralysis
Useful for treatment of Pediculas humanus capitis, Pediculus humanus corporis, or Phthirius pubis. Used in small children.
Usually combined with piperonyl butoxide (PBX)= synergist that inhibits insect p450 and therefore inactivation of the drug.

Front 110

Permithrin

Back 110

Nix-1, Elimite, Acticin, others

Hint 110

Anti-ectoparasitics
Bind to voltage dependant Na channel-->blocks arm, leaves in open formation-->constant Na influx-->contractility= paralysis
Treatment of lice and scabies

Front 111

Spinosad (spinosyn A and D)

Back 111

Natroba

Hint 111

Anti-ectoparasitics
MOA: Causes neuronal excitation in insects – 100% mortality due to paralysis
Approved for treatment of head lice for patients > 4 yo
Contains benzyl alcohol= toxic in babies and neonates with low-birth weight

Front 112

Mebendazole

Back 112

Vermox

Hint 112

Antihelmintic Agents
MOA: Selective inhibition of helminth microtubule assembly. Secondary mech: inhibition of the worm’s ability to syn ATP
Active against Nematodal helminths (roundworms, hookworms, pinworms)

Front 113

Albendazole

Back 113

Zental

Hint 113

Antihelmintic Agents
MOA: Selective inhibition of helminth microtubule assembly. Secondary mech: inhibition of the worm’s ability to syn ATP
Active against Nematodal helminths (roundworms, hookworms, pinworms)

Front 114

Ivermectin

Back 114

Mectizan, Stromectol

Hint 114

Antihelmintic Agents
MOA: Binds with high affinity to glutamate-gated Cl- channels(only found in invertebrates and highly expressed in nematode pharyngeal muscle)-->Immobilizes affected organisms by inducing paralysis of musculature
Now used solely for control of parasitic Nematodes, insects, ticks, and mites in livestock and domestic animals
Excellent activity against E. vermicularis – Pinworm and A.lumbricoides – Roundworm. Drug of choice for onchocerciasis, or river blindness caused by Onchocerca volvulus, a helminth

Front 115

Praziquantel

Back 115

Biltricide

Hint 115

Antihelmintic Agents
MOA: Ca+2 influx across the tegument (cover), result: muscle contraction= paralysis, Inhibition of phosphoinositide metabolism, result: affects contractility, Drug-induced damage to tegument, leading to antibody attack on intra-worm antigens
Spectrum: Cestode and Trematode (Schistosoma sp and tapeworms)

Front 116

Pyrantel Pamoate

Back 116

Pin-X (OTC)
Drontal ® - combo with praziquantel

Hint 116

Antihelmintic Agents
MOA: Depolarizing NM blocking agent--> leads to paralysis of the organism. Also activates N receptors on the organism-->contractions followed by paralysis
Directed against pinworm, roundworm, hookworm only
Safe b/c confined to GI tract, killing off any worms there

Front 117

Amphotericin B

Back 117

Fungizone, others

Hint 117

Antifungal agent
Polyene membrane disruptor
MOA: Destructs fungal membrane: binds to ergosterol and form pores--> cause leakage (K, H2O)-->cell die. Also inc’s generation of ROS-->oxidative damage (pleiotropic effect)
Spectrum: Covers all fungi, yeast, and Aspergillus sp. Not used on tinea due to toxicity
AE: Liver & kidney toxicity (esp when combined with other treatment like AGs)

Front 118

Nystatin

Back 118

Mycostatin, others

Hint 118

Antifungal agent
Polyene membrane disruptor
MOA: Destructs fungal membrane: binds to ergosterol and form pores--> cause leakage (K, H2O)-->cell die. Also inc’s generation of ROS-->oxidative damage (pleiotropic effect)
Spectrum: Effective only against Candida sp.--> Candidiasis. Oral suspension for premature or low birth infants (underdeveloped immune sys--> flushes out candida in GI tract to prevent candidiasis). Oral thrush – swish and swallow!
Not absorbed from the GIT, vagina, or skin= benefit
AE: Highly toxic

Front 119

Amphotericin B (liposomal)

Back 119

Abelcet, others

Hint 119

Antifungal agent
Polyene membrane disruptor

Front 120

Ketoconazole

Back 120

Nizoral

Hint 120

Azole
Systemic & Topical (shampoo)
MOA: CYP450-14a-demethylase inhibitor. Whole molecule is held into active site--> triazole or imidazole moiety is held closest to the heme--> binds covalently to the heme-->inhibits oxidative transfer that the heme is normally responsible for. Dec ergosterol, inc lanosterol--> used instead in membranes--> leaky--> die
Spectrum: Wide- Candida sp., Blastomyces dermatitidus, Paracoccidiodes brasiliensis, Coccidioides immitus, Histoplasma capsulatum , Tinea, Pityrosporum ovale (dandruff). Poor efficacy in Immunosuppressed patients and in meningitis. Generally used only if lower cost outweighs use of other azoles.
AE: Potent substrate of 3A4 and 2C9= Inc's []'s of macrolides, statins, warfarin,and PHY, N/V, anorexia, menstrual irregularities, teratogenic, acute sterility, dec'd libido, hair growth

