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Flashcards in Antimicrobials Deck (136)
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0
Q

Penicillin V

A

Prototype B lactam antibiotic–Oral form

MOA: binds PBPs and blocks transpeptidase crosslinking

Uses: mostly gram positive (s. Pneumo, s. Pyogenes, actinomyces); Also used for N? Meningitidis and T. pallidum. Bactericidal for gram positive cocci, gram positive rods, gram negative cocci, and spirochetes. Penicillinase sensitive.

TOXICITY: hypersensitivity reactions, hemolytic anemia.

RESISTANCE: penicillinase in bacteria (a type of B lactamase) cleaves B lactam ring

1
Q

Penicillin G

A

Prototype B lactam antibiotic–IV and IM form

MOA: binds PBPs and blocks transpeptidase crosslinking

Uses: mostly gram positive (s. Pneumo, s. Pyogenes, actinomyces); Also used for N? Meningitidis and T. pallidum. Bactericidal for gram positive cocci, gram positive rods, gram negative cocci, and spirochetes. Penicillinase sensitive.

TOXICITY: hypersensitivity reactions, hemolytic anemia.

RESISTANCE: penicillinase in bacteria (a type of B lactamase) cleaves B lactam ring

2
Q

Ampicillin

A

Penicillinase-sensitive penicillin

MOA: same as penicillin. Wider spectrum; penicillinase sensitive. Also combine with clavulanic acid to protect against B-lactamase.

USES: extended-spectrum penicillin–Haemophilus influenzae, E. Coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci (ampicillin/amoxicillin HELPSS kill enterococci)

TOXICITY: hypersensitivity reactions; rash; pseudo membranous colitis

RESISTANCE: penicillinase in bacteria (a type of B lactamase) cleaves B-lactam ring

3
Q

Oxacillin

A

Penicillinase-resistant penicillin

MOA: same as penicillin. Narrow spectrum; penicillinase resistant because bulky R group blocks access of B lactamase to B lactam ring.

USE: S. aureus (except MRSA; resistant because of altered PBP target site)

TOXICITY: hypersensitivity reactions, interstitial nephritis

4
Q

Pipercillin

A

Antipsuedomonal

MOA: same as penicillin. Extended spectrum.

USES: Pseudomonas spp. And gram negative rods; susceptible to penicillinase; use with B lactamase inhibitors.

TOXICITY: hypersensitivity reactions

5
Q

Cephalosporins

A

Inhibits peptidoglycan cross-linking; less susceptible to penicillinase than penicillin

1st generation: cefazolin, cephalexin

2nd generation: cefaclor, cefprozi, cefoxitin

3rd generation: cefpodoxime, cefotaxime, ceftriaxone

4th generation: cefepime

6
Q

1st generation cephalosporins

A

Cefazolin, cephalexin

PEcK: Proteus mirabilis, E. coli, Klebsiella pneumoniae

Don’t penetrate CNS

7
Q

2nd generation cephalosporins

A

Cefaclor, cefprozi, cefoxitin; extended gram negative spectrum

HEN PEcKS: Haemophilus influenzae, Enterobacter, Neisseria, Proteus, E. Coli, Klebsiella, Serratia

8
Q

3rd generation cephalosporins

A

Cefpodoxime, cefotaxime, ceftriaxone

Serious gram negative infections resistant to other beta lactams

Penetrates the CNS-meningitis, gonorrhea, pseudomonas

Less effective against gram positive than 1st

9
Q

4e generation cephalosporins

A

Cefepime

Increased activity against pseudomonas and gram positive

Enhanced resistance to beta lactamase

Crosses the BBB

10
Q

Imipenem

A

Cabapenem

MOA: broad-spectrum, B-lactamase-resistant capbapenem. Inhibit cell wall synthesis. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decreased inactivation of drug in renal tubules.

USES: gram positive cocci, gram negative rods, and anaerobes. Wide spectrum, but significant side effects limit use to life threatening infections or after other drugs have failed.

TOXICITY: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.

11
Q

Vancomycin

A

MOA: inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors. Bacteriocidal.

USES: gram positive only–serious, multidrug-resistant organisms, including MRSA, enterococci, and Clostridium difficile (oral dose for pseudomembranous colitis)

TOXICITY: well tolerated in general–but NOT trouble free. Nephrotoxicity, ototoxicity, thrombophlebitis, diffuse flushing–red many syndrome (can largely prevent by pretreatment with antihistamines and slow infusion rate)

RESISTANCE: occurs in bacterial via amino acid modification of D-ala D-ala to D-ala D-lac

12
Q

Tobramycin

A

Aminoglycoside–30S inhibitor

MOA: bactericidal; inhibits formation of inititation complex and causes misreading of mRNA. Also blocks translocation. Requires O2 for uptake; therefore ineffective against anaerobes.

USES: severe, gram negative rod infections. Synergistic with B lactam antibiotics.

