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155 Cards in this Set

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Empiric therapy is:
presumptive
Gram + bacteria stain:
blue or purple
Gram (-) bacteria stain:
red or pink
Skin & Soft Tissues are usually infected by gram:
positive bacteria
Intra-abdominal bacteria tend to be:
gram (-) or anaerobes
Which ABX inhibit cell wall synthesis?
Penicillins
Cephalosporins
Carbapenems
Monobactams (aztreonam)
Vancomycin
Penny Ceded Carl Many Vaginas
Which ABX inhibit protein synthesis?
Chloramphenicol
Tetracyclines
Glycylcycline (tigecycline)
Macrolides
Clindamycin
Streptogramins
(quinupristin/dalfopristin)
Oxazolidinones (linezolid)
Aminoglycosides
Chlorinated Tetras Glide Macroscopically Close Strumming Oxen Along
Which ABX alter nucleic acid metabolism?
Rifamycins
Quinolones
Which ABX inhibit folate metabolism?
Trimethoprim
Sulfonamides
Bactericidal:
kill organisms, reducing their concentration
Bacteriostatic agents cause:
inhibition of bacterial growth but doesn't kill them.
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
Time-dependent ABX must exceed ____ percent of the MIC.
40-50
What are the 6 main factors in ABX selection?
PK, Resistance, Efficacy, Safety & tolerability, Dosing & administration, Cost
Which class of ABX are conc. dependent?
Aminoglycosides, Daptomycin, Metronidazole, Polymixins, and Quinilones
Amanda Quintupled Dad's Metrosexual Polyuria
What differentiates the penicillins?
The right side of their Beta-lactam chains
How do Beta-Lactams work generally?
By inhibiting the 3rd (last) step of cell wall synthesis (transpeptidation)
What is the process involved in Beta-Lactam action specifically?
They inactivate penicillin-binding proteins (PBPs) by bind to them, resulting in autolysin mediated autolysis and cell death.
Beta is Bound
What are the pharmodynamics of B-Lactams?
Time-dependent killing and bacteriacidal
The Beta Band Killed Time
What two classes act as cell wall inhibitors?
Beta-lactams and glycopeptides
The Wall Yielded to Beta Waves and Glycolysis
What families are cell wall inhibitors?
Penicillins, Cephalosporins, Monobactam (aztreonam), Carbapenams, Vancomycin
Penny Vandalized the WALL with Ceph, Monk, Azrael, and Carl
What is the spectrum of natural PCN action?
Narrow; it works on spirochetes (Treponema pallidum) and select bacteria
What is the drug of choice for syphilis?
PCN G
Which form of natural PCN is available IV?
K+ or Na+ salt
Which IM form of natural PCN has a bioavailability equivalent to IV admin?
Procaine
High Biologists Procrastinate
Which penicillinase-resistant PCNs are available IM/IV?
Nafcillin & Oxacillin
Nefarious Oxen Inject Pennies
Which penicillinase-resistant PCNs are available PO only?
Cloxacillin, Dicloxacillin
Penny has a Clock with a Mouth
Penicillinase-resistant PCNs are ______ spectrum?
Narrow
Penicillinase-resistant PCNs work only on gram ____ bacteria
positive
Which Penicillinase-resistant PCNs is most often used and for what?
Methicillin for MSSA
Aminopenicillins include:
ampicillin & amoxicillin
Which of the Aminopenicillins is available parenterally?
Ampicillin
Inject Amplitude
Aminopenicillins are ______ spectrum.
narrow
Aminopenicillins are similar to _____ in their spectrum, adding a few more bacteria.
PCN Gs
Aminopenicillins are the drug of choice for:
enterococcus and listeria
Amin Entered Listlessly
Which two classes of PCNs are good for pseudomonas infections?
Carboxypenicillins and Ureidopenicillins
Carbon's Pseudonym is Urea
What is the primary Ureidopenicillin and what is its spectrum of activity?
Piperacillin and it is broad spectrum, but particularly good against gram (-) bacteria (pseudomonas)
The Piper was Broadly Negative for Urea
Ticarcillin is a:
Carboypenicillin
Ticarcillin is available:
parenterally
Carboxypenicillins and Ureidopenicillins are used clinically for:
gram (-) Enterobacter and pseudomonas infections; UTIs, RTIs, Bactremias, & intra-abdominal infections
Carbon and Urea Negatively affected Urine Reabsorption Adamantly with Brio
What are B-Lactamase inhibitors and what do they do?
They bind to enzymes, increasing B-Lactam spectrum activity
What are the B-Lactamase inhibitors?
Clavulanic Acid, sulbactam, tazobactam
Lacrimose Clowns Acidly Suckled on Tazo Tea
What is the absorption of PCNs?
PO formulations are incompletely absorbed. Amoxicillin has higher F than ampicillin.
Poor Absorption Amplified Orally
Which class of PCNs are hepatically metabolized?
Penicillinase-resistan penicillins
What is the average half-life of the PCNs?
~0.8-1 hr
Why are PCNs good for UTIs?
Because they have have high urinary concentrations?
How well are PCNs distributed? What are the exceptions?
Very well. Exceptions are eyes, brain, CSF, or prostate.
