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226 Cards in this Set
- Front
- Back
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antibacterial spectrum
|
range of microorganisms that an antibiotic affects
narrow to broad spectrum (know relative spectra) |
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bacteriostatic
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inhibiting growth of microorganisms, but not necessarily killing them
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bacteriocidal
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killing microorganisms
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Which is a barrier to drug penetration, gram negative or gram positive outer membrane?
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gram negative
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Bottom line of MRSA epidemiology studies
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demonstrate need for sensitivity testing
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2 general rules for combined therapy with ABS
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use one drug
avoid fixed dose combinations |
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Group 1 ABS
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penicillins
cephalosporins vancomycin bacitracin aminoglycosides fluoroquinolones polymyxin |
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Group 2 ABS
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choloramphenicol
tetrocyclines erythromycin retapamulin quinupristin/dalforpristin linezolid clindamycin sufonamides |
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3 possible indications for combinations of ABS
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severe infection, etiology unknown
treatment of mixed infections to delay emergence of resistant microorganisms, e.g.: TB |
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5 biochemical mechanisms of resistance
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metabolism to an inactive chemical
change in the target site reducation in cellular transport upregulation of efflux pumps increased level of a competitive antagonist |
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6 host determinants of response to ABS
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immune system status
age history of allergy pregnancy hepatic or renal disorders durgs in breastmilk |
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what pH range inactivates penicillins
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pH < 6
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at what pH range are aminoglycosides more active
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alkaline pH
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window in which you should see evidence of improvement
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48 - 72 hours
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3 factors in enhancing efficacy
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start treatment early
proper dose, route and duration of dosing sensitivity testing (gram stain) |
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When did MRSA develop resistance to cephalosporins?
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1982
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What species gave S. aureus the vancomycin resistance gene?
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E. faecalis
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effect of pus on ABS
|
ph < 7
- decreased activity aminoglycosides - possible inactivation penicillins proteins may bind drugs |
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effect of low oxygen tension
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impairs phagocytic activity of WBCs
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3 steps in synthesis of bacterial cell wall
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synthesis of basic building blocks
peptidoglycan formation linking & crosslinking of the peptidoglycan units |
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2 basic building blocks of bacterial cell wall
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UDP-acetyl-glucosamine
UDP-acetyl-muramylpentapeptide |
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main enzyme that cross links the peptidoglycan units
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transpeptidase
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mechanism of beta-lactams
|
prevent cross-linking peptides from binding to the tetra-peptide side chains in cell walls
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2 drugs that inhibit formation of the peptidoglycan units
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vancomycin
bacitracin |
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drugs that inhibit cross linking of linear peptidoglycan strands
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beta-lactams: penicillins & cephalosporins
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vancomycin
mechanism of action |
inhibits peptidoglycan formation
|
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vancomycin spectrum
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narrow (G+)
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vancomycin absorption/distribution
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not absorbed from the GI tract
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vancomycin termination
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renal excretion
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vancomycin toxicity
|
nephrotoxic
hearing loss |
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vancomycin substitutes in cases of resistance
|
quinopristin/dalfopristin
linezolid |
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what kind of infections is vancomycin important for (barring resistance)
|
G+ staph infections
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vancomycin administrion route
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i.v.
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vancomycin distribution
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most body fluids
|
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does vancomycin distribute well to the CNS
|
No
only distributes to CNS when meninges inflamed |
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Bacitracin mechanism
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inhibits peptidoglycan formation
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Bacitracin spectrium
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G+
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Bacitracin absorption
|
not absorbed from the GI tract
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Bacitracin toxicity
|
nephrotoxic
limited to topical use |
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Which peptidoglycan formation inhibitor can be used to treat GI infections?
|
bacitracin
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What kinds of ABS are often combined with bacitracin?