TOXICITY: nephrotoxicity, neuromuscular blockade, ototoxicity (especially when used with loop diuretics), teratogenic.

RESISTANCE: bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.

13
Q

Doxycycline

A

MOA: bacteriostatic; binds 30s and prevents attachment of aminoacyl-tRNA; limited CNS penetration. Doxycycline is fecally eliminated and can be used in patients with renal failure. Do not take with milk (calcium), antacids (calcium or magnesium), or iron-containing preparations because divalent cations inhibit absorption in gut.

USES: Borrelia burgdorferi, M pneumoniae. Drug’s ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamydia. Also used to treat acne.

TOXICITY: GI distress, discoloration of Teeth and inhibition of bone growth in children, photosensitivity. Contraindicated in pregnancy.

RESISTANCE: decreased uptake or increased efflux out of bacterial cells by plasmid-encoded transport pumps.

14
Q

Erythromycin

A

Macrolide

MOA: binds 50S subunit and inhibits translocation. Bacteriostatic.

Uses: atypical pneumonias-mycoplasma, chlamydia, legionella, STDs (chlamydia), gram positive cocci (strep if allergic to penicillin)

TOXICITY: GI motility issues, arrhythmia caused by prolonged QT, Canute cholestatic hepatitis, rash, eosinophilia. Increases serum concentration of theophyllines, oral anticoagulants.

RESISTANCE: methylation of 23s rRNA-binding site prevents binding of drug.

15
Q

Clindamycin

A

MOA: blocks peptide transfer (translocation) at 50s ribosomal subunit. Bacteriostatic.

USES: anaerobic infections (e.g. Bacteroides spp., Clostridium perfringens) in aspiration pneumonia, lung abscesses, and oral infections. Also effective against invasive Group A strep infection. **treats anaerobes above the diaphragm vs metronidazole

TOXICITY: pseudomembranous colitis (C. Difficile overgrowth), fever, diarrhea

16
Q

Linezolid

A

Oxazolidinone

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

USES: gram positive species including MRSA and VRE

TOXICITY: bone marrow suppression (especially thrombocytopenia), peripheral neuropathy, serotonin syndrome

RESISTANCE: point mutation of ribosomal RNA

17
Q

Sulfamethoxazole

A

Sulfonamide

MOA: inhibits folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase. Bacteriostatic.

Uses: gram positive, gram negative, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.

TOXICITY: hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (Tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (e.g. Warfarin)

RESISTANCE: altered enzyme (bacterial dihydropteroate synthase), decreased uptake, or increased PABA synthesis

18
Q

Trimethoprim

A

MOA: Inhibitor of dihydrofolate reductase. Bacteriostatic.

USES: used in combination with sulfonamides, causing sequential block of folate synthesis. Combination used for UTIs, shigella, salmonella, pneumocystis jirovecii pneumonia treatment and prophylaxis, toxoplasmosis prophylaxis.

TOXICITY: megaloblastic anemia, thrombocytopenia, leukopenia

19
Q

Ciprofloxacin

A

fluoroquinolone

MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.

Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms

TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.

RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.

20
Q

Metronidazole

A

MOA: Forms free radical toxic metabolites in bacterial cell that Damage DNA. Bactericidal, antiprotozoal.

USES: treats GET GAP–Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C. Difficile). Used with a proton pump inhibitor and clarithromycin for “triple therapy” against H. Pylori.

TOXICITY: disulfiram-like reaction (severe flushing, tachycardia, hypotension) with alcohol (thought to be due to its inhibition of alcohol oxidizing enzymes–>accumulation of acetaldehyde); headache, metallic taste

21
Q

Amoxicillin

A

Penicillinase-sensitive penicillin

MOA: same as penicillin. Wider spectrum; penicillinase sensitive. Also combine with clavulanic acid to protect against B-lactamase.

USES: extended-spectrum penicillin–Haemophilus influenzae, E. Coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, Shigella, enterococci (ampicillin/amoxicillin HELPSS kill enterococci)

TOXICITY: hypersensitivity reactions; rash; pseudo membranous colitis

RESISTANCE: penicillinase in bacteria (a type of B lactamase) cleaves B-lactam ring

21
Q

Nafcillin

A

Penicillinase-resistant penicillin

MOA: same as penicillin. Narrow spectrum; penicillinase resistant because bulky R group blocks access of B lactamase to B lactam ring.

USE: S. aureus (except MRSA; resistant because of altered PBP target site)

TOXICITY: hypersensitivity reactions, interstitial nephritis

22
Q

Dicloxacillin

A

Penicillinase-resistant penicillin

MOA: same as penicillin. Narrow spectrum; penicillinase resistant because bulky R group blocks access of B lactamase to B lactam ring.

USE: S. aureus (except MRSA; resistant because of altered PBP target site)

TOXICITY: hypersensitivity reactions, interstitial nephritis

23
Q

Ticarcillin

A

Antipsuedomonal

MOA: same as penicillin. Extended spectrum.

