Antibiotics Flashcards
Gram + Antibiotics
Beta lactams
- Penicillines
- Cephas
- Carbapenems
Macrolides
- Erythromycin
- Azithromycin
Glycopeptides
- Vancomycin
**Gram+ but may vary
Gram Negative antibiotics
Aminoglycosides
Fluoroquinolones
2-4th cephalosporins
Gram - and Fx2-4
Broad spectrum antibiotics
Tetracyclines
TMS
Chloramphenicol
vanc
linazolid
2nd-4th gen cephas
carbapenems
**Tries to look very casual clocking 2-4
Anaerobic coverage
Azithromycin
Chloramphenicols
Metronidazole
Lincosamides –> clindamycin
Beta Lactams
- Pens: clostridium, peptostreptococci, actinomyces, fusobacterium
-Aminopen-clav against bacterioides
-cephas
** Anaerobes are clearly more like Bitches
Bacteriostatic antibiotics
Interferes with protein production, DNA replocation or cellular metabolism
- Stops reproduction but depends on immune system to kill bacteria
Tetracyclines
Chloramphenicol
Lincosamides (clindamycin)
Macrolides
3 types of resistance
- intrinsic: inherent feature of microbes to be resistant to drug (ex: pseudomonas is intrinsically resistant to beta lactams)
- Circumstantial: susceptible in vitro, but resistant in vivo (ex: inactivated by platelets or cant reach site like CSF)
- Acquired: change in phenotypic characteristic
Inhibitory quotient
Cmax/MIC
High inhibitory quotient must be achieved to reliably kill offending organism with concentration dependent antibiotics
MRS
MC Staph pseudointermedium then aureus
-MOA: acquired mecA gene –> alters PBP
- Also resistent to clinda, fluoroquinolones, macrolides & TMS
Escalation protocols:
- Aminoglycosides - will not act in puss or cellular debris
- Vancomycin drug of choice ((linesolid indicated if resistant or oral therapy needed))
-Tetracyclines, chloramphenicol, rifampin
*Staph be calling man fucking tyrant
MDR Enterococcus
E. Faecalis & E. Faecium
INtrinsic resistance to cephas, clinda, aminoglycosides & fluoroquinolones
Acquired MOA: aminoglycoside-modifying enzymes (AME) or alterations on PBP5
Fluoroquinolone + Cepha use assd with development of vanc resistent MDRE!!!
Treatment options:
-Gentamicin + amp –> synergistic ( no other Aminos synergistic)
- Vancomycin (linesolid indicated if resistant or oral therapy needed)
**Often nosocomial
Pseudomonas aeroginosa
Intrinsic resistance: majority beta lactams (exc ticarcillin, pipercarcillin ceftazadime & carbapenems), quinolones & aminoglycosides
Acquired 3 MOAs:
- Decreased intracellular drug due to efflux pumps or altered membrane structure
-Enzymes modify/destroy antibiotics
-Modify target of antibiotics (DNA gyrase mutation)
Treatment often requires amikacin or carbapenem
RNA synthase inhibitors
- Inhibits RNA polymerase
- lipohilic
- Hepatic clearance
- ABX: Rifampin
Side effects: discolored urine, GI, hepatotoxicity, hypersensitivity
Protein Synthesis Inhibitors
- Inhibit 30s & 50s ribosome units –> prevent mRNA translation
30s inhib: aminoglycosides, tetracyclines
50s inhib: macrolides, chloramphenicol, clindamycin
DNA synthesis inhibitors
-INhibits DNA gyrase & topisomerase IV
- lipophilic
-Renal/hepatic clearance
- ABX: fluoroquinolones, metronidazole
Side Effects: GI, nephrotoxicity, cartilage damage, hepatotox, hypersensitivity
Cephalosporins
- Inhibit cell wwall synthesis
- Bacteriocidal
- Hydrophilic–> renal clearance
- Time dependent
- Aerobic bacteria
- 1st gen> Gram + coverage
- 3 & 4 gen > gram+ & Gram -
*3rd gen ideal for CNS
Ceftazadime –> labeled for pseudomonas
Carbapenems
- Cell wall synthesis inhibition
- Hydrophilic – renal clearance
- Time dept
- Bacteriocidal
- 4 quad coverage
-Withstand beta lactamases (even ESBL)
Imipenem: inc Gram + for E. Faecalis –> neuro signs poss
Meropenem: inc gram - including pseudomonas
Etrapenem: no activity against enterococci
Macrolides
Inhibit ribosomal 50s subunit
-Lipophilic –> hepatic clearance
- Concentration dependent- azithromycin
- Time dep + conc enhanced– erythromycin
-Aerobic Gram + & - & atypical bacteria
-bacteriostatic
- Concentrated in macs–> get to infection
Side effects: GI upset, hypersensitivity–> products of streptomyxces species
Vancomycin
- Cell wall synthesis inhibition
- Hydrophilic - renal clearance
- Time Dept
- Gram + coverage, MRSA, & enterococcus sp
- Bacteriocidal
Augmented renal clearance
- In critically ill: increased renal clearance due to increase CO with decrease SVR
- Human Study: antibiotic clearance 3x with normal Crea
**MC in trauma, sepsis, blood malignancies & pancreatitis
TMS combos
- Inhibit enzymes in folic acid synthesis pathway
- Sulfas–> static
- trimethoprim - cidal
- Sulfa+ trimetho = cidal
- Gram +/- & protozoa
- Renal excretion, metabolism by liver
Side effects: KCS (reversible), hepatitis, hemolytic anemia, leukopenia, GI
Hypersensitivities in Dobies
Chloramphenicol
- Inhibits ribosomal 50s subunit
- Bacteriostatic
- Time dependent
- 4 quadrant coverage, rickettsial, mycoplasma, chlamydia
- EXTENSIVE liver metabolism
- Gram neg resistance via acetylation & inactivated by bascterial enzymes
Side effects: GI upset, hypersensitivity
Nitromidazoles
- ie metronidazole
- Disrupt DNA by forming reactive intermediates
- Bacteriocidal
- Concentration dept
- ONly active in anaerobic conditions
Excellent distribution –> including CNS & abscess
Lincosamides
- Inhibit protein synthesis via binding 50s ribosomeal subunit
- bacteriostatic
- Gram + aerobes, most anaerobes, intracellular bacteria
- Reach high concentrations in abscesses
Ex: clindamycin, lincomycin (less active against anaerobes)
Antibiotics for resistant infections
- Carbapenems
- Glycopeptides –> vancomycin
- Oxazolidinones –> linazolid
Oxazolidinones
MOA: inhibit protein synthesis by binding to bacterial 23s rRNA of 50s subunit
-Static against most bacteria, maybe cidal in vivo
- Resistant Gram + bacteria (streptococci, enterococci)
Ex: linezolid $$$