|
drugs with G-neg spectrum
e.g.: polymyxin B or an aminoglycoside |
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2 rings in penicillins
|
beta-lactam ring
thiazolidiene ring |
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peniciliin toxicity
|
relatively safe
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penicillins distribution
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CNS poor, unless meninges are inflamed
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penicillins - termination of action
|
renal excretion
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Penicillin G
acid stability penicillinase sensitivity |
Penicillin G
acid stability - low penicillinase sensitivity - yes |
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Phenoxymethyl penicillin
acid stability penicillinase sensitivity |
acid stability - high
penicillinase sensitivity - yes |
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Methicillin
acid stability penicillinase sensitivity |
acid stability - low
penicillinase sensitivity - no |
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dicoxacillin
acid stability penicillinase sensitivity |
acid stability - high
penicillinase sensitivity - no |
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nafcillin
acid stability penicillinase sensitivity |
acid stability - low
penicillinase sensitivity - no |
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amoxacillin
acid stability penicillinase sensitivity |
acid stability - high
penicillinase sensitivity - yes |
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ticarcillin
acid stability penicillinase sensitivity |
acid stability - low
penicillinase sensitivity - yes |
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piperacillin
acid stability penicillinase sensitivity |
acid stability - low
penicillinase sensitivity - yes |
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three penicillins that are broad spectrium
|
amoxacillin
ticarcillin piperacillin |
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three penicillins that are NOT penicillinase sensitive
|
methicillin
dicloxacillin nafcillin |
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how do penicillins work?
|
bind transpeptidase
--> penicilloyl-enzyme (inactive) |
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PBP
|
penicillin binding protein
|
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|
penicillin binding proteins
definition |
variety of enzymes involved in the terminal stages of assembly of bacterial cell wall
by definition, inhibited by penicillin and other beta-lactams |
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most prominent PBP
|
transpeptidase
|
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form of penicillin that achieves the highest blood level
|
Penicillin G, given i.m.
|
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form of penicillin that lasts the longest in the blood
|
procain penicillin G
|
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penicillinase mechanism of resistance
|
most prominent mechanism of resistance
breaks beta-lactam ring |
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3 penicillins with good acid stability and resistance to penicillinase
|
oxacillin
dicoxacillin cloxacillin |
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2 penicillins that are broad spectrum compared to penicillin G
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amoxicillin
carbenicillin |
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carbenicillin notes
|
not administered orally
penicillinase sensitive |
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2 beta-lacatamse inhibitors
|
Clavulanic Acid
Tazbactam |
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Azlocillin
|
new broad spectrum penicillin
not absorbed from the GI tract penicillinase sensitive |
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adverse reactions to azlocillin
|
some GI upset
bone marrow suppression |
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4 ABS which are effective against anaerobes
|
piperacillin
clindaymycin imipenem 3rd generation cephalosporins |
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structural difference between penicillins and cephalosporins
|
instead of a thizolidine ring, cephalosporins have a dihydrothizine (6 membered) ring
|
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2 1st generation cephalosporins
|
similar to broad spectrium penicillins
not effective aginst anerobes cephalexin (oral) cephazolin (i.m.) |
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second generation cephalosporin
|
cefaclor
not effective against G-neg |
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third generation cephalosporins
|
cefotaxime
cefixime less effective against G+ more effective against G(-) & anerobes distributes to CNS |
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fourth generation cephalosporin
|
cefepime
|
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mechanism of resistance against cephalosporins
|
beta-lactamases
|
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adverse effects of cephalosporins
|
irritation at site of injection
GI upset bone marrow suppression renal toxicity, esp. w/ an aminoglycoside |
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Carbapenems
|
very broad spectrium beta-lactam
- G+, G(-), anerobes combined with cillistatin, inhibits renal enzymes that catabolize it i.v. administration required |
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Monobactams
|
braod spectrum beta-lactam for G(-)
narrow spectrum for G+ important for G+ staph infections i.v. administration required |
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Polymixin
|
a group of structurally related antibiotics that bind to and disrupts bacterial cell membranes
|
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polymixin absorption
|
not absorbed from GI tract
decrease bowel flora prior to surgery |
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polymixin toxicity
|
nephrotoxic - topical use only
|
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polymixin spectrum
|
narrow G(-)
e.g.: pseudomonas: skin, eye, mucus membranes |
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polymixin resistance
|
development of resistance relatively rare
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polyene antifungals (2 examples)
|
nystatin
amphtericin B |
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Polyene antifungals
mechanism of action |
bind to ergosterol-containing receptors on cell membrane
|
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amphotericin B
administration toxicity |
must be administered i.v.