USES: Pseudomonas spp. And gram negative rods; susceptible to penicillinase; use with B lactamase inhibitors.

TOXICITY: hypersensitivity reactions

24
Q

Clavulanic acid

A

B-lactamase inhibitor. Often added to penicillin antibiotics to proct the antibiotic from destruction by B-lactamase (penicillinase)

25
Q

Sulbactam

A

B-lactamase inhibitor. Often added to penicillin antibiotics to proct the antibiotic from destruction by B-lactamase (penicillinase)

26
Q

Tazobactam

A

B-lactamase inhibitor. Often added to penicillin antibiotics to proct the antibiotic from destruction by B-lactamase (penicillinase)

27
Q

Cefazolin

A

1st generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections

TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.

28
Q

Cephalexin

A

1st generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae.

TOXICITY: 1st generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections

TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.

29
Q

Cefoxitin

A

2nd generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: HEN PEcKS (gram positive cocci)–Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens

TOXICITY: 1st generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections

TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.

30
Q

Cefaclor

A

2nd generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: HEN PEcKS (gram positive cocci)–Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens

TOXICITY: 1st generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections

TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.

31
Q

Cefuroxime

A

2nd generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: HEN PEcKS (gram positive cocci)–Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens

TOXICITY: 1st generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections

TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.

32
Q

Ceftriaxone

A

3rd generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bactericidal.

USES:

TOXICITY: 1st generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections

TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.

33
Q

Cefotaxime

A

3rd generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bactericidal.

USES: serious gram negative infections resistant to other B-lactams

TOXICITY: 1st generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections

TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.

34
Q

Ceftazidime

A

3rd generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bactericidal.

USES: serious gram negative infections resistant to other B-lactams–Pseudomonas

TOXICITY: 1st generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections

TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.

35
Q

Cefepime

A

4th generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bactericidal.

USES:

TOXICITY: 1st generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections

TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.

36
Q

Ceftaroline

A

5th generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bactericidal.

USES: broad gram positive and gram negative organism coverage, including MRSA; does not cover pseudomonas.

TOXICITY: 1st generation cephalosporin

MOA: B-lactam drug that inhibits cell wall synthesis but are less susceptible to penicillinases. Bacteriocidal.

USES: PEcK (gram positive cocci)–Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to surgery to prevent S. aureus wound infections

TOXICITY: hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction (inhibits acetaldehyde dehydrogenase and causes hangover symptoms, severe flushing hypotension, tachycardia with alcohol). Exhibits cross reactivity with penicillins. Increases nephrotoxicity of aminoglycosides.

37
Q

Aztreonam

A

MOA: a monobactam; resistant to B-lactamase. Prevents peptidoglycan cross-linking by binding to penicillin-binding protein 3. Synergistic with aminoglycosides. No cross-allergenicity with penicillins.

USES: gram negative rods only–no activity against gram positive or anaerobes. For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides.

TOXICITY: usually nontoxic. Occasional GI upset.

38
Q

Meropenem

A

Cabapenem

MOA: B-lactamase-resistant capbapenem. Inhibit cell wall synthesis. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules.

USES: gram positive cocci, gram negative rods, and anaerobes. Wide spectrum, but significant side effects limit use to life threatening infections or after other drugs have failed.

TOXICITY: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels. **meropenem has a decreased risk of seizures and is stable to dehydropeptidase I

39
Q

Ertapenem

A

Newer Cabapenem

MOA: broad-spectrum, B-lactamase-resistant capbapenem. Inhibit cell wall synthesis. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decreased inactivation of drug in renal tubules.

USES: gram positive cocci, gram negative rods, and anaerobes. Wide spectrum, but significant side effects limit use to life threatening infections or after other drugs have failed. Limited pseudomonas coverage.

TOXICITY: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.

40
Q

Doripenem

A

Newer Cabapenem

MOA: broad-spectrum, B-lactamase-resistant capbapenem. Inhibit cell wall synthesis. Always administered with cilastatin (inhibitor of renal dehydropeptidase I) to decreased inactivation of drug in renal tubules.

USES: gram positive cocci, gram negative rods, and anaerobes. Wide spectrum, but significant side effects limit use to life threatening infections or after other drugs have failed. Limited pseudomonas coverage.

TOXICITY: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.

41
Q

Gentamicin

A

Aminoglycoside–30S inhibitor

MOA: bactericidal; inhibits formation of inititation complex and causes misreading of mRNA. Also blocks translocation. Requires O2 for uptake; therefore ineffective against anaerobes.

USES: severe, gram negative rod infections. Synergistic with B lactam antibiotics.

TOXICITY: nephrotoxicity, neuromuscular blockade, ototoxicity (especially when used with loop diuretics), teratogenic.

RESISTANCE: bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.

