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155 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Empiric therapy is:
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presumptive
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Gram + bacteria stain:
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blue or purple
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Gram (-) bacteria stain:
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red or pink
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Skin & Soft Tissues are usually infected by gram:
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positive bacteria
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Intra-abdominal bacteria tend to be:
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gram (-) or anaerobes
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Which ABX inhibit cell wall synthesis?
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Penicillins
Cephalosporins Carbapenems Monobactams (aztreonam) Vancomycin |
Penny Ceded Carl Many Vaginas
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Which ABX inhibit protein synthesis?
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Chloramphenicol
Tetracyclines Glycylcycline (tigecycline) Macrolides Clindamycin Streptogramins (quinupristin/dalfopristin) Oxazolidinones (linezolid) Aminoglycosides |
Chlorinated Tetras Glide Macroscopically Close Strumming Oxen Along
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Which ABX alter nucleic acid metabolism?
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Rifamycins
Quinolones |
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Which ABX inhibit folate metabolism?
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Trimethoprim
Sulfonamides |
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Bactericidal:
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kill organisms, reducing their concentration
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Bacteriostatic agents cause:
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inhibition of bacterial growth but doesn't kill them.
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What is the minimum inhibitory
concentration? |
The lowest concentration of drug that prevents
visible bacterial growth after 24 hours of incubation in a specified growth medium |
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Time-dependent ABX must exceed ____ percent of the MIC.
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40-50
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What are the 6 main factors in ABX selection?
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PK, Resistance, Efficacy, Safety & tolerability, Dosing & administration, Cost
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Which class of ABX are conc. dependent?
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Aminoglycosides, Daptomycin, Metronidazole, Polymixins, and Quinilones
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Amanda Quintupled Dad's Metrosexual Polyuria
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What differentiates the penicillins?
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The right side of their Beta-lactam chains
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How do Beta-Lactams work generally?
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By inhibiting the 3rd (last) step of cell wall synthesis (transpeptidation)
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What is the process involved in Beta-Lactam action specifically?
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They inactivate penicillin-binding proteins (PBPs) by bind to them, resulting in autolysin mediated autolysis and cell death.
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Beta is Bound
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What are the pharmodynamics of B-Lactams?
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Time-dependent killing and bacteriacidal
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The Beta Band Killed Time
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What two classes act as cell wall inhibitors?
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Beta-lactams and glycopeptides
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The Wall Yielded to Beta Waves and Glycolysis
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What families are cell wall inhibitors?
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Penicillins, Cephalosporins, Monobactam (aztreonam), Carbapenams, Vancomycin
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Penny Vandalized the WALL with Ceph, Monk, Azrael, and Carl
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What is the spectrum of natural PCN action?
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Narrow; it works on spirochetes (Treponema pallidum) and select bacteria
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What is the drug of choice for syphilis?
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PCN G
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Which form of natural PCN is available IV?
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K+ or Na+ salt
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Which IM form of natural PCN has a bioavailability equivalent to IV admin?
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Procaine
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High Biologists Procrastinate
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Which penicillinase-resistant PCNs are available IM/IV?
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Nafcillin & Oxacillin
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Nefarious Oxen Inject Pennies
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Which penicillinase-resistant PCNs are available PO only?
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Cloxacillin, Dicloxacillin
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Penny has a Clock with a Mouth
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Penicillinase-resistant PCNs are ______ spectrum?
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Narrow
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Penicillinase-resistant PCNs work only on gram ____ bacteria
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positive
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Which Penicillinase-resistant PCNs is most often used and for what?
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Methicillin for MSSA
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Aminopenicillins include:
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ampicillin & amoxicillin
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Which of the Aminopenicillins is available parenterally?
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Ampicillin
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Inject Amplitude
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Aminopenicillins are ______ spectrum.
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narrow
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Aminopenicillins are similar to _____ in their spectrum, adding a few more bacteria.
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PCN Gs
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Aminopenicillins are the drug of choice for:
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enterococcus and listeria
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Amin Entered Listlessly
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Which two classes of PCNs are good for pseudomonas infections?
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Carboxypenicillins and Ureidopenicillins
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Carbon's Pseudonym is Urea
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What is the primary Ureidopenicillin and what is its spectrum of activity?