toxicity: nephrotoxic, GI upset newwe lipid based products are less toxic |
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nystatin toxicity
|
severe nephrotoxicity - limited to topical use
|
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fungal cell membrane characteristic important to azole antifungals
|
ergosterol in fungal cells vs. cholesteraol in mammalian cells
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azole mechanism of action
|
inhibits 14-alpha-sterol demethylase (fungal specific)
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azole administration
|
oral
|
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|
ketoconazole & itraconazole
absorption CNS distribution termination |
low gastric pH enhances absorption
does not distribute to CSF excreted in bile & urine |
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fluconazole
absorption CNS distribution termination |
oral absorption is not affected by pH
can be administered by i.v. does distribute well to CNS renal excretion |
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adverse effects of azoles
|
GI upset, vomiting, anorexia
ketoconazole: some decrease in steroid biosynthesis inhibition of cytochrome P450 metabolism of other drugs |
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ergosterol synsthesis pathway
|
acetyl CoA --> HMG CoA --> mevalonate --> squalene --> lanosterol --> ergosterol
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step in ergosterol synthesis pathway catalyzed by 14-alpha-sterol demethylase
|
lanosterol --> ergosterol
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terbinifine
mechanism of action absorption |
inhibits squalene epoxidase
(catalyzes squalene to lanosterol) well absorbed after oral administration |
|
|
5-fluorcytosine
mechanism of action absorption distribution termination toxicity |
metabolized to 5-fluorouracil (5-FU)
well absorbed after oral administration distributes to CNS renal exretion suppression of bone marrow activity |
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ABS that affect nucleic acids
|
fluorquinolones - ciprofloxacin & levofloxacin
rifampin nitrofurantoin |
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fluoroquinolones mechanism of action
|
inhibition of gyrases/topoisomerases, selective for bacterial enzymes
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fluoroquinolone spectrum
|
bacteriocidal, primarily G(-), not anerobes
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fluoroquinolones administration
|
oral
i.m. i.v. |
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fluoroquinolone termination
|
some metabolism by liver
renal exretion active in urine some exretion in bile-feces |
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fluoroquinolone toxicity
|
GI upset
CNS excitement cartilage damage |
|
|
uses of fluoroquinolones
|
UTIs
bone infections resp. tract infections |
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rifampin mechanism
|
inhibits RNA plymerase, blocks initiation
|
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rifampin spectrium
|
more effectivee aginst G+ than G(-)
b/c of penetration difference, not sensitivity of RNA polymerase |
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rifamin absorption
|
well absorbed from GI tract
can also be given i.m. & i.v. |
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rifampin distribution
|
total body water (orange tint)
|
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rifampin termination
|
bile-feces
metabolized by liver metabolite active but more readily exreted |
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rifampin toxicity
|
induces drug metabolizing enzymes
increases metabolism of anticoagulants teratogenic mild GI upset |
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nitrofurantoin - hypothesized mechanism of action
|
bacterial enzymes reduce drug, which causes it to damage DNA
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nitrofurantoin absorption
|
well absorbed from GI tract
|
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nitrofurantoin termination
|
rapid renal excretion (turns urine brown)
|
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nitrofurantoin adverse effects
|
nitrofuantoin:
N/V diarrhea HA pulmonary fibrosis (rare) |
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2 drug families that act on the 30S ribosomal subunit
|
aminoglycosides
tetracyclines |
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aminoglycosides mechanism of action
|
inhibit protein synthesis
mis-incorporation of amino acids bacteriocidal |
|
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aminoglycoside spectrum
|
G(-)
|
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aminoglycoside absorption and administration
|
poorly absorbed from GI trat
i.m., i.v. and s.c. |
|
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aminoglycoside distribution
|
poor lipid solubility
poor distribution to CNS |
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aminoglycoside termination
|
not metabolized
renal exrection |
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adverse effects of aminoglycosides
|
1* tubular nephrotoxicity, esp. w/ cephalosporins
vestibular & auditory toxicity NMJ blocking |
|
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to minimize aminoglycoside toxicity...
