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24 Cards in this Set

  • Front
  • Back
What is the spectrum of penicillins?
How do they work?
What infections are they good for?
*effective agst G+, easy G-, anaerobes
*Bactericidal - inhibit cell wall synthesis
*Good for UTI's
Name two examples of natural penicillins

What is their spectrum?
Pen G and Pen V

G+, G-, spirochetes
Name two penicillinase-resistant penicillins

What is their spectrum?
Cloxacillin and dicloxacillin

Effective against penicillinase producing G+ cocci, especially Staph
Name two aminopenicillins

What is their spectrum?
Ampicillin and amoxicillin are aminopenicillins

Broad spectrum with increased G- activity
Extended spectrum penicillins include _____.

These are even more effective agst ___ and also work against _____
Carbenicillin, ticarcillin, piperacillin

more effective against G- and Pseudomonas
Potentiated penicillins include

These inactivate _____
Clavamox, timentin

Inactivate beta-lactamases
Penicillins as a class are primarily effective against ____ bacteria and increase in ____ activity

They are (bactericidal/bacteristatic)
Primarily effective against G+
Increase in G-

Penicillins < aminopenicillins < extended spectrum

Penicillins are bactericidal
T/F Penicillin is an appropriate antibiotic to use in rodents and lagomorphs

elimination of G+ gut flora can lead to fatal colibacillosis
What is the spectrum of cephalosporins?
Are they static or cidal?
How do they work?
Good against G+, some G- (more with each generation), and anaerobes

Cephalosporins are bactericidal

They work by inhibiting cell wall synthesis
More effective against actively growing bacteria
Name 6 1st generation cephalosporins
Cephalothin, cefazolin, cephapirin, cephadine, cephalexin, cefadroxil

Most G+, poor G-
Name 4 3rd generation cephalopsporins
Cefotaxime, moxolactom, cefoperazone, ceftiofur (use in bovine resp dz - no withdrawal)

Good G+, much improved G-
What is the spectrum of aminoglycosides?
Primarily G- aerobes, some G+, pseudomonas, atypical mycobacterium (nocardia, actinomyces)

Inactive against fungi, viruses, and most anaerobes
What is the MOA of aminoglycosides?

Are they cidal or static?
Irreversibly bind to the 30S ribosome and INHIBIT PROTEIN SYNTHESIS

Name four examples of aminoglycosides
amikacin (SID, parvo pups)
Where do aminoglycosides accumulate?
Inner ear and kidneys
What are some adverse effects of aminoglycosides?
NEPHROTOXIC - casts in urine, inc BUN/CREA, reversible when drug is d/c

OTOTOXIC - 8th CN toxicity, auditory and vestibular symptoms may be irreversible

NM BLOCKADE - can occur resulting in apnea and paralysis, respiratory failure
What is the spectrum of the fluoroquinolones?

Are they cidal or static?
Good G- aerobes, facultative anaerobes, atypical mycobacterium, chlamydia, mycoplasma, ehrlichia, BRD

They are cidal (except recently shown to be static in cats)
Name three examples of fluroquinolones
Enrofloxacin (QD, prostate, RMSF, de-ethylated to cipro)
Name some contraindications to fluoroquinolones
Contraindicated in young animals due to cartilage defects

Enrofloxacin will cause retinal detachment (blindness) in cats at 5 mg/kg
How do fluoroquinolones work?
FQ inhibit DNA gyrase and prevent DNA synthesis
What is the spectrum of sulfonamides?

Are they static or cidal?
G+, easy G-, anaerobes, nocardia and actinomyces

How do sulfonamides work?
Sulfonamides inhibit folic acid pathyway (PABA/pteridine is not converted to DHFA)

*Many bacteria have developed resistance
How do potentiated sulfonamides work?

Name an example
Bactericidal, inhibits bacterial thymidine synthesis in folic acid pathway

An example is TMPS
What are some of the side effects of sulfonamides
*Most drug side effects of all antibiotics
Allergic reactions, hepatotoxic, KCS, hypothyroidism, crystalluria, thyrotoxic, anemia, BM toxicity (aplastic anemia, thrombocytopenia, hypoprothrombinemia)