What needs to be taken into consideration when calculating dosage of PCNs?
Renal function
The ACDs of PCNs are available:
PO
What is the ABX of choice for gout?
a PCN
What are the AEs of PCNs?
Hypersensitivity, diarrhea, nephritis, seizure @ high dose, thrombophlebitis (injection site), elevated liver enzymes, hypokalemia, hypernatremia, platelet dysfunction
Penciled Hyper Dinosaurs Seize Thrones High Above the Liver
Modifications of the R1 side chain in cephalosporins alters what?
antibacterial activity
Modifications of the R2 side chain in cephalosporins alters what?
Metabolism and PKs
MTT side chain in cephalosprorins causes what?
Increased risk of bleeding
Which cephalosporins achieve adequate CSF concentration for meningitis Tx?
cefuroxime, cefotaxime, ceftriaxone, ceftazidime, and cefepime
Furious Tax Trials Dimed Pine
What is the trend in the generations of cephalosporins?
Increasingly broad spectrum and increasingly active against gram (-) bacteria
Spores Broadly Dispersed Negatives
Which cephs. are prodrugs?
Cefuroxime & cefpodoxime
What is the distribution of cephs.?
Wide with variable protein binding
What determines dosing freq. in cephs?
half-life
How are cephs eliminated?
Renally
What are the exceptions to the normal path of exit for cephs?
Ceftriaxone and cefoperazone are hepatic
Triad Zone Livers
What are the AE of cephs.?
Same as PCNs.
What is the only monobactam?
aztreonam
Old smart phone
aztreonam has what spectrum?
Narrow and gram (-) only (pseudomonas)
The Treo is Narrow and Negative
What are the PKs of aztreonam?
IV only, high F, good CSF conc., renal elim., ~2 hr half-life
Ivies Flourish Cendantly Reaching Two Lives
What advantage does aztreonam have?
It's structure is different enough from the other B-Lactams that it can be used in those with a hypersensitivity to them.
What AE does aztreonam have?
Rash
Carbapenams differ how?
In their 5-ring structure?
What is special about carbapenems?
They are EXTREMELY broad spectrum
Which Carbapenems are broad action?
Imipenem and meropenem
Imps Merrily Carve Broadly
What can't carbapenems treat?
MRSA
When are carbapenems indicated?
For severe, ABX infections
Why is imipenem coformulated with cilastatin?
To inhibit a kidney enzyme that would degrade the imipenem
What are the PKs of carbapenems?
IV, IM only, high F, can infiltrate CSF, primarily renal
Cartoon Images Distribute Widely Into Cartoon Network and leave Ren & stimpy
Which cabapenem is give qd?
ertapenem
What are the AEs of carbapenems?
Hypersensitivity, seizures, diarrhea, & increased liver enzymes
All B-Lactams are Preg. Cat B except for ________which Cat C
imipenem
What is the MoA for Vanco?
Inhibits cell wall synthesis by inhibiting SECOND stage peptidoglycan synthesis
What is the spectrum of vanco?
Gram + only, including MRSA; considered broad spectrum gram + agent
What are the PKs of vanco?
Poor oral F, high fluid bioavailability, protein binding ~30-55%, renal excretion
What are the PDs of vanco?
Bacteriacidal, time-dependent, and trough levels are to be monitored and should be 10-20mcg/ml
Vinny Murdered Tim and threw him in a Trough
What are the AEs of vanco?
H1 mediated rash dependent upon infusion rate, nephrotoxicity, and ototoxicity
Histrionic Vandals Redden Ears and Kidneys
Protein synthesis inhibitors are all _______________ except for ______________.
bacteriostatic; aminoglycosides
Static Produce Aminates
All protein synthesis inhibitors bind to the 50S ribosomal subunit except for ___________ and __________
aminoglycosides; tetracyclines
30 Soldiers Abort Sides
Chloramphenicol is rarely used because:
it causes hemopathies (aplastic anemia in 20 %, "gray baby" syndrome, & reversible bone marrow supression
What is spectrum of chloramphenicol?
Broad with all 3 types of bacteria
PKs of chloroamphenicol:
Well absorbed from GI tract, high F, hepatic, bacteriostatic
The MoA of tetracyclines is:
inhibition of the 30S ribosomal subunit
Doxycycline is good for:
Lyme's disease
The Foxy Doc Went to Lyme
What spectrum are tetracyclines?
Relatively narrow-spectrum
Tetracyclines are bacteriostatic/bacteriacidal.
bacteriostatic
What class is an alt. to macrolides for resp. illness?
Tetracyclines
Why are tetracyclines OK for PCN -sensitive pts?
Completely different class
What are the PKs of tetracyclines?
-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
Tetracycline AEs:
Preg Cat D
GI
Photosensativity
Hepatic/renal toxicity
Permanent brown discoloration of teeth
Dizziness
What is Fanconi syndrome and what class of ABX is it associated with?
proximal renal tubule toxicity; assoc with outdated tetracycline
Glycylcycline (tigecycline)is indicated for:
Mycobacteria in institutional setting and is broad spectrum
Tigecycline's PKs:
IV only