42
Q

Neomycin

A

Aminoglycoside–30S inhibitor

MOA: bactericidal; inhibits formation of inititation complex and causes misreading of mRNA. Also blocks translocation. Requires O2 for uptake; therefore ineffective against anaerobes.

USES: severe, gram negative rod infections. Synergistic with B lactam antibiotics. Neomycin for bowel surgery.

TOXICITY: nephrotoxicity, neuromuscular blockade, ototoxicity (especially when used with loop diuretics), teratogenic.

RESISTANCE: bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.

43
Q

Amikacin

A

Aminoglycoside–30S inhibitor

MOA: bactericidal; inhibits formation of inititation complex and causes misreading of mRNA. Also blocks translocation. Requires O2 for uptake; therefore ineffective against anaerobes.

USES: severe, gram negative rod infections. Synergistic with B lactam antibiotics.

TOXICITY: nephrotoxicity, neuromuscular blockade, ototoxicity (especially when used with loop diuretics), teratogenic.

RESISTANCE: bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.

44
Q

Streptomycin

A

Aminoglycoside–30S inhibitor

MOA: bactericidal; inhibits formation of inititation complex and causes misreading of mRNA. Also blocks translocation. Requires O2 for uptake; therefore ineffective against anaerobes.

USES: severe, gram negative rod infections. Synergistic with B lactam antibiotics.

TOXICITY: nephrotoxicity, neuromuscular blockade, ototoxicity (especially when used with loop diuretics), teratogenic.

RESISTANCE: bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation.

45
Q

Tetracycline

A

MOA: bacteriostatic; binds 30s and prevents attachment of aminoacyl-tRNA; limited CNS penetration. Do not take with milk (calcium), antacids (calcium or magnesium), or iron-containing preparations because divalent cations inhibit absorption in gut.

USES: Borrelia burgdorferi, M pneumoniae. Drug’s ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamydia. Also used to treat acne.

TOXICITY: GI distress, discoloration of Teeth and inhibition of bone growth in children, photosensitivity. Contraindicated in pregnancy.

RESISTANCE: decreased uptake or increased efflux out of bacterial cells by plasmid-encoded transport pumps.

46
Q

Minocycline

A

MOA: bacteriostatic; binds 30s and prevents attachment of aminoacyl-tRNA; limited CNS penetration. Do not take with milk (calcium), antacids (calcium or magnesium), or iron-containing preparations because divalent cations inhibit absorption in gut.

USES: Borrelia burgdorferi, M pneumoniae. Drug’s ability to accumulate intracellularly makes it very effective against Rickettsia and Chlamydia. Also used to treat acne.

TOXICITY: GI distress, discoloration of Teeth and inhibition of bone growth in children, photosensitivity. Contraindicated in pregnancy.

RESISTANCE: decreased uptake or increased efflux out of bacterial cells by plasmid-encoded transport pumps.

47
Q

Azithromycin

A

Macrolide

MOA: binds 50S subunit and inhibits translocation. Bacteriostatic.

Uses: atypical pneumonias-mycoplasma, chlamydia, legionella, STDs (chlamydia), gram positive cocci (strep if allergic to penicillin)

TOXICITY: GI motility issues, arrhythmia caused by prolonged QT, Canute cholestatic hepatitis, rash, eosinophilia. Increases serum concentration of theophyllines, oral anticoagulants.

RESISTANCE: methylation of 23s rRNA-binding site prevents binding of drug.

48
Q

Clarithromycin

A

Macrolide

MOA: binds 50S subunit and inhibits translocation. Bacteriostatic.

Uses: atypical pneumonias-mycoplasma, chlamydia, legionella, STDs (chlamydia), gram positive cocci (strep if allergic to penicillin)

TOXICITY: GI motility issues, arrhythmia caused by prolonged QT, Canute cholestatic hepatitis, rash, eosinophilia. Increases serum concentration of theophyllines, oral anticoagulants.

RESISTANCE: methylation of 23s rRNA-binding site prevents binding of drug.

49
Q

Chloramphenicol

A

MOA: blocks peptidyltransferase at 50s ribosomal subunit. Bacteriostatic.

USES: meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae) and Rocky Mountain Spotted Fever (Rickettsia rickettsii)

TOXICITY: anemia (dose dependent), aplastic anemia (dose independent), gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase)

RESISTANCE: plasmid-encoded acetyltransferase inactivates the drug.

50
Q

Sulfisoxazole

A

Sulfonamide

MOA: inhibits folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase. Bacteriostatic.

Uses: gram positive, gram negative, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.

TOXICITY: hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (Tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (e.g. Warfarin)

RESISTANCE: altered enzyme (bacterial dihydropteroate synthase), decreased uptake, or increased PABA synthesis

51
Q

Sulfadiazine

A

Sulfonamide

MOA: inhibits folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase. Bacteriostatic.

Uses: gram positive, gram negative, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.