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Piperacillin and it is broad spectrum, but particularly good against gram (-) bacteria (pseudomonas)
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The Piper was Broadly Negative for Urea
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Ticarcillin is a:
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Carboypenicillin
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Ticarcillin is available:
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parenterally
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Carboxypenicillins and Ureidopenicillins are used clinically for:
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gram (-) Enterobacter and pseudomonas infections; UTIs, RTIs, Bactremias, & intra-abdominal infections
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Carbon and Urea Negatively affected Urine Reabsorption Adamantly with Brio
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What are B-Lactamase inhibitors and what do they do?
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They bind to enzymes, increasing B-Lactam spectrum activity
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What are the B-Lactamase inhibitors?
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Clavulanic Acid, sulbactam, tazobactam
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Lacrimose Clowns Acidly Suckled on Tazo Tea
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What is the absorption of PCNs?
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PO formulations are incompletely absorbed. Amoxicillin has higher F than ampicillin.
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Poor Absorption Amplified Orally
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Which class of PCNs are hepatically metabolized?
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Penicillinase-resistan penicillins
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What is the average half-life of the PCNs?
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~0.8-1 hr
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Why are PCNs good for UTIs?
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Because they have have high urinary concentrations?
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How well are PCNs distributed? What are the exceptions?
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Very well. Exceptions are eyes, brain, CSF, or prostate.
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What needs to be taken into consideration when calculating dosage of PCNs?
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Renal function
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The ACDs of PCNs are available:
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PO
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What is the ABX of choice for gout?
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a PCN
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What are the AEs of PCNs?
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Hypersensitivity, diarrhea, nephritis, seizure @ high dose, thrombophlebitis (injection site), elevated liver enzymes, hypokalemia, hypernatremia, platelet dysfunction
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Penciled Hyper Dinosaurs Seize Thrones High Above the Liver
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Modifications of the R1 side chain in cephalosporins alters what?
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antibacterial activity
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Modifications of the R2 side chain in cephalosporins alters what?
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Metabolism and PKs
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MTT side chain in cephalosprorins causes what?
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Increased risk of bleeding
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Which cephalosporins achieve adequate CSF concentration for meningitis Tx?
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cefuroxime, cefotaxime, ceftriaxone, ceftazidime, and cefepime
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Furious Tax Trials Dimed Pine
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What is the trend in the generations of cephalosporins?
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Increasingly broad spectrum and increasingly active against gram (-) bacteria
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Spores Broadly Dispersed Negatives
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Which cephs. are prodrugs?
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Cefuroxime & cefpodoxime
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What is the distribution of cephs.?
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Wide with variable protein binding
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What determines dosing freq. in cephs?
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half-life
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How are cephs eliminated?
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Renally
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What are the exceptions to the normal path of exit for cephs?
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Ceftriaxone and cefoperazone are hepatic
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Triad Zone Livers
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What are the AE of cephs.?
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Same as PCNs.
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What is the only monobactam?
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aztreonam
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Old smart phone
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aztreonam has what spectrum?
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Narrow and gram (-) only (pseudomonas)
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The Treo is Narrow and Negative
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What are the PKs of aztreonam?
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IV only, high F, good CSF conc., renal elim., ~2 hr half-life
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Ivies Flourish Cendantly Reaching Two Lives
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What advantage does aztreonam have?
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It's structure is different enough from the other B-Lactams that it can be used in those with a hypersensitivity to them.
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What AE does aztreonam have?
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Rash
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Carbapenams differ how?
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In their 5-ring structure?
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What is special about carbapenems?
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They are EXTREMELY broad spectrum
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Which Carbapenems are broad action?
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Imipenem and meropenem
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Imps Merrily Carve Broadly
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What can't carbapenems treat?
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MRSA
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When are carbapenems indicated?
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For severe, ABX infections
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Why is imipenem coformulated with cilastatin?
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To inhibit a kidney enzyme that would degrade the imipenem
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What are the PKs of carbapenems?
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IV, IM only, high F, can infiltrate CSF, primarily renal
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Cartoon Images Distribute Widely Into Cartoon Network and leave Ren & stimpy
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Which cabapenem is give qd?
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ertapenem
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What are the AEs of carbapenems?
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Hypersensitivity, seizures, diarrhea, & increased liver enzymes
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All B-Lactams are Preg. Cat B except for ________which Cat C
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imipenem
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What is the MoA for Vanco?
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Inhibits cell wall synthesis by inhibiting SECOND stage peptidoglycan synthesis
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What is the spectrum of vanco?
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Gram + only, including MRSA; considered broad spectrum gram + agent
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What are the PKs of vanco?
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Poor oral F, high fluid bioavailability, protein binding ~30-55%, renal excretion
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What are the PDs of vanco?