Very tissue bound

Eliminated via feces

Pregnancy Cat D
Tigecycline's AEs:
Same as tetras + n/v & hepatotoxicity
Macrolide PDs & MoA
PD: Bacteriostatic
MoA: 50S inhibitor
Macrolide spectrum:
Relatively narrow gram (-) & +
Which macrolide has no IV formulation?
Clarithromycin
Which macrolide is NOT a CYP450 inhibitor?
z-pak
The two macrolides that inhibit substrates inhibit which CYP450?
3A4
Macrolide absorption:
Eryth base enteric coated
Macrolide distribution:
Eryth: Billiary, shorter half-life

Clarith: CYP450/renal, long half-life

Azith: Biliary/Fecal, long half life
Macrolide AEs:
Eryth inhibit GI motility, cholestatic hepatitis, ototox

All can cause QT prolongation
Clindamycin MoA and SoA:
50S inhibitor

Relatively narrow, gram + & anaerobic only
Clindamycin PD & Indications:
Bacteriostatic

Integ infections

Acne (topically)
Clindamycin PK:
Nearly completely absorbed, poor CSF dist., >90% protein bound

Extensive hepatic metabolism; excreted in bile and urine

Preg Cat B
Clindamycin AEs:
Diarrhea
Rash
Elevated liver enzymes
What are the 2 streptogramins?
quinupristin/dalfoprisin in a synergistic formulation
Pristine Synergy
Streptogramin spectrum:
Gram + ONLY
Streptogramin PK:
IV only / D5 only (no NS)

No CSF

Hepatic metabolism by conjug.

Biliary Excretion
Streptogramin PD:
each is bacteriostatic; may be bactericidal in combo
Streptogramin is an inhibitor of:
3A4
Streptogramin rarely used:
due to toxicity (liver)
The only oxazolidinone is:
linezolid
Linezolid MoA & Class:
50S inhibitor

Synthetic
Linezold SoA, PD, & Indications:
Gram + only

Broad Spectrum

Mycobacteria

Bacteriostatic

Resistant gram + bacteria
Linezolid PK:
100 % oral bioavailability including CSF

Excreted in urine (non-enzymatic oxidation)
Linezolid AEs and tetra:
Bone marrow suppression (thrombocytopenia, anemia, leukopenia)

