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37 Cards in this Set

  • Front
  • Back
Bactericidal Abx
Penicillin, Cephalosporins, Vancomycin, Aminoglycosides, Fluoroquinilones, Metronidazole
Penicillin Mechanism of Action
Pen G = IV
Pen V = Oral
1)Binds Penicillin binding proteins
2)Blocks transpeptidase cross linking of cell wall
3)Activates autolytic enzymes
Penicillin Use and Toxicity
Uses- Bactericidal for Gram (+) cocci (Strep), rods (listeria, etc), gram (-) cocci (Neisseria) and spirochetes

Toxicity- Hypersensitivity reactions (Type I) and hemolytic anemia (Type 2)
Methicillin, Naficillin, Dicloxacillin
MOA- same as penicillin but resistant to B-lactamase

Uses- adds S.aureus coverage but no MRSA (has altered PBP, not penicillinase)

Toxicity- Hypersensitivity
Methicillin- Interstitial Nephritis
Ampicillin, Amoxicillin
MOA- same as Penicillin, still susceptible to B-lactamse (no S. aureus)

Can combine with clavulonic acid (B-lactamase inhibitor)
AmOxicillin better Oral
Amoxicillin, Ampicillin
Use and Toxicity
Use- Extended spectrum Penicillin for gram (+) and (-)
H. flu
entercocci and strep

Toxicity- Rash, Pseudomembranous colitis
Ticarcillin, Carbenicillin, and Piperacillin
MOA- same as penicillin but with extended spectrum

Use- All Gram (+) except S.aureus
All Gram (-) rods and cocci
Cephalosporins MOA and Toxicity
MOA- B-lactam drugs that inhibit cell wall cross linking by binding PBP
Less susceptible to B-lactamases

Toxicity- Hypersensitivity (seen in ~5% pts allergic to penicillin)
Acts like disulfiram in EtOH metabolism causing nausea while drinking (esp Cefamandole)
Worsens aminoglycoside nephrotoxicity
1st generation Cephalosporins
Cefazolin, Cephalexin

Uses- Gram (+) plus PEcK
2nd generation Cephalosporins
Cefoxitin, Cefaclor, Cefuroxime

Uses- Gram (+) plus HEN PEcKS
H.flu, Enterobacter, Nisseria, Proteus, E.coli,Klebsiella, Serratia
3rd Generation Cephalosporins
Ceftriaxone, Cefotaxime, Ceftazidime

Uses- serious gram (-) infxns resistant to other Penicillins, etc
Adds Pseudomonas
Meningitis, gonorrhea
4th Generation Cephalosporins
Cefepime, Cefpiramide

Best for Pseudomonas and Gram (+) coverage
MOA- Bind PBP3 to block cross linking, and is resistant to B-lactamases
Acts in synergy with Aminoglycosides
No Cross reactivity with Penicillin allergy

Uses- Gram (-) rods
Klebsiella, Pseudomonas, Serratia
No Gram (+) activity
Use in pen allergic pts and pts with renal failure (no aminoglycosides)

Toxic- minor GI
Imipenem/Cilastatin, Meropenum
MOA- B-lactamase resistant carbapenum
Cilastatin inhibits renal dihydropeptidase to decrease inactivation

Use-Everything, esp Enterobacter

Toxicity- GI distress, Rash, Seizures at high levels
MOA- Inhibits cell wall synthesis by binding D-Ala D-Ala precursor (resistance via change to D-Ala D-Lac)

Use- MRSA, C. difficile, Enterococcus

Toxicity- NOT many
Thrombophlebitis and Red Man Syndrome if infused too fast (block with Antihistamines--not an allergy)
30S inhibitors are _____ and ______

50S inhibitors are _____, _____, ______, and _______

"buy AT 30, CELL at 50"
Aminoglycosides and Tetracyclin

Chloramphenicol, Erythromycin, Lincomycin, and cLindomycin (CELL)
Aminoglycosides (GNATS)

GNATS do NOT kill anaerobes
Gentamycin, Neomycin, Amikacin, Tobramycin, Streptomycin