Front 121

Itraconazole

Back 121

Sporanox

Hint 121

Azole
Systemic
MOA: CYP450-14a-demethylase inhibitor. Whole molecule is held into active site--> triazole or imidazole moiety is held closest to the heme--> binds covalently to the heme-->inhibits oxidative transfer that the heme is normally responsible for. Dec ergosterol, inc lanosterol--> used instead in membranes--> leaky--> die
Spectrum: Oral caps DOC for, Indolent, nonmeningeal infections due to thermally dimorphic fungi. Maintenance therapy of HIV patients with disseminated Histoplasmosis or other fungal infections. Aspergillus (non-AIDS or non-immunocompromised) & Tinea. Solution is effective and indicated for Candidiasis – oropharyngeal and esophogeal
Take w/food to inc absorption (imp in AIDS pts)
AE: Extensively metabolized by 3A4--> concurrent use w/statins can lead to rhabdo and ARF, steroid imbalances (rare)

Front 122

Posoconazole

Back 122

Noxafil

Hint 122

Azole
Systemic
MOA: CYP450-14a-demethylase inhibitor. Whole molecule is held into active site--> triazole or imidazole moiety is held closest to the heme--> binds covalently to the heme-->inhibits oxidative transfer that the heme is normally responsible for. Dec ergosterol, inc lanosterol--> used instead in membranes--> leaky--> die
Spectrum: Approved for prevention of invasive Aspergillus and Candida in immunocompromised patients (esp., hematopoietic stem cell transplant)
AE: Extensively metabolized by 3A4--> concurrent use w/statins can lead to rhabdo and ARF, steroid imbalances (rare)

Front 123

Fluconazole

Back 123

Diflucan

Hint 123

Azole
Systemic
MOA: CYP450-14a-demethylase inhibitor. Whole molecule is held into active site--> triazole or imidazole moiety is held closest to the heme--> binds covalently to the heme-->inhibits oxidative transfer that the heme is normally responsible for. Dec ergosterol, inc lanosterol--> used instead in membranes--> leaky--> die
Spectrum: Candidiasis - oropharyngeal and esophageal, Cryptococcosis – DOC for AIDS patient maintenance (Can be used after stabilization by Amphotericin B in AIDS/meningitis), DOC for Coccidioides immitus – induced meningitis. Less active than itraconazole against thermally dimorphic fungi and tinea. NO activity against Aspergillus sp.
Crosses BBB, can be dose 1qd= chief benefit
AE: Mainly metabolized by 2C9= doubles [wafarin]-->bleeding

Front 124

Voriconazole

Back 124

Vfend

Hint 124

Azole
Systemic
MOA: CYP450-14a-demethylase inhibitor. Whole molecule is held into active site--> triazole or imidazole moiety is held closest to the heme--> binds covalently to the heme-->inhibits oxidative transfer that the heme is normally responsible for. Dec ergosterol, inc lanosterol--> used instead in membranes--> leaky--> die
Spectrum: Improved activity against mold-->Invasive Aspergillosis – different than fluconazole, Disseminated Candidiasis (AIDS and transplant), Esophageal Candidiasis
Cross BBB
AE: Mainly metabolized by 2C9= doubles [wafarin]-->bleeding

Front 125

Clotrimazole

Back 125

Lotrimin, Mycelex, Mycelex Troche

Hint 125

Azole
Topical
Not approved for systemic use (extensive 1st pass)
MOA: CYP450-14a-demethylase inhibitor. Whole molecule is held into active site--> triazole or imidazole moiety is held closest to the heme--> binds covalently to the heme-->inhibits oxidative transfer that the heme is normally responsible for. Dec ergosterol, inc lanosterol--> used instead in membranes--> leaky--> die
Spectrum: Excellent activity only against Tinea and Cutaneous Candida, used cutaneously or vaginally

Front 126

Econazole

Back 126

Spectazole

Hint 126

Azole
Topical
Not approved for systemic use (extensive 1st pass)
MOA: CYP450-14a-demethylase inhibitor. Whole molecule is held into active site--> triazole or imidazole moiety is held closest to the heme--> binds covalently to the heme-->inhibits oxidative transfer that the heme is normally responsible for. Dec ergosterol, inc lanosterol--> used instead in membranes--> leaky--> die
Spectrum: Excellent activity only against Tinea and Cutaneous Candida, used cutaneously or vaginally

Front 127

Butoconazole

Back 127

Femstat 3

Hint 127

Azole
Topical
Not approved for systemic use (extensive 1st pass)
MOA: CYP450-14a-demethylase inhibitor. Whole molecule is held into active site--> triazole or imidazole moiety is held closest to the heme--> binds covalently to the heme-->inhibits oxidative transfer that the heme is normally responsible for. Dec ergosterol, inc lanosterol--> used instead in membranes--> leaky--> die
Spectrum: Excellent activity only against Tinea and Cutaneous Candida, used cutaneously or vaginally

Front 128

Miconazole

Back 128

Monistat

Hint 128

Azole
Topical
Not approved for systemic use (extensive 1st pass)
MOA: CYP450-14a-demethylase inhibitor. Whole molecule is held into active site--> triazole or imidazole moiety is held closest to the heme--> binds covalently to the heme-->inhibits oxidative transfer that the heme is normally responsible for. Dec ergosterol, inc lanosterol--> used instead in membranes--> leaky--> die
Spectrum: Excellent activity only against Tinea and Cutaneous Candida, used cutaneously or vaginally