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Bacteriacidal, time-dependent, and trough levels are to be monitored and should be 10-20mcg/ml
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Vinny Murdered Tim and threw him in a Trough
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What are the AEs of vanco?
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H1 mediated rash dependent upon infusion rate, nephrotoxicity, and ototoxicity
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Histrionic Vandals Redden Ears and Kidneys
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Protein synthesis inhibitors are all _______________ except for ______________.
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bacteriostatic; aminoglycosides
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Static Produce Aminates
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All protein synthesis inhibitors bind to the 50S ribosomal subunit except for ___________ and __________
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aminoglycosides; tetracyclines
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30 Soldiers Abort Sides
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Chloramphenicol is rarely used because:
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it causes hemopathies (aplastic anemia in 20 %, "gray baby" syndrome, & reversible bone marrow supression
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What is spectrum of chloramphenicol?
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Broad with all 3 types of bacteria
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PKs of chloroamphenicol:
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Well absorbed from GI tract, high F, hepatic, bacteriostatic
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The MoA of tetracyclines is:
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inhibition of the 30S ribosomal subunit
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Doxycycline is good for:
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Lyme's disease
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The Foxy Doc Went to Lyme
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What spectrum are tetracyclines?
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Relatively narrow-spectrum
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Tetracyclines are bacteriostatic/bacteriacidal.
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bacteriostatic
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What class is an alt. to macrolides for resp. illness?
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Tetracyclines
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Why are tetracyclines OK for PCN -sensitive pts?
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Completely different class
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What are the PKs of tetracyclines?
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-Oral F is incomplete
-Chelates to Fe, Mg, Al, Zn, Ca -Widely distributed, including CSF -Tetra = renal -Mino = liver -Doxy = fecal |
Bound Biologists Cheer Wide Distribution of Tetra Rings, Mean Lives, and Doughy Feces
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Tetracycline AEs:
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Preg Cat D
GI Photosensativity Hepatic/renal toxicity Permanent brown discoloration of teeth Dizziness |
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What is Fanconi syndrome and what class of ABX is it associated with?
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proximal renal tubule toxicity; assoc with outdated tetracycline
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Glycylcycline (tigecycline)is indicated for:
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Mycobacteria in institutional setting and is broad spectrum
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Tigecycline's PKs:
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IV only
Very tissue bound Eliminated via feces Pregnancy Cat D |
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Tigecycline's AEs:
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Same as tetras + n/v & hepatotoxicity
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Macrolide PDs & MoA
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PD: Bacteriostatic
MoA: 50S inhibitor |
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Macrolide spectrum:
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Relatively narrow gram (-) & +
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Which macrolide has no IV formulation?
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Clarithromycin
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Which macrolide is NOT a CYP450 inhibitor?
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z-pak
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The two macrolides that inhibit substrates inhibit which CYP450?
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3A4
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Macrolide absorption:
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Eryth base enteric coated
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Macrolide distribution:
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Eryth: Billiary, shorter half-life
Clarith: CYP450/renal, long half-life Azith: Biliary/Fecal, long half life |
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Macrolide AEs:
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Eryth inhibit GI motility, cholestatic hepatitis, ototox
All can cause QT prolongation |
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Clindamycin MoA and SoA:
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50S inhibitor
Relatively narrow, gram + & anaerobic only |
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Clindamycin PD & Indications:
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Bacteriostatic
Integ infections Acne (topically) |
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Clindamycin PK:
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Nearly completely absorbed, poor CSF dist., >90% protein bound
Extensive hepatic metabolism; excreted in bile and urine Preg Cat B |
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Clindamycin AEs:
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Diarrhea
Rash Elevated liver enzymes |
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What are the 2 streptogramins?