|
maintain hydration
avoid other potential nephortoxic drugs |
|
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2 bacteria that indicate aminoglycoside use
|
pseduomonas
klebdiella resistant to other drugs |
|
|
mechanisms of aminoglycoside resistance
|
aminoglycoside antibiotics induce bacterioal biofilm formation, which resist ABS tx.
esp. in P. aeruginosa & E. coli |
|
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3 limiting factors in aminoglycoside use
|
toxicity
rapid development of resistance lack of oral absorption |
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4 examples of aminoglycosides
|
gentamicin
amikacin tobramycin metilmicin |
|
|
Oral/parenteral tetracyclines
|
tetracycline
oxytetracycline doxycycline*** - preferred |
|
|
tetracyclines - adverse effects
|
tetracyclines:
GI upset hepatotoxicity (mild) discoloration of teeth crosses placenta photosensitivity |
|
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tetracycline spectrum
|
bactera (G+ & G(-))
actinomycetes richettsiae mycoplasma chlamydia entamoeba histolytica |
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Drugs that act on the 50S ribosomal subunit
|
chloramphenicol
macrolides: - erythromycin - clarithromycin - azithromycin - telithromycin retapulmin clindamycin |
|
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choloramphenicol spectrum
|
broad spectrum antibacterial
rickettsiae |
|
|
chloramphenicol resistance
|
metabolism
lack of uptake altered receptor |
|
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chloramphenicol
absorption distribution termination |
well absorbed from GI
distributes to total body water, including CSF metabolized by liver, conjugated with glucuronic acid --> renal excretion |
|
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toxicity associated with chloramphenicol
|
toxic bone marrow suppression
aplastic anemia |
|
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Toxic bone marrow suppression
appearance of marrow peripheral blood dose-response time of appearance common symptoms prognosis |
Toxic bone marrow suppression
appearance of marrow - normocellular peripheral blood - anemia dose-response - dose related time of appearance - during treatment common symptoms - anemia prognosis - recovery |
|
|
Aplastic anemia associated with chloramphenicol
appearance of marrow peripheral blood dose-response time of appearance common symptoms prognosis |
aplastic anemia associated with chloramphenicol
appearance of marrow - hypoplastic/aplastic peripheral blood - pancytopenia dose-response - not dose related time of appearance = days/months later common symptoms - purpura and/or hemorrhage prognosis - often fatal |
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4 macrolides
|
erythromycin
clarithromycin azithromycin telithromycin |
|
|
erythromycin spectrum
|
antibacterial
similar to Pen G (mostly G+) effective against penicillinase-producing organisms & mycoplasma |
|
|
erythromycin
absorption distribution termination |
well absorbed from GI
pain upon injection - oral route preferred does not penetrate BBB metablized in liver --> bile/feces only 2-5% excreted in urine (no need for dose adjustment wrt renal impairment) |
|
|
erythromycin adverse effects
|
mild liver toxicity
mild GI upset |
|
|
clarithromycin
|
new
slightly more broad spectrum than erythromycin |
|
|
azithromycin
|
derived from erythromycin
better oral absorption more broad spectrum longer half life and higher tissue concentrations |
|
|
telithromycin
|
erythromycin derivative
well absorbed w/ oral administration mebolized by liver, excreted mainly in bile |
|
|
telithromycin adverse effects
|
GI upset