Front 129

Terconazole

Back 129

Terazol

Hint 129

Azole
Topical
Not approved for systemic use (extensive 1st pass)
MOA: CYP450-14a-demethylase inhibitor. Whole molecule is held into active site--> triazole or imidazole moiety is held closest to the heme--> binds covalently to the heme-->inhibits oxidative transfer that the heme is normally responsible for. Dec ergosterol, inc lanosterol--> used instead in membranes--> leaky--> die
Spectrum: Excellent activity only against Tinea and Cutaneous Candida, used cutaneously or vaginally

Front 130

Tioconazole

Back 130

Vagistat-1, others

Hint 130

Azole
Topical
Not approved for systemic use (extensive 1st pass)
MOA: CYP450-14a-demethylase inhibitor. Whole molecule is held into active site--> triazole or imidazole moiety is held closest to the heme--> binds covalently to the heme-->inhibits oxidative transfer that the heme is normally responsible for. Dec ergosterol, inc lanosterol--> used instead in membranes--> leaky--> die
Spectrum: Excellent activity only against Tinea and Cutaneous Candida, used cutaneously or vaginally

Front 131

Oxyconazole

Back 131

Oxystat, others

Hint 131

Azole
Topical
Not approved for systemic use (extensive 1st pass)
MOA: CYP450-14a-demethylase inhibitor. Whole molecule is held into active site--> triazole or imidazole moiety is held closest to the heme--> binds covalently to the heme-->inhibits oxidative transfer that the heme is normally responsible for. Dec ergosterol, inc lanosterol--> used instead in membranes--> leaky--> die
Spectrum: Excellent activity only against Tinea and Cutaneous Candida, used cutaneously or vaginally

Front 132

Naftifine

Back 132

Naftin

Hint 132

Squalene Epoxidase Inhibitor
MOA: Inhibits fungal squalene epoxidase--> squalene build up--> toxic. Also, dec ergosterol
Spectrum: Limited to treatment of fungal infections of the skin and nails by tinea. Can also treat cutaneous candida (diaper yeast infection)

Front 133

Terbinafine

Back 133

Lamisil

Hint 133

Squalene Epoxidase Inhibitor
MOA: Inhibits fungal squalene epoxidase--> squalene build up--> toxic. Also, dec ergosterol
Spectrum: Limited to treatment of fungal infections of the skin and nails by tinea. Can also treat cutaneous candida (diaper yeast infection). Greater affinity at nail tinea

Front 134

Butenafine

Back 134

Mentax

Hint 134

Squalene Epoxidase Inhibitor
MOA: Inhibits fungal squalene epoxidase--> squalene build up--> toxic. Also, dec ergosterol
Spectrum: Limited to treatment of fungal infections of the skin and nails by tinea. Can also treat cutaneous candida (diaper yeast infection)

Front 135

Tolnaftate

Back 135

Tinactin

Hint 135

Squalene Epoxidase Inhibitor
MOA: Inhibits fungal squalene epoxidase--> squalene build up--> toxic. Also, dec ergosterol
Spectrum: Limited to treatment of fungal infections of the skin and nails by tinea. Can also treat cutaneous candida (diaper yeast infection)

Front 136

Flucytosine

Back 136

Ancobon, 5FU, others

Hint 136

Miscellaneous Antifungal Agents
MOA: Fungal enzyme converts drug into 5-FU-->inhibit thymidylate synthetase by competing with uracil-->can’t be converted to thymine--> unable to synthesize DNA. 5-FU is also ribosylated and phosphorylated; 5-dUMP also inhibits thymidylate syn; 5-FdUTP is incorporated into DNA-->cant base pair--> missense DNA-->apoptosis
Spectrum: Cryptococcus neoformans, Candida sp.(Candida use is decreased with advent of fluconazole). Typically never used alone, usu w/ Amph B for serious infections
Toxicity arises due to some normal flora's ability to convert to 5-FU

Front 137

Griseofulvin

Back 137

Grifulvin, others

Hint 137

Miscellaneous Antifungal Agents
MOA: Inhibits fungal tubulin; After po administration, it becomes incorporated into kerratin precursor cells and into kerratin cells – which then cannot support fungal growth
Spectrum: Active against all three Tinea-causing genus. Clinical use now limited to Tinea infections of skin and nails.
AE: Interacts with Ocs (dec effectiveness), limited to superficial infections due to high SE profile

Front 138

Caspofungin

Back 138

Cancidas

Hint 138

Echinocandins
MOA: Inhibits cell wall synthesis; Inhibit b-glucan synthase--> cant make b-glucans--> cant make cell wall--> permeable-->cell lysis
Spectrum: Effective against Candida sp. and Aspergillus sp. ONLY. Uses: Invasive aspergillosis in those who fail or are intolerant of approved drugs, esophageal candidiasis, INCLUDES AZOLE RESISTANT SP. If add to voriconazole--> high levels of synergy for aspergillosis
Relatively SE free

Front 139

Anidulafungin

Back 139

Eraxis

Hint 139

Echinocandins
MOA: Inhibits cell wall synthesis; Inhibit b-glucan synthase--> cant make b-glucans--> cant make cell wall--> permeable-->cell lysis
Spectrum/uses: Esophageal candidiasis and invasive candidiasis, including candidemia
Relatively SE free

Front 140

Micafungin

Back 140

Mycamine

Hint 140

Echinocandins
MOA: Inhibits cell wall synthesis; Inhibit b-glucan synthase--> cant make b-glucans--> cant make cell wall--> permeable-->cell lysis
Spectrum/uses: Candidiasis, candidemia, and prophylaxis of candida infections in bone marrow transplant patients