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quinupristin/dalfoprisin in a synergistic formulation
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Pristine Synergy
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Streptogramin spectrum:
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Gram + ONLY
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Streptogramin PK:
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IV only / D5 only (no NS)
No CSF Hepatic metabolism by conjug. Biliary Excretion |
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Streptogramin PD:
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each is bacteriostatic; may be bactericidal in combo
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Streptogramin is an inhibitor of:
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3A4
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Streptogramin rarely used:
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due to toxicity (liver)
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The only oxazolidinone is:
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linezolid
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Linezolid MoA & Class:
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50S inhibitor
Synthetic |
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Linezold SoA, PD, & Indications:
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Gram + only
Broad Spectrum Mycobacteria Bacteriostatic Resistant gram + bacteria |
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Linezolid PK:
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100 % oral bioavailability including CSF
Excreted in urine (non-enzymatic oxidation) |
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Linezolid AEs and tetra:
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Bone marrow suppression (thrombocytopenia, anemia, leukopenia)
Cat C |
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Aminoglycosides include:
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Gentamicin, tobramycin, amikacin, streptomycin
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Aminoglycosides MoA:
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30S inhibition
Aerobic and energy-dependent |
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Aminoglycosides SoA:
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Aerobic gram (-) organisms
Gram + w/ cell wall-active agt |
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Aminoglycosides PDs:
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Rapidly bacteriacidal, concentration-dependent, post-ABX effect (fail to grow at concentrations below MIC)
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Aminoglycosides PKs:
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Renal elim
Poor GI absorption Rapid IM absorption |
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Aminoglycoside AEs & Tetra:
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Nephrotoxicity (8-26%) (reversible)
Ototoxicity (irreversible) Neuromuscular blockade (rare) |
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Aminoglycoside dosing:
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Narrow therapeutic index
Dose based on lean or adjusted body weight |
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Quinolones MoA:
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Alter nucleic acid metabolism
Target DNA gyrase and topoisomerase IV (loosens chromosome) |
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Quinolones SoA:
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Gram (-)
"Atypicals" |
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Quinolones PK:
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Good oral absorption
Chelates w/ cations High F Mostly renal, some hepatic (moxi mostly hepatic) Concentration-dependent Bactericidal |
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Quinolones Safety:
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Arthritis
QT Prolongation CNS Cat C |
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What are the folic acid inhibitors?
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Sufonamides & trimethoprim/sulfamethoxazole
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trimethoprim/sulfamethoxazole SoA:
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Ltd gram (+) & (-) coverage
Drug of choice for PCP in immunocompromised pts as Tx and prophylaxis |
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Sulfonamide PKs:
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Var. absorption
Wide dist. ~65 % protein bound Excreted in Urine Bacteriostatic |
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Sulfonamides AEs:
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**Hypersensitivity (SJS & sulfa alergy)
KERNICTERUS (encephalopathy) in nenoates Crystalluria (crystals in kidneys/increased Cr) |
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Sulfonamide interactions:
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Sulfonylurea hypoglycemic agents, AEDs, warfarin
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The two urinary tract antiseptics are:
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Methanamine and nitrofurantoin
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Methenamine properties:
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Prodrug that decomposes in H20 to form formaldehyde
H+ increase in urine promotes formaldehyde action Produces NH3 (hepatotoxic) USED AS PROPHYLAXIS FOR UTIs |
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Nitrofurantoin MoA & SoA:
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MoA: enzymatically reduced, binds to ribosomal proteins, damaging DNA (theory)
SoA: Limited to some gram (-) & (+); narrow spectrum |
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Nitrofurantoin PKs:
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40-50 % absorption
Renal elim CrCl > 40ml/min ONLY |
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Nitrofurantoin AEs:
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anemia, elevated liver enzymes, neuropathies, n/v/d
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Metronidazole MoA:
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Enters via e- transport protein ferrodoxin, reduced, binds to DNA, breaking DNA (thought)
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Metronidazole SoA, PK:
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SoA: anaerobes only
PK: IV/PO Hepatic metabolism/renal excretion Good oral F |
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Metronidazole AEs:
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**CNS (ataxia, dysarthia, dizziness, confusion, excitation, depression seizures)
Peripheral neuropathies (burning/tingling) Metallic taste Avoid EtOH |
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Daptomycin MoA, Class, Spectrum:
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Ion leakage causes cell death
Cyclic lipopeptide Gram + only (including MRSA, VRE) |
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Daptomycin PKs/PDs:
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Concentration dependent bactericidal (like quinolones and aminoglycosides)
Poor oral absorption Renal elim. |
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Daptomycin AE:
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***Myositis (muscle pain or weakness due to increased creatine kinase)***
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Polymixins MoA & SoA:
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Lysis gram (-) cell wall by changing permeability in cytoplasm
Gram (-) only |
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Polymixins PK/PD:
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Concentration dependent
Highly tissue bound Cleared via glomular filtration |
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Polymixins AEs:
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Binding greatest to kidney and brain = cumulative toxicity
Renal toxicity Neurotoxicity |
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B-Lactams PD Parameters:
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Time-dependent
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Vanco PD Parameters:
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Time dependent & prolonged persistent effects
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Aminoglycosides & Meronidazole PD Parameters:
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Concentration dependent & prolonged persistent effects
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