HA blurred vision altered taste perception liver toxicity |
|
|
telithromycin use
|
limited to serious respiratory infections
|
|
|
retapamulin
|
pleuromutilin derivative
topical treatment use against staph & strept |
|
|
retapamulin mechanism of action
|
binds 50S ribosomal subunit & inhibits protein synthesis
inhibits peptide bond formation AND binding of tRNA to the ribosome |
|
|
clindamycin is a derivative of _____
|
lincomycin
|
|
|
drugs for vancomycin-resistant organisms
|
quinupristin/dalfopristin
linezolid |
|
|
quinupristin/dalfopristin mechanism
|
bind to 50S ribosome subunit -
inhibit protein synthesis |
|
|
quinupristin/dalfopristin spectrum
|
G+
staph, strept, enterocococcus |
|
|
quinupristin/dalfopristin
absorption termination |
i.v. route
not absorbed from GI tract metabolized in liver, excreted in bile |
|
|
quinupristin/dalfopristin adverse effects
|
pain
inflammation edema thrombophlebitis at infusion site arthralgia & myalgias |
|
|
linezolid mechanism
|
binds to 50S, blocks formation of 70S
|
|
|
linezolid spectrum
|
G+
staph, strep & enterococcus more broad spectrum than quinupristin/dalfopristin |
|
|
linezolid
absorption termination |
well absorbed from Gi tract
metabolized in liver & excreted in urine |
|
|
linezolid adverse effects
|
mild GI upset
thrombocytopenia (reversible) monitor platelet counts if Rx longer than 2 weeks |
|
|
antibiotics that affect intermediary metabolism
|
antimetabolites:
- sulfonamides (sulfa drugs) - trimethoprim - flucytosine (5-flurocytosine) |
|
|
antimetabolites - general mechanism
|
competes with endogenous substrate for enzyme active site
|
|
|
sulfonamides mechanism of action
|
analogs of p-aminobenzoic acid
(PABA requried for synthesis of folic acid) - basis for selective toxicity |
|
|
sulfonamides spectrum
|
broad: many G+ & G(-)
resistance is frequent bacteriostatic |
|
|
sulfonamides
absorption distribution termination |
well absorbed from Gi tract
distribute to total body water, including CNS renal excretion |
|
|
sulfonamides toxicity
|
dermal immune reactions
- keratoconjunctivitis (HSR) crystaluria some liver toxicity anemia |
|
|
trimethoprim
|
inhibits dihydrofolate reductase,
blocking reduction of dihydrofolate to tetrahydrofolate ultimately inhibits synthesis of nucleic acids & proteins |
|
|
example of sequential inhibition
|
sulfa + trimethoprim
sulfa blocks PABA --> folate trimethorprim blocks Folate --> tetrahydrofolate |
|
|
flucytosine (5-fluorocytosine) mechanism
|
metabolized by the FUNGI to 5-FU
blocks nucleic acid synthesis |
|
|
flucytosine
absorption termination |
well absorbed from GI tract
distributes to total body water excreted in urine, not metabolized |
|
|
flucytosine toxicity
|
depression of bone marrow
GI upset |
|
|
urinary tract antispectics (2 examples)
|
nitrofurantoin
methenamine |
|
|
methenamine mechanism
|
hydrolized to formaldahyde & NH4+
bacteriocidal in acid baceteriostatic in alkaline environment |
|
|
methenamine
absorption distribution termination |
usually administered with mandelic acid or ascorbic acid to lower urinary pH (increases activity of drug - best when pH < 6)
well absorbed from GI renal excretion |
|
|
methenamine counterindications
|
do NOT use with sulfonamides
|
|
|
Compare immunological, interferon & chemical antiviral therapies:
- level of effectiveness - spectrum - duration of effect |
Effectiveness
- immunological: high - IFN: moderate/high - chem: low/moderate Spectrum - immunological: narrow - IFN: broad - chem: narrow Duration - immunological: long - IFN: short - chem: short |
|
|
Process of viral infection
|
entry of the virus into the host cell, release of viral genome