TOXICITY: hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (Tubulointerstitial nephritis), photosensitivity, kernicterus in infants, displace other drugs from albumin (e.g. Warfarin)

RESISTANCE: altered enzyme (bacterial dihydropteroate synthase), decreased uptake, or increased PABA synthesis

52
Q

Norfloxacin

A

fluoroquinolone

MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.

Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms

TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.

RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.

53
Q

Levofloxacin

A

fluoroquinolone

MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.

Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms

TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.

RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.

54
Q

Ofloxacin

A

fluoroquinolone

MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.

Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms

TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.

RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.

55
Q

Sparfloxacin

A

fluoroquinolone

MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.

Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms

TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.

RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.

56
Q

Moxifloxacin

A

fluoroquinolone

MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.

Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms

TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.

RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.

57
Q

Gemifloxacin

A

fluoroquinolone

MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.

Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms

TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.

RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.

58
Q

Enoxacin

A

fluoroquinolone

MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.

Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms

TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.

RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.

59
Q

Nalidixic acid

A

Quinolone

MOA: inhibits DNA gyrate (topoisomerase II) and topoisomerase IV. bactericidal. Must not be taken with antacids.

Uses: gram negative rods of urinary and GI tracts, Neisseria, some gram positive organisms

TOXICITY: GI upset, super infections, skin rashes, headache, dizziness. Less commonly, can cause tendonitis, tendon rupture, leg cramps, and myalgias. Contraindicated in pregnancy, nursing mothers, and children under 18 due to possible damage to cartilage. Some may cause prolonged QT interval. May cause tendon rupture in people over 60y and in patients taking prednisone.

RESISTANCE: chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.

60
Q

Isoniazid

A

Antimycobacterial prophylaxis against M. Tuberculosis

MOA: decreases synthesis of mycolic acids. Bacterial catalase-peroxidase (encoded by KatG) needed to convert INH to active metabolites

USES: Mycobacterium tuberculosis. The only agent used as solo prophylaxis against TB.

TOXICITY: neurotoxicity (usually presents as peripheral neuropathy),hepatotoxicity. Pyridoxine (vitamin B6) can prevent neurotoxicity (INH competes with B6 in synthesis of neurotransmitters and increases its urinary excretion leading to B6 deficiency)

**INH is metabolized by acetylation in the liver. Different half-lives in fast vs. slow acetylators–bimodal curve of drug concentration show pharmacological polymorphism in drug metabolism.

61
Q

Rifampin

A

MOA: inhibits DNA-dependent RNA polymerase

USES: part of multi-agent drug therapy for Mycobacterium tuberculosis; delays resistance to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus Influenzae type B.

TOXICITY: minor hepatotoxicity and drug interactions (increases P-450); orange body fluids. Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation.

MECHANISM OF RESISTANCE: mutations reduce drug binding to RNA polymerase. Monotherapy rapidly leads to resistance.

62
Q

Rifabutin

A

MOA: inhibits DNA-dependent RNA polymerase

USES: part of multi-agent drug therapy for Mycobacterium tuberculosis; delays resistance to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with Haemophilus Influenzae type B.

TOXICITY: minor hepatotoxicity and drug interactions (increases P-450); orange body fluids. Rifabutin favored over rifampin in patients with HIV infection due to less cytochrome P-450 stimulation.

63
Q

Pyrazinamide

A

MOA: uncertain. Thought to acidify intracellular environment via conversion to pyrazinoic acid. Effective in acidic pH of phagolysosomes, where TB engulfed by macrophages is found.

USES: P one RIPE therapy for Mycobacterium tuberculosis

TOXICITY: hyperuricemia, hepatotoxicity

64
Q

Ethambutol

A

MOA: decreases carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase

USES: Mycobacterium tuberculosis

TOXICITY: optic neuropathy (red-green color blindness)

65
Q

Prophylaxis-endocarditis with surgical or dental procedures

A

Penicillins

66
Q

Prophylaxis-Gonorrhea

A

Ceftriaxone

67
Q

Prophylaxis-history of recurrent UTI

A

TMP-SMX

68
Q

Prophylaxis-meningococcal infections

A

Ciprofloxacin (DOC), rifampin for children

69
Q

Prophylaxis-pregnancy women carrying group B strep

A

Ampicillin

70
Q

Prophylaxis-prevention of gonococcal or chlamydial conjunctivitis in newborn

A

Erythromycin ointment

71
Q

Prophylaxis-prevention of post surgical infection due to S. Aureus

A

Cefazolin

72
Q

Prophylaxis-strep pharyngitis in child with prior rheumatic fever

A

Oral penicillin

73
Q

Prophylaxis-syphillis

A

Benzathine penicillin G

74
Q

Prophylaxis in HIV-Pneumocystis pneumonia

A

CD4<200 TMP-SMX

75
Q

Prophylaxis in HIV-pneumocystis pneumonia and toxoplasmosis

A

CD4<100 TMP-SMX

76
Q

Prophylaxis HIV-Mycobacterium avium complex

A

CD4<50 Azithromycin

77
Q

Amphotericin B

A

Anti-fungal

MOA: binds ergosterol and forms membrane pores that allow leakage of electrolytes

USES: serious systemic mycoses, not for non-invasive infections. Cryptococcus, Blastomyces, Coccidioides, Histoplasma, Candida, Mucor. Intrathecally for fungal meningitis. Supplement K+ and Mg++ because of altered renal tubule permeability.