Front 141

Amantadine

Back 141

Symmetrel

Hint 141

Antiinfluenzal Agents
MOA: Block proton entry through M1 and M2 channels--> no fusion and release--> virus destroyed by lysosome
Spectrum: limited to Influenza A virus
Most effective if given within 48 hours of onset of symptoms
Can be utilized for prophylaxis in high risk patient if vaccine cannot be given
Almost all flu isolates are resistant
SE: Due to inc in DA release from neuronal sites (crosses BBB)-->Nightmares, hallucinations, insomnia, headache

Front 142

Rimantadine

Back 142

Flumadine

Hint 142

Antiinfluenzal Agents
MOA: Block proton entry through M1 and M2 channels--> no fusion and release--> virus destroyed by lysosome
Spectrum: limited to Influenza A virus
Most effective if given within 48 hours of onset of symptoms
Can be utilized for prophylaxis in high risk patient if vaccine cannot be given
SE: Less CNS affects than Amantadine

Front 143

Zanamivir

Back 143

Relenza

Hint 143

Antiinfluenzal Agents
NA inhibitor
MOA: Drug acts as a competitive inhibitor of the enzyme-->Virion cant be cleaved from the cell surface-->no release--> immune cells can then come clean up
Spectrum: Potently and selectively inhibits Influenza A and B serotypes. Should be used with 1st 48 hrs and if done so, will reduce the duration by 1.5 days. Can be used in resistant strains
Considerations: Must be delivered locally by intranasal or dry powdered inhalation. Proprietary inhaler requires a cooperative patient and instruction by the healthcare provider – especially if used in children= Y not used often

Front 144

Oseltamivir

Back 144

Tamiflu

Hint 144

Antiinfluenzal Agents
NA inhibitor
MOA: Drug acts as a competitive inhibitor of the enzyme-->Virion cant be cleaved from the cell surface-->no release--> immune cells can then come clean up
Spectrum: Potently and selectively inhibits Influenza A and B serotypes. At higher doses and longer treatment times, active against H5N1 and pandemic H1N1
Orally bioavailable, Eliminated by kidney proximal tubules-->Co-administration with probenacid--> dec elimination-->less can be used

Front 145

Acyclovir

Back 145

Zovirax

Hint 145

Antiherpesvirus Agents
MOA: Obligate chain terminator; Thymidine kinase is herpes virus dependant, cellular kinase are from the host cell--> forms acyclovir triphos--> directly competes with GTP-->inhibits DNA polymerase-->terminates replication
Clinical use limited to Herpesviruses- HSV-1, HSV-2, HHV-3; The gold standard for treatment of common Herpesvirus infections
Mycophenolate Mofetil (Immunosuppressant) potentiates the effects of acyclovir by depleting normal pools of dGTP

Front 146

Valacyclovir

Back 146

Valtrex

Hint 146

Antiherpesvirus Agents
MOA: Obligate chain terminator; Thymidine kinase is herpes virus dependant, cellular kinase are from the host cell--> forms acyclovir triphos--> directly competes with GTP-->inhibits DNA polymerase-->terminates replication. Valine is cleaved to yield acyclovir, Valine yields greater oral F-->high blood concentrations
Clinical use limited to Herpesviruses- HSV-1, HSV-2, HHV-3, EBV, CMV
SE: nephrotoxicity particularly when given IV

Front 147

Cidofovir

Back 147

Vistide

Hint 147

Antiherpesvirus Agents
MOA: Converted to active diphosphate form by host cell enzyme. Competes with dCTP for incorporation into the growing DNA strand. Acts as a competitive viral DNA polymerase inhibitor. Not dependent of HSV TK for monophosphorylation-->more toxicity. Poor oral F--> used topical or injection
Spectrum: Human Herpes, Papilloma Virus - cause of genital warts, cervical cancer, Pox Virus – i.e, monkeypox, not as effective in smallpox. Good activity against (val)acyclovir resistant Herpes, especially TK- or altered strains.
Uses: Approved for CMV in AIDs patients; Used in acyclovir-resistant HSV in AIDs patients, acyclovir resistant systemic infections, and Keratitis (topical)
Considerations: Nephrotoxic – Co-administration with probenecid PREVENTS nephrotoxicity. Mutagenic, gonadotoxic, embryotoxic, teratogenic, rodent carcinogen.

Front 148

Penciclovir

Back 148

Denavir

Hint 148

Antiherpesvirus Agents
MOA: NOT an obligate chain terminator. Compete with GTP for viral DNA polymerase--> 3'OH present but less rigid structure--> causes kinks in chain-->DNA falls apart. Dependent on viral TK monophosphorylation
Spectrum: Active against HSV, HHV3, and HBV. Only 5% oral F--> limited to topical creams

Front 149

Famciclovir

Back 149

Famvir

Hint 149

Antiherpesvirus Agents
Prodrug of pencyclovir
MOA: Readily absorbed orally and rapidly cleaved and oxidized in intestine walls to yield pencyclovir. NOT an obligate chain terminator. Compete with GTP for viral DNA polymerase--> 3'OH present but less rigid structure--> causes kinks in chain-->DNA falls apart. Dependent on viral TK monophosphorylation
Spectrum: Active against HSV, HHV3, and HBV

