atibiotic study guide Flashcards
Drugs that weaken cell walls
PCNs Cephalosporins Carbapenems Fosfomycin Vancomycin
Bacteriostatic Inhibitors of Protein Synthesis
Macrolides
Tetracyclines
Ketolides
Competitive Antimetabolite in the Synthesis of Folic Acid
Sulfonamides
CA-MRSA
Sulfonamides (less effective secondary to resistance):
Sulfonamides (less effective secondary to resistance):
PCN
Staph (Skin, bone, joint)
Penicillinase Resistant Penicillins (PRPs):
Strep and Group A Strep (GAS)
Natural and broad-specturm
Β-Lactamase Inhibiting Compounds (BLIC):
respiratory, S. pneumoniae, GAS
staph and strep (Gr + activity)
Cephalosporins 1st and 4th generations
Cephalsporin 2nd gen
Moderate Gr+ activity
Cephlasporin 3rd
more Gram - coverage than Gram + coverage
Some Staph, indicated for CA-MRSA
Tetracyclines
Staph, poor activity S. pneumonaie
Fluoroquinolones
variable activity against Gram + Strep and Staph; some Gram + bacilli (Gut)
Macrolides
UTI (growing resistance TMP-SMX), less respiratory coverage secondary to
resistance. Special use Pneumocystis carinii
Sulfonamides
Gram – cocci and some Gram –
bacilli (UTI, although growing resistance)
Penicillins Natural
: Gram – bacilli, pseudomonas BLIC: Gram + and
Gram –
Extended spectrum (Ticarcillin, Piperacillin)
aerobic Gr- (GI/GU); not effective against anaerobes
Fluoroquinolones
Some Gram – (Gut). Campylobacter, Legionella Cover Weird Intracellular (atypical):
Chlamydia, Ureaplasma, Mycoplasma
Macrolides
Gram - ; limited by side effects Cover weird Intracellular (atypical): Chlamydia,
Ureaplasma, Mycoplasm
Tetracyclines
. Decreased Permeability
(e.g., Pseudomonas)
Antibiotic Efflux Pump
• (e.g., S. pneumoniae vs. quinolones, macrolides)
Drug Inactivation
(e.g., -lactamase from H. influenzae, Staph, E. coli, Klebsiella)
Altered Target Site
(e.g., S.pneumoniae (altered PBPs), S. pneumonia vs macrolides (ribosomal methylase), S.
pneumoniae vs quinolones (GyrA, Topo4))
Gram +
(SSE) Strep, Staph, Enterococcus – Skin, soft tissue, respiratory
Gram -
H. flu, Neisseria, Moraxella – Respiratory, Meningtitis, GU
(EKP): E-coli, Klebsiella, Proteus – GU
(ESP) Enterobacter, Serratia, Providencia – GI
Salmonella, Shigella – GI
Atypicals
Chlamydia, Mycoplasm, Legionella – Respiratory, GU
Pseudomonas
—Respiratory, other
Bacteroides
GI, Respiratory
SSE infection site
Skin, soft tissue
Respiratory tract
GI/GU
SSE Treatment
Gr + Action: PCNs, Carbapenems, macrolides,
clindamycin, tetracyclines, fluoroquinolones,
cephalosporins
PCNs* Aminoglycosides*, glycopeptides
HNM Infection site
AOM, sinusitis, bronchitis
Meningitis
GU
AOM, sinusitis, bronchitis
HNM treatment
Gr- action: Macrolides, carbapenems,
ketolides, fluoroquinolones, 3/4
cephalosporins,
EKP infection site
UTI, GI
ESP Infection Site
GI
Salmonella, Shingella Infection site
GI
EKP treatment
Gr- action:Carbapenems, aminoglycoside
fluoroquinolones, 2/3/4 cephalosporins,
TMP-SMX
ESP Treatment
Stronger Gr- action: Carbapenems, 3/4
cephalosporins, fluoroquinolones,
aminoglycosides
Salmonella, Schigella Treatment
TMP-SMS, PCN (Shigella
Pseudomonals Infection site
Pneumonia, various
Bacterioides infection site
GI, Aspiration Pneumonia
Bacteroids treatment
Carbapenems, Clindamycin, Tetracycline
Pneumona, various treatment
Aminoglycoside, βlactam,quinolone,3cef
Immediate (Most emergent: urticare, angioedema, anaphylaxis)
Type 1
Cytotoxic (Activation of the complement cascade: PCNS and Sulfa most common)
Type 2
Delayed Immune Complex Reactions (Complement fixation induced and lodged in small
blood vessels skin, kidneys, joints: Serum Sickness)
Type 3
Cell Mediated Reaction (topical applications; hypersensitivity)
Type 4