TOXICITY: fever/chills, hypotension, nephrotoxicity (causes both decreased GFR and divert toxic effects on tubular epithelium), arrhythmias, anemia, IV phlebitis. Hydration decreases nephrotoxicity. Liposomal Amphotericin decreases toxicity.

78
Q

Nystatin

A

MOA: same as Amphotericin B (binds ergosterol and forms pores in membranes). Topical form because too toxic for systemic use.

USES: only mucocutaneous infections, not systemic. “Swish and swallow” for oral candidiasis; topical for diaper rash or vaginal candidiasis.

79
Q

Fluconazole

A

MOA: inhibits fungal (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to

USES: local and less serious systemic mycoses; chronic suppression of cryptococcal meningitis in AIDS patients and Candida infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.

TOXICITY: testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), increases levels of P450 metabolized drugs (cyclosporine, warfarin)

80
Q

Ketoconazole

A

MOA: inhibits fungal (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to

USES: local and less serious systemic mycoses; chronic suppression of cryptococcal meningitis in AIDS patients and Candida infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.

TOXICITY: testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), increases levels of P450 metabolized drugs (cyclosporine, warfarin)

81
Q

Clotrimazole

A

MOA: inhibits fungal (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to

USES: local and less serious systemic mycoses; chronic suppression of cryptococcal meningitis in AIDS patients and Candida infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.

TOXICITY: testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), increases levels of P450 metabolized drugs (cyclosporine, warfarin)

82
Q

Miconazole

A

MOA: inhibits fungal (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to

USES: local and less serious systemic mycoses; chronic suppression of cryptococcal meningitis in AIDS patients and Candida infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.

TOXICITY: testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), increases levels of P450 metabolized drugs (cyclosporine, warfarin)

83
Q

Itraconazole

A

MOA: inhibits fungal (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to

USES: local and less serious systemic mycoses; chronic suppression of cryptococcal meningitis in AIDS patients and Candida infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.

TOXICITY: testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), increases levels of P450 metabolized drugs (cyclosporine, warfarin)

84
Q

Voriconazole

A

MOA: inhibits fungal (ergosterol) synthesis, by inhibiting the P-450 enzyme that converts lanosterol to

USES: local and less serious systemic mycoses; chronic suppression of cryptococcal meningitis in AIDS patients and Candida infections of all types. Itraconazole for Blastomyces, Coccidioides, Histoplasma. Clotrimazole and miconazole for topical fungal infections.

TOXICITY: testosterone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), increases levels of P450 metabolized drugs (cyclosporine, warfarin)

85
Q

Flucytosine

A

MOA: inhibits DNA and RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase–blocks thymidylate synthetase

USES: systemic fungal infections (especially meningitis caused by cryptococcus) in combination with Amphotericin B

TOXICITY: bone marrow suppression

86
Q

Caspofungin

A

MOA: inhibits cell wall synthesis by inhibiting synthesis of B-glucan

USES: invasive aspergillosis, candida.

TOXICITY: GI upset, flushing (by histamine release)

87
Q

Micafungin

A

MOA: inhibits cell wall synthesis by inhibiting synthesis of B-glucan

USES: invasive aspergillosis, candida.

TOXICITY: GI upset, flushing (by histamine release)

88
Q

Anidulafungin

A

MOA: inhibits cell wall synthesis by inhibiting synthesis of B-glucan

USES: invasive aspergillosis, candida.

TOXICITY: GI upset, flushing (by histamine release)

89
Q

Terbinafine

A

MOA: inhibits the fungal enzyme squalene epoxidase (ergosterol biosynthesis inhibitor)

USES: used to treat dermatophytoses–especially onychomycosis (fungal infection in finger or toe nails)

TOXICITY: GI upset, headaches, hepatotoxicity, taste disturbance

90
Q

Griseofulvin

A

MOA: interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues (e.g. Nails)

USES: oral treatment of superficial infections–inhibits growth of dermatophytes (tinea, ringworm)

TOXICITY: teratogenic, carcinogenic, confusion, headaches, increases P450 and warfarin metabolism.

91
Q

Chloroquine

A

MOA: blocks detoxification of heme into hemozoin. Heme accumulates and is toxic to plasmodia.