Front 150

Ganciclovir

Back 150

Cytovene, Vitrasert

Hint 150

Antiherpesvirus Agents
MOA: NOT an obligate chain terminator. Compete with GTP for viral DNA polymerase--> 3'OH present but less rigid structure--> causes kinks in chain-->DNA falls apart. In HSV, dependent on viral TK monophosphorylation. In CMV, monophosphorylated by CMV phosphotransferase
Spectrum: Active against all Herpesviruses, but especially against HHV5
Uses: Indicated for CMV Retinitis, for prophylaxis and suppression of CMV in transplant and AIDS patients, HSV keratitis. Used for more serious infections
AE: Highly toxic; 1/3 of patients experience CNS or bone-marrow toxicity. Teratogenic, embryotoxic, reproductive toxicity, myelotoxic, mutagen, potential carcinogen

Front 151

Valganciclovir

Back 151

Valcyte

Hint 151

Antiherpesvirus Agents
Prodrug of Ganciclovir-->inc oral F
MOA: NOT an obligate chain terminator. Compete with GTP for viral DNA polymerase--> 3'OH present but less rigid structure--> causes kinks in chain-->DNA falls apart. In HSV, dependent on viral TK monophosphorylation. In CMV, monophosphorylated by CMV phosphotransferase
Spectrum: Active against all Herpesviruses, but especially against HHV5
Uses: Indicated for CMV Retinitis, for prophylaxis and suppression of CMV in transplant and AIDS patients, HSV keratitis. Used for more serious infections
AE: Highly toxic; 1/3 of patients experience CNS or bone-marrow toxicity. Teratogenic, embryotoxic, reproductive toxicity, myelotoxic, mutagen, potential carcinogen

Front 152

Idoxuridine

Back 152

Virudox, others

Hint 152

Antiherpesvirus Agents
Iodinated thymidine analog
MOA: Compete w/thymine for DNA polymerase. NOT a chain terminator-->but I can’t H-bond with adenine--> DNA falls apart in the middle
Spectrum: Active against various DNA viruses; More potent antiviral activity than any of the dGTP analogues
Uses: Used topically in treatment of HSV keratitis and keratconjuntivitis
Very toxic to normal human cells

Front 153

Trifluridine

Back 153

Viroptic, others

Hint 153

Antiherpesvirus Agents
Trifluoromethane thymidine analog
MOA: Compete w/thymine for DNA polymerase. NOT a chain terminator-->but CF2 can’t H-bond with adenine--> DNA falls apart in the middle
Spectrum: Active against various DNA viruses; More potent antiviral activity than any of the dGTP analogues
Uses: Used topically in treatment of HSV keratitis and keratconjuntivitis
Very toxic to normal human cells

Front 154

Vidarabine

Back 154

Vira-A, Ara-A

Hint 154

Antiherpesvirus Agents
Adenosine analog with arabinose instead of ribose sugar
MOA: mono-, di-, and tri- phosphorylated by cellular kinases to form active dATP mimic. Active triphosphate inhibits viral and cellular DNA polymerase and is inserted into growing DNA chain. NOT an obligate chain terminator.
Spectrum: Active against Herpesviruses
Highly toxic= reserve drug

Front 155

Docosanol

Back 155

Abreva (OTC)

Hint 155

Antiherpesvirus Agents
MOA: Inhibits the fusion of the HSV virion to the host cell plasma membrane-->Prevents viral entry
Spectrum: Active against many lipid-enveloped viruses, including HSV
Uses: Approved only for topical treatment of orolabial HSV (dec's duration)

Front 156

Zidovudine

Back 156

Retrovir, AZT, ZDV

Hint 156

Nucleoside/nucleotide Reverse Transcriptase Inhibitors (NRTIs)
Structural mimic of thymidine
MOA: OBLIGATE CHAIN TERMINATOR. Must be mono-, di-, and tri- phosphorylated by HOST thymidine Kinase and other enzymes. Triphosphorylated AZT (dAzTP) competes with dTTP for a place on RT
Spectrum: Potent inhibitor of HIV-1 and HIV-2 RT
AE: High [ ]'s of monophosphate accumulate in cell = toxicity--> accumulates in bone marrow (rapidly dividing cells)-->Causes bone marrow suppression, anemia and erythroid stem cell toxicity

Front 157

Stavudine

Back 157

Zerit, d4T

Hint 157

Nucleoside/nucleotide Reverse Transcriptase Inhibitors (NRTIs)
Thymidine mimic
MOA: OBLIGATE CHAIN TERMINATOR; Must be activated by cellular kinases to the triphosphate. Triphosphorylated D4T (dAzTP) competes with dTTP for a place on RT
Spectrum: Potent inhibitor of HIV-1 and HIV-2 RT (higher affinity than AZT
Considerations: Less affinity for Thymidine kinase--> monophosphate does not accumulate in cells=Dec toxicity. If given with AZT, AZT will compete for phosphorylation by TK lose effectiveness

Front 158

Lamivudine

Back 158

Epivir, 3TC

Hint 158

Nucleoside/nucleotide Reverse Transcriptase Inhibitors (NRTIs)
Cytosine analog
MOA: OBLIGATE CHAIN TERMINATOR; Must be activated by cellular kinases to the triphosphate. Triphosphorylated 3TC competes with dCTP for a place on RT
Spectrum: Activity against HIV-1, HIV-2, HBV. Synergistic effects with other nucleoside RT inhibitors, except emtricitabine
Considerations: Induces M184V mutation--> resistance develops rapidly. M184V is selective for less virulence-->pts may be left on the drug to select for these less virulent mutants