Cat C
Aminoglycosides include:
Gentamicin, tobramycin, amikacin, streptomycin
Aminoglycosides MoA:
30S inhibition

Aerobic and energy-dependent
Aminoglycosides SoA:
Aerobic gram (-) organisms

Gram + w/ cell wall-active agt
Aminoglycosides PDs:
Rapidly bacteriacidal, concentration-dependent, post-ABX effect (fail to grow at concentrations below MIC)
Aminoglycosides PKs:
Renal elim
Poor GI absorption
Rapid IM absorption
Aminoglycoside AEs & Tetra:
Nephrotoxicity (8-26%) (reversible)
Ototoxicity (irreversible)
Neuromuscular blockade (rare)
Aminoglycoside dosing:
Narrow therapeutic index

Dose based on lean or adjusted body weight
Quinolones MoA:
Alter nucleic acid metabolism

Target DNA gyrase and topoisomerase IV (loosens chromosome)
Quinolones SoA:
Gram (-)

"Atypicals"
Quinolones PK:
Good oral absorption
Chelates w/ cations
High F
Mostly renal, some hepatic (moxi mostly hepatic)
Concentration-dependent
Bactericidal
Quinolones Safety:
Arthritis
QT Prolongation
CNS

Cat C
What are the folic acid inhibitors?
Sufonamides & trimethoprim/sulfamethoxazole
trimethoprim/sulfamethoxazole SoA:
Ltd gram (+) & (-) coverage

Drug of choice for PCP in immunocompromised pts as Tx and prophylaxis
Sulfonamide PKs:
Var. absorption
Wide dist.
~65 % protein bound
Excreted in Urine
Bacteriostatic
Sulfonamides AEs:
**Hypersensitivity (SJS & sulfa alergy)

KERNICTERUS (encephalopathy) in nenoates

Crystalluria (crystals in kidneys/increased Cr)
Sulfonamide interactions:
Sulfonylurea hypoglycemic agents, AEDs, warfarin
The two urinary tract antiseptics are:
Methanamine and nitrofurantoin
Methenamine properties:
Prodrug that decomposes in H20 to form formaldehyde

H+ increase in urine promotes formaldehyde action

Produces NH3 (hepatotoxic)

USED AS PROPHYLAXIS FOR UTIs
Nitrofurantoin MoA & SoA:
MoA: enzymatically reduced, binds to ribosomal proteins, damaging DNA (theory)

SoA: Limited to some gram (-) & (+); narrow spectrum
Nitrofurantoin PKs:
40-50 % absorption
Renal elim
CrCl > 40ml/min ONLY
Nitrofurantoin AEs:
anemia, elevated liver enzymes, neuropathies, n/v/d
Metronidazole MoA:
Enters via e- transport protein ferrodoxin, reduced, binds to DNA, breaking DNA (thought)
Metronidazole SoA, PK:
SoA: anaerobes only

PK: IV/PO
Hepatic metabolism/renal excretion
Good oral F
Metronidazole AEs:
**CNS (ataxia, dysarthia, dizziness, confusion, excitation, depression seizures)

Peripheral neuropathies (burning/tingling)

Metallic taste

Avoid EtOH
Daptomycin MoA, Class, Spectrum:
Ion leakage causes cell death

Cyclic lipopeptide

Gram + only (including MRSA, VRE)
Daptomycin PKs/PDs:
Concentration dependent bactericidal (like quinolones and aminoglycosides)

Poor oral absorption

Renal elim.
Daptomycin AE:
***Myositis (muscle pain or weakness due to increased creatine kinase)***
Polymixins MoA & SoA:
Lysis gram (-) cell wall by changing permeability in cytoplasm

Gram (-) only
Polymixins PK/PD:
Concentration dependent
Highly tissue bound
Cleared via glomular filtration
Polymixins AEs:
Binding greatest to kidney and brain = cumulative toxicity

Renal toxicity

Neurotoxicity
B-Lactams PD Parameters:
Time-dependent
Vanco PD Parameters:
Time dependent & prolonged persistent effects
Aminoglycosides & Meronidazole PD Parameters:
Concentration dependent & prolonged persistent effects