USES: plasmodial erythrocyte infection (not liver). treatment of plasmodial species other than P. Falciparum (frequency of resistance to falciparum is too great). Resistance due to membrane pump that decreases intracellular concentration of drug. Treat P. Falciparum with artemether/lumafantrine or atovoquone/proguanil. For life-threatening malaria, use quinidine in US or artesunate.

TOXICITY: retinopathy, pruritis

92
Q

Artemether/lumefantrine

A

MOA: not known; drug combo artemisinin derivative and lumafantrine

USES: acute, uncomplicated p. Falciparum; treat chloroquine-resistant strains; NOT prophylaxis or severe

93
Q

Mebendazole

A

Anti-helminthic

MOA: binds worm tubulin and interferes with organellar transport–immobilizes helminth.

USES: enterobiasis (pinworm), trichuriasis (whip worm), ascariasis

94
Q

Praziquantel

A

Antihelminthic therapy

MOA: increases cellular calcium–>permeability leads to death of organism

USES: all species of schistosoma, infection due to liver flukes

95
Q

Zanamivir

A

MOA: inhibits viral neuraminidase–prevents new viral particles from being released

USES: treatment and prevention of both influenza A and B

96
Q

Oseltamivir

A

MOA: inhibits viral neuraminidase–prevents new viral particles from being released

USES: treatment and prevention of both influenza A and B

97
Q

Acyclovir

A

MOA: monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells, so few adverse effects. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination.

USES: HSV and VZV. Weak activity against EBV. No activity against CMV. Used for HSV-induced mucocutaneous and genital lesions as well as encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.

TOXICITY: obstructive crystalline nephropathy and acute renal failure if not adequately hydrated. When the concentration in collecting duct exceeds it’s solubility.

RESISTANCE: mutated viral thymidine kinase,

98
Q

Famciclovir

A

MOA: monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells, so few adverse effects. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination.

USES: HSV and VZV. Weak activity against EBV. No activity against CMV. Used for HSV-induced mucocutaneous and genital lesions as well as encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.

TOXICITY: obstructive crystalline nephropathy and acute renal failure if not adequately hydrated. When the concentration in collecting duct exceeds it’s solubility.

RESISTANCE: mutated viral thymidine kinase,

99
Q

Valacyclovir

A

MOA: monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells, so few adverse effects. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination.

USES: HSV and VZV. Weak activity against EBV. No activity against CMV. Used for HSV-induced mucocutaneous and genital lesions as well as encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV. Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.

TOXICITY: obstructive crystalline nephropathy and acute renal failure if not adequately hydrated. When the concentration in collecting duct exceeds it’s solubility.

RESISTANCE: mutated viral thymidine kinase,

100
Q

Ganciclovir

A

MOA: synthetic analog of 2-deoxyguanine. Converted to ganciclovir mono phosphate by CMV during infection; subsequently, cellular kinases catalyze the formation of gancyclovir diphosphate and triphosphate–activated drug inhibits DNA polymerase and suppresses chain elongation.

USES: CMV, especially in immunocompromised patients. Valganciclovir, a prodrug of ganciclovir, has better oral bioavailability.

TOXICITY: leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.

RESISTANCE: mutated CMV DNA polymerase or lack of viral kinase.

101
Q

Foscarnet

A

MOA: viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme. Does not require activation by viral kinase.

USES: CMV retinitis in immunocompromised patients when ganciclovir fails; acyclovir-resistant HSVZ

TOXICITY: nephrotoxicity, electrolyte abnormalities can lead to seizures. Foscarnet is a pyrophosphate analog that can chelate calcium and cause magnesium wasting leading to decreased PTH which exacerbates hypocalcemia. (Remember dramatic decreases in magnesium inhibit PTH)

RESISTANCE: mutated DNA polymerase

102
Q

Cidofovir

A

MOA: preferentially inhibits viral DNA polymerase. Does not require phosphorylation by viral kinase.

USES: CMV retinitis in immunocompromised patients; acyclovir-resistant HSV. Long half life.

TOXICITY: nephrotoxicity (co administer with probenecid and IV saline to decrease toxicity)

103
Q

Ribavirin

A

MOA: inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase

USES: RSV! Chronic hepatitis C

TOXICITY: hemolytic anemia. Severe teratogen

104
Q

Atazanavir

A

Protease inhibitor

MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.

TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria

105
Q

Darunavir

A

Protease inhibitor

MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.

TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria

106
Q

Fosamprenavir

A

Protease inhibitor

MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.

TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria

107
Q

Indinavir

A

Protease inhibitor

MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.

TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria

108
Q

Lopinavir

A

Protease inhibitor

MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.

TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria

109
Q

Ritonavir

A

Protease inhibitor

MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses. Ritonavir can boost other drug concentrations by inhibiting p-450

TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria. Inhibitor of CYP-450 so increases drug concentrations of those metabolized by CYP -450.

110
Q

Saquinavir

A

Protease inhibitor

MOA: assembly of virions depends on HIV-1 protease, which cleaves the polypeptide products of HIV mRNA into their functional parts. Thus, protease inhibitors prevent maturation of new viruses.