Front 159

Emtricitabine

Back 159

Emtriva, FTC

Hint 159

Nucleoside/nucleotide Reverse Transcriptase Inhibitors (NRTIs)
Fluorinated cytosine analog
MOA: OBLIGATE CHAIN TERMINATOR; Must be activated by cellular kinases to the triphosphate. Triphosphorylated 3TC competes with dCTP for a place on RT
Spectrum: Potent inhibitor of resistant HIV-1 and HIV-2 strains
Considerations: Cross resistance seen with lamivudine (Similar M184V effect)

Front 160

Didanosine

Back 160

Videx, dDI

Hint 160

Nucleoside/nucleotide Reverse Transcriptase Inhibitors (NRTIs)
A prodrug, biotransformed to dideoxyadenosine
OBLIGATE CHAIN TERMINATOR; Must be activated by cellular kinases to the triphosphate. Triphosphorylated dDI competes with dATP for a place on RT
Spectrum: Highly potent (10X > AZT) against HIV-1, HIV-2 in T cells and monocytes
Considerations: Should not be co-administered with AZT as it will lose potency

Front 161

Abacavir

Back 161

Ziagen, ABC

Hint 161

Nucleoside/nucleotide Reverse Transcriptase Inhibitors (NRTIs)
Active triphosphorylated metabolite is a mimic of dGTP
MOA: OBLIGATE CHAIN TERMINATOR; Must be activated by cellular kinases to the triphosphate. Triphosphorylated ABC competes with dGTP for a place on RT
Considerations: HYPERSENSITIVITY- Significance is that repeated challenge with ABC can evoke rapid onset and more severe reactions, including death. Any pt on this drug should be counseled on this possibility (gene predisposes)

Front 162

Tenofovir

Back 162

Viread, TDF

Hint 162

Nucleoside/nucleotide Reverse Transcriptase Inhibitors (NRTIs)
Ester analog of adenosine
MOA: Cleaved after absorption, yielding monophosphate. Requires only two phosphorylation steps=works faster. OBLIGATE CHAIN TERMINATOR; Must be activated by cellular kinases to the triphosphate. Triphosphorylated TDF competes with dATP for a place on RT
AE: Causes severe lactic acidosis--> liver/kidney damage

Front 163

AZT and Lamivudine

Back 163

Combivir

Hint 163

NRTI Combo Drugs

Front 164

AZT, Lamivudine, and Abacavir

Back 164

Trizivir

Hint 164

NRTI Combo Drugs
Caution: ABC hypersensitivity

Front 165

Abacavair and Lamivudine

Back 165

Kivexa

Hint 165

NRTI Combo Drugs
Caution: ABC hypersensitivity

Front 166

Emtricitabine and Tenofovir

Back 166

Truvada

Hint 166

NRTI Combo Drugs

Front 167

Emtricitabine, Tenofovir and Efavirenz (nNRTI)

Back 167

Atripla

Hint 167

NRTI Combo Drugs

Front 168

Nevirapine

Back 168

Viramune

Hint 168

Non-Nucleoside Reverse Transcriptase Inhibitors (nNRTIs)
1st generation
MOA: Binds to allosteric site on the enzyme--> changes conformation of active site-->enzyme cant pick up bases=inhibited. NOT phosphorylated by cellular or viral enzymes
Spectrum: Active only against HIV-1. Excellent synergistic effects with AZT or combos of NRTIs
Considerations: High level resistance develops rapidly if used in monotherapy, due to mutations in RT. Inducer of CYP450-3A and -2B6, decreases concentrations of Antivirals**: Efavirenz (nNRTI), Lopinavir (PI), Nelfinavir (PI), Saquinavir (PI), Indinavir (PI), and Clarithromycin, Ketoconazole, OCs

Front 169

Delaviradine

Back 169

Rescriptor

Hint 169

Non-Nucleoside Reverse Transcriptase Inhibitors (nNRTIs)
1st generation
MOA: Binds to allosteric site on the enzyme--> changes conformation of active site-->enzyme cant pick up bases=inhibited. NOT phosphorylated by cellular or viral enzymes
Spectrum: Active only against HIV-1. Only used in combinations
Considerations: High level resistance develops rapidly if used in monotherapy, due to mutations in RT. Evidence that resistance to delavirdine may restore AZT susceptibility to AZT resistant HIV

Front 170

Efavirenz

Back 170

Sustiva

Hint 170

Non-Nucleoside Reverse Transcriptase Inhibitors (nNRTIs)
1st generation
MOA: Binds to allosteric site on the enzyme--> changes conformation of active site-->enzyme cant pick up bases=inhibited. NOT phosphorylated by cellular or viral enzymes
Spectrum: Active only against HIV-1. Only used in combinations (due to occurence of high level resistance)
Considerations: Large benefit is 1 QD dosing. Teratogenic, women of childbearing age warned to use two methods of contraception. CYP450 interactions lowers levels of PIs, as with other nNRTIs