Requires O2 for uptake --> ineffective against anaerobes
Aminoglycosides MOA, Use, Toxicity
MOA- blocks 30S initiation complex to cause misreading of mRNA --> bactericidal
No anaerobe activity

Use- Severe Gram(-) infxns, act in synergy with B-lactams
Req'd for Enterobacter
Neomycin used before bowel sx

Toxicity- Nephrotoxic (in combo with cephalosporins), Ototoxic (combo with loop duiretics), and Teratogenic

1) BLocks aminoacyl-tRNA from binding ribosome-->bacteriostatic
2) inhibited by cations --> can't take w/ antacids, milk, iron, etc

1) VACUUM THe BedRoom
Vibrio, Acne, Chlamydia,Ureaplasma, Urealyticum, Mycoplasma,Tularemia,H.pylori,Borrelia (Lyme), Rickettsia

2) Tooth discoloration, GI distress, bone growth inhibition, photosensity, Teratogenic

1) MOA
2) Use
1) ADH antagonist even though it's an ABx

2) Used to trt SIADH
Macrolides (ACE)

1) MOA
2) Use
Azithromycin, Clarithromycin, Erythromycin

1) blocks 23S RNA subunit of 50S ribosome to prevent translocation of growing peptide into P site

2)Atypical Pneumonia - Mycoplasma, Legionella, Psitticosis,
STDs- Chlamydia, Neisseria
Trt of Strep if Pen allergy
Simple Gram (-)like E.coli, H.flu
1)Macrolides Toxicity

2) 2 drugs increased while on this Abx (inhibits p450)
1)MC is GI disturbance
Skin Rash, Change in taste (clarithromycin), Eosinophilia, Tosades de Pointes (w/ 3rd antihistamine and Cisapride)

2)Blood thinners, theophylline
MOA- Bacterostatic via blocking 50S pepidyltransferase (blocks addition of amino acid onto growing peptide)

Use- Meningitis if other therapies fail

Toxicity- Anemia, Aplastic Anemia, gray baby syndrome
MOA- Bacterostatic via 50S

Use- Anaerobic infxns (Bacteroides, Clostridium, mouth bacteria), and Staph?Strep

Toxicity- Pseudomembranous colitis, fever, diarrhea
Sulfonamides (SMX)
1) MOA
2) Use
3) Toxicity
1)Inhibits PABA --> Dihydrofolate (dihydropteroate synthase)

2) Gram (+) and Gram (-), simple UTI's

3) Hypersensitivity, hemolysis if G6PD deficient, nephrotoxic, kernicterus

1) MOA- inhibits Dihydrofolate--> THF to prevent DNA synthesis

2) used in combo with SMX to trt recurrent UTIs, Shigella, Salmonella, PCP

3) Toxic- megaloblastic anemia, granulocytopenia, leukopenia
(all end in -oxacin)

Quinolones hurt your bones
1) MOA- inhibits DNA gyrase and is bactericidal

2)Use- gram (-) UTI and GI infxns, Pseudomonas, Neisseria, Gram (+)

3) Toxic- GI upset, headache, cartilage damage (teratogenic), tendonitis, myaglia
MOA- toxic metabolites in cell wall --> cidal

Uses- Protozoa (Giardia, Entamoeba, Trichomonas
Triple Therapy for Ulcers

Toxic- acts like disulfiram for EtOH use, metallic taste
MOA- binds cell membranes like a detergent and disrupts them (mixes up membrane)

Use- Resistant Gram (-) infxns

Toxic- Neurotoxic, Acute Tubular Necrosis
Penicillin/Cephalosporin Resistance
B-lactamase cleaves the ring
Aminoglycoside Resistance
Modification via acetylation, adenylation, or phosphorylation
Vancomycin Resistance
Terminal D-Ala in cell wall is changed to D-Lac to decrease affinity
Chloramphenicol Resistance
Modified by acetylation
Macrolide Resistance
Methylation of RNA near the 50S binding site
Tetracycline Resistance
blocked uptake or increase efflux out of the cell
Sulfonamides Resistance
Altered Dihydropteroate synthase enzyme, or increased PABA synthesis to overwhelm the drug