TOXICITY: hyperglycemia, GI intolerance, lipodystrophy, nephropathy, hematuria

111
Q

Abacavir

A

NRTI

MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleoside–needs to be phosphorylated to be active.

TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis

112
Q

Didanosine

A

NRTI

MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleoside–needs to be phosphorylated to be active.

TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis

113
Q

Emtricitabine

A

NRTI

MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleoside–needs to be phosphorylated to be active.

TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis

114
Q

Lamivudine

A

NRTI

MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleoside–needs to be phosphorylated to be active.

TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis

115
Q

Stavudine

A

NRTI

MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleoside–needs to be phosphorylated to be active.

TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis

116
Q

Tenofovir

A

NRTI

MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleotide–does NOT need to be phosphorylated to be active.

TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis

117
Q

Zidovudine

A

Formerly AZT

NRTI

MOA: competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain (lack a 3’ OH group). Nucleoside–needs to be phosphorylated to be active. Used for general prophylaxis and during pregnancy to decrease risk of transmission to fetus.

TOXICITY: bone marrow suppression (can be reversed with granulocyte-stimulating factor and erythropoietin), peripheral neuropathy, lactic acidosis, rash, anemia, pancreatitis

118
Q

Efavirenz

A

NNRTI

MOA: bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides.

TOXICITY: rash and hepatotoxicity are common. Vivid dreams and CNS symptoms common with efavirenz. Contraindicated in pregnancy.

119
Q

Nevirapine

A

NNRTI

MOA: bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides.

TOXICITY: rash and hepatotoxicity are common.

120
Q

Delavirdine

A

NNRTI

MOA: bind to reverse transcriptase at site different from NRTIs. Do not require phosphorylation to be active or compete with nucleotides.

TOXICITY: rash and hepatotoxicity are common. Contraindicated in pregnancy.

121
Q

Raltegravir

A

Integrase inhibitor

MOA: inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase

TOXICITY: hypercholesterolemia

122
Q

Enfuvirtide

A

Fusion inhibitor

MOA: binds gp41 and inhibits viral entry

TOXICITY: skin reaction at injection site

123
Q

Maraviroc

A

Fusion inhibitor

MOA: binds CCR-5 on surface of T cells/monocytes, inhibiting interaction with gp120

TOXICITY: skin reaction at injection site

124
Q

Daptomycin

A

MOA: lipopeptide that disrupts cell membrane of gram positive cocci.

USES: S. Aureus skin infections, bacteremia, endocarditis, VRE

TOXICITY: myopathy, rhabdomyolysis

125
Q

Metronidazole

A

MOA: forms toxic free radical metabolites on the bacterial cell that damage DNA. Bactericidal, antiprotozoal.

USES: treats Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, Anaerobes (Bacteroides, C. Difficile). Used with a proton pump and clarithromycin for triple therapy against h. Pylori.

TOXICITY: disulfiram-like reactions (severe flushing, tachycardia, hypotension) with alcohol, headache, metallic taste

126
Q

Interferons

A

MOA: glycoproteins normally synthesized by virus-infected cells, exhibiting a wide range of antiviral and antitumoral properties

USES: IFN-a: chronic hepatitis B and C, Kaposi sarcoma, hairy cell leukemia, condyloma acuminatum, renal cell carcinoma, malignant melanoma. IFN-B: MS. IFN-gamma: chronic granulomatous disease.

TOXICITY: neutropenia, myopathy

127
Q

Ribavirin

A

MOA: inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase. IMP cannot be converted to GMP.

USES: chronic HCV, also used in RSV (palivizumab preferred in children)

TOXICITY: hemolytic anemia, severe teratogen

128
Q

Simeprevir

A

MOA: HCV protease inhibitor; prevents viral replication

USES: chronic HCV in combination with ribavirin and peginterferon Alfa.

TOXICITY: photosensitivity reactions, rash

129
Q

Sofosbuvir

A

MOA: inhibits HCV RNA-dependent RNA polymerase acting as a chain terminator

USES: chronic HCV in combination with ribavirin, +/- peginterferon Alfa.

TOXICITY: fatigue, headache, nausea

130
Q

Red man syndrome

A

Diffuse flushing following vancomycin treatment. Cn largely prevent by pretreatment with antihistamines and slow infusion rate

131
Q

Prophylaxis for M. Tuberculosis

A

Isoniazid

132
Q

Prophylaxis for M. Avium-intracellulare

A

Azithromycin, rifabutin

133
Q

Palivizumab

A

Monoclonal antibody against F protein of paramyxoviruses. Prevents pneumonia caused by RSV infection in premature infants.

134
Q

Fidaxomicin

A

Treatment for recurrent cases of C. Difficile. Inhibits sigma subunit of RNA polymerase. Oral drug with limited systemic absorption.