Front 171

Etravirine

Back 171

Intelence

Hint 171

Non-Nucleoside Reverse Transcriptase Inhibitors (nNRTIs)
2nd generation
MOA: Binds to allosteric site on the enzyme--> changes conformation of active site-->enzyme cant pick up bases=inhibited. NOT phosphorylated by cellular or viral enzymes
Spectrum: Effective against some 1st gen-resistant nNRTI isolates. Not for use in initial treatment regimens
Considerations: Inducer of CYP3A4, Inhibitor of CYP2C9 and CYP2C19

Front 172

Rilpivarine

Back 172

Edurant (Complera – with TDF and FTC)

Hint 172

Non-Nucleoside Reverse Transcriptase Inhibitors (nNRTIs)
2nd generation
MOA: Binds to allosteric site on the enzyme--> changes conformation of active site-->enzyme cant pick up bases=inhibited. NOT phosphorylated by cellular or viral enzymes
Spectrum: Effective against some 1st gen-resistant nNRTI isolates. Not for use in initial treatment regimens
Considerations: Inducer of CYP3A4, Inhibitor of CYP2C9 and CYP2C19. Longer t1/2= favorable 1QD dosing

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Saquinavir

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Invirase

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Protease Inhibitors
MOA: Mimics polyprotein transition state-->bind reversibly to this site and prevent the protease from cleaving the polyprotein-->This blocks virion maturation, preventing the subunit proteins (RT, gp120, etc…) from being post-translationally cleaved.
Spectrum: Potent HIV-1 Protease inhibitor
Considerations: All PIs are substrates for P-Glycoprotein efflux pumps--> will be pumped out of CD4+ cells (T-cells, Mpahges, etc). Substrate and inhibitor of CYP450 isozymes (least potent), Dyslipidemia***, glucose imbalances, When given with ritonavir, blood levels are boosted and dosing is made to be more compliant, but may cause arrhymias

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Indinavir

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Crixivan

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Protease Inhibitors
MOA: Mimics polyprotein transition state-->bind reversibly to this site and prevent the protease from cleaving the polyprotein-->This blocks virion maturation, preventing the subunit proteins (RT, gp120, etc…) from being post-translationally cleaved.
Spectrum: 10X more active on HIV-1 protease than HIV-2 protease
Considerations: Numerous protease mutations lead to resistance, esp in monotherapy. All PIs are substrates for P-Glycoprotein efflux pumps--> will be pumped out of CD4+ cells (T-cells, Mpahges, etc). Substrate and inhibitor of CYP450 isozymes, Dyslipidemia***, glucose imbalances

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Ritonavir

Back 175

Norvir

Hint 175

Protease Inhibitors
MOA: Mimics polyprotein transition state-->bind reversibly to this site and prevent the protease from cleaving the polyprotein-->This blocks virion maturation, preventing the subunit proteins (RT, gp120, etc…) from being post-translationally cleaved.
Spectrum: Potent HIV-1 Protease inhibitor, major benefit comes from ability to inhibit CYP3A-isoforms--> tremendously inc’s oral F
Considerations: All PIs are substrates for P-Glycoprotein efflux pumps--> will be pumped out of CD4+ cells (T-cells, Mphages, etc). Substrate and inhibitor of CYP450 isozymes (most potent--> can be used to inc the oral F of other PIs), Dyslipidemia***, glucose imbalances, co-admin of
ritonavir and saquinavir can lead to arrythmias

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Nelfinavir

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Viracept

Hint 176

Protease Inhibitors
MOA: Mimics polyprotein transition state-->bind reversibly to this site and prevent the protease from cleaving the polyprotein-->This blocks virion maturation, preventing the subunit proteins (RT, gp120, etc…) from being post-translationally cleaved.
Spectrum: Active against HIV-1 & 2

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Lopinavir

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Kaletra (with ritonavir)

Hint 177

Protease Inhibitors
MOA: Mimics polyprotein transition state-->bind reversibly to this site and prevent the protease from cleaving the polyprotein-->This blocks virion maturation, preventing the subunit proteins (RT, gp120, etc…) from being post-translationally cleaved.
Spectrum: Active against HIV-1 & 2
AE: pronounced hyperlipidemic effect

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Fosamprenavir

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Lexiva

Hint 178

Protease Inhibitors
MOA: Mimics polyprotein transition state-->bind reversibly to this site and prevent the protease from cleaving the polyprotein-->This blocks virion maturation, preventing the subunit proteins (RT, gp120, etc…) from being post-translationally cleaved.
Spectrum: Active against HIV-1 & 2

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Tipranavir

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Aptivus

Hint 179

Protease Inhibitors
MOA: Mimics polyprotein transition state-->bind reversibly to this site and prevent the protease from cleaving the polyprotein-->This blocks virion maturation, preventing the subunit proteins (RT, gp120, etc…) from being post-translationally cleaved.
Spectrum: Active against HIV-1 & 2
Considerations: higher side effect profile – hyperlipidemia, hepatitis, glucose imbalance

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Atazanavir

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Reyataz

Hint 180

Protease Inhibitors
MOA: Mimics polyprotein transition state-->bind reversibly to this site and prevent the protease from cleaving the polyprotein-->This blocks virion maturation, preventing the subunit proteins (RT, gp120, etc…) from being post-translationally cleaved.
Spectrum: Active against HIV-1 & 2
Considerations: Can be dosed once daily, less dyslipidemic effect

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Darunavir

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Prezista

Hint 181

Protease Inhibitors
2nd Generation
MOA: Mimics polyprotein transition state-->bind reversibly to this site and prevent the protease from cleaving the polyprotein-->This blocks virion maturation, preventing the subunit proteins (RT, gp120, etc…) from being post-translationally cleaved.
Spectrum: Active against HIV-1 & 2. Higher efficacy compared to other PIs. Benefit is activity in presence of multiple protease mutations. Higher barrier against resistance

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Enfuvirtide

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Fuzeon

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HIV Fusion Inhibitor
MOA: Binds to GP41 and inhibits the fusion of viral and cell membranes
Spectrum: Active only against HIV-1
Not 1st line due to $

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Maraviroc

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Selzentry

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HIV Entry Inhibitors
MOA: Antagonizes CCR5 so that conformational changes do not occur
Spectrum: Only useful in adults with CCR5-tropic HIV1 detectable disease
Considerations: Patients must undergo screening to determine tropism before initiation. SEs: cough, upper respiratory infections, systemic allergies--> all due to blockage of chemokine receptor. CYP3A substrate-->inducers/inhibitors alter PK profile (dose). P-GP substrate. Contraindicated with St. Johns Wort--> substantial dec [Maraviroc]. BBW – potential hepatotoxicity

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Raltegravir

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Isentress

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Integrase Inhibitors
Uses: Indicated for combination use with other antiretroviral drugs in adults with prior treatments, that have: a) Evidence of viral replication b)HIV-1 strains resistant to multiple agents
AE: Creatine kinase increases, myopathy and rhabdomyolysis

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Isoniazid

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Various

Hint 185

Antimycobacterial Agents
MOA: Prodrug-->req’s catalase peroxidase to form active species. Reactive isoniazide metabolite acetylates inhA-->loses ability to create mycolic acid--> bacteria loses cell wall and stability. Bacteria loses "acid-fastness". Bacteriostatic for “resting” bacilli, but bacteriocidal for dividing ones. Penetrates host cells with ease= necessary
Spectrum: Highly selective for Mycobacteria sp.
Considerations: Resistance is profound--> generally used alone for prophylaxis and in combo for treatment. Must be given concurrently with pyridoxine To prevent peripheral neuritis (neuropathy). Metabolized by liver NAT2: Metabolite of acetylation= hepatotoxin--> fast acetylators= more likely to have hepatic toxicity; Slow acetylators more at risk for peripheral neuropathy (more isoniazid). DI: affects metabolism of PHY (inc’s [ ])--> monitor levels if given concurrently

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Rifampin

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Rimactane, Rifamate (with Isoniazid)

Hint 186

Antimycobacterial Agents
MOA: Binds and prevents formation of the polymerase on the DNA--> prevents transcription of mRNA and translation of proteins
Spectrum: Excellent activity against most Gram + and many gram – bacteria: Streptococcus and Staphylococcus (Not MRSA), N. meningitidis and H. influenzae. Highly active against Mycobacteria tuberculosis. Increases the activity of Streptomycin and Isoniazid (synergism). Exclusively used as combination treatment
AE: GI disturbance and rash are common. Potentially hepatotoxic – caution in those with hepatic history. Orange pigmentation--> any body fluids (urine and feces)= warn of this. Potent inducer of CYP450-3A4 and -2C and could decrease effectiveness of OCs (use barrier method), warfarin, RT inhibitors AND protease inhibitors, and azole antifungals. NEVER use with HIV drugs

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Rifabutin

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Mycobutin

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Antimycobacterial Agents
MOA: Binds and prevents formation of the polymerase on the DNA--> prevents transcription of mRNA and translation of proteins
Spectrum: Better activity against MAC than rifampin. Highly active against Mycobacteria tuberculosis. Increases the activity of Streptomycin and Isoniazid (synergism). Exclusively used as combination treatment
Considerations: Cross resistance occurs between rifampin and rifabutin with both M. tuberculosis and MAC. Well tolerated in AIDs patients, doesn’t induce CYP to same degree as rifampin does with anti-virals-->can be substitued for rifampin

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Rifapentine

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Priftin

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Antimycobacterial Agents
MOA: Binds and prevents formation of the polymerase on the DNA--> prevents transcription of mRNA and translation of proteins
Spectrum: Highly active against Mycobacteria tuberculosis. Increases the activity of Streptomycin and Isoniazid (synergism). Exclusively used as combination treatment
Considerations: Much longer t ½ compared to rifampin and rifabutin-->can be given less frequently

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Ethambutol

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Myambutol

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Antimycobacterial Agents
MOA: Blocks arabinosyl transferase, which converts an arabinofuranosyl sugar to arabinogalactans
Spectrum: Mycostatic agent, quickly taken up by Mycobacterium (TB and MAC)
Considerations: Major SE is Optic Neuritis, leads to decreased visual acuity and loss of red/green differentiation-->usu reversible. Baseline visual acuity test should be done.

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Pyrazinamide

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Various

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Antimycobacterial Agents
MOA: Inhibits mycolic acid synthesis(target unknown) in slightly acidic pH. Dependent on Tuberculin pyrazinamidase, which creates the active agent (mutation yields resistance)
Always used in combo therapy

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Cycloserine

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Various

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Antimycobacterial Agents
MOA: Inhibits D-alanine racemase and D-alanine ligase-->effect formation of peptidoglycan
Spectrum: TB activity only
Considerations: Reserve drug due to CNS SE's: NMDA receptor agonism & dec synthesis/metabolism of GABA--> seizures. Inc risk of suicide in depressed pts