- adsorption - penetration - uncoating replication of viral genome assemply of virus particles and release from host cell |
|
|
5 antiherpes drugs
|
acyclovir
valacyclovir ganciclovor idoxuridine vidarabine |
|
|
drug for Hep B
|
adefovir dipivoxil
|
|
|
acyclovir
chemical structure mechanism |
guanosine nucleoside analogs
nucleic acid chain termination |
|
|
acyclovir
absorption distribution termination |
oral, topical
distributes to CSF renal excretion |
|
|
acyclovir toxicity
|
mild GI upset
HA renal toxicity |
|
|
gancyclovir
|
guanosine nucleoside analog
spectrum: Herpes, CMV oral administration |
|
|
gancyclovir toxciity
|
bone marrow
CNS teratogenic (more incoprorated into host DNA than acyclovir) |
|
|
acyclovir spectrum
|
herpes
CMV EBV |
|
|
iododeoxyuridine
|
thymidine analog
DNA viruses, herpes also affects mammalian DNA |
|
|
vidarabine
|
adenosine analog
spectrum: DNA viruses mechanism not clear (chain termination?) |
|
|
adefovir didivoxil
|
adenosine analog
oral pro-drug mechanism: inhibits viral polymerase |
|
|
Anti-influenza A drugs
|
amantadine
oseltamivir zanamivir |
|
|
Amantadine mechanism
|
specific for influenza A virus (treat & prevent)
mechanism - inhibits proton channel (M2) |
|
|
Amantadine
absorption termination |
oral administration
renal excretion |
|
|
amantadine toxicity
|
minor GI upset
CNS: nervous, light headed, difficulty concentrating |
|
|
M2 protein in influenza
|
proton chennel M2 mediates influx of H+
facilitates release of viral nucleic acid thus, amantadine blocks viral uncoating |
|
|
oseltamivir mechanism
|
treats and prevents influenza A
inhibits viral neuramidase (conformational change) |
|
|
neuraminidiase
|
cleaves terminal sialic acid residues necessary for release of viral particles from cells
|
|
|
oseltamivir
administration termination |
oral route OK
renal excretion |
|
|
oseltamivir toxicity
|
mild GI upset
|
|
|
zanamivir mechanism
|
treat and prevent influenza A & B
mechanism same as oseltamivir, except no conformational change |
|
|
zanamivir
absorption termination |
not well absorbed from absorption
intranasal delivery or dry powder inhablation renal excretion |
|
|
zanamivir toxicity
|
well tolerated, some wheezing/bronchospams reported
|
|
|
siRNA therapy is being developed for what viral disease
|
HSV
|
|
|
IFNs - general mechanism
|
block penetration, uncoating, RNA & protein synthesis
|
|
|
3 types of IFN
|
alpha (used most, recombinant)
beta (produced by most cells) gamma (less direct antiviral activity, stimulate T cells) |
|
|
IFN administration
|
injection, i.v.
|
|
|
IFN use
|
hep B, hep C
|
|
|
IFN toxicity
|
fever
chills HA depress bone marrow CNS: confusion, behavior changes |
|
|
lamivudine
uses mehcanism |
Hep B
non-nucleoside inhibitor of DNA polymerase and reverse transcriptase mechanism same as oseltamivir, w/o conformational change |
|
|
lamivudine
absorption termination |
not well absorbed by GI tract
intranasal delivery or dry powerder inhalation renal excretion |
|
|
lamivudine toxicity
|
well tolerated
some wheezing/bronchospasm reported |
|
|
lamivudine structure
|
cytidine analog
|
|
|
AZT, aka:
|
zidovudine
|
|
|
nucleoside reverse transcriptase inhibitors
|
zidovudine (AZT)
didanosine |
|
|
non-nucleoside reverse trasncriptase inhibitors
|
nevirapine
efavirenz |
|
|
zidovudine (AZT)
|
thymidine analog
oral administration metabolized by liver & renal excretion |
|
|
zidovudine toxicity
|
fatigue
nausea HA anemia |
|
|
didanosine
|
dideoxyinosine, a purine nucleoside analog
oral administration with antacid or buffer |
|
|
didanosine toxicity
|
GI upset
peripheral neuropathy pancreatitis |
|
|
nevirapine
|
non-nucleoside reverse transcriptase inhibitor
oral administration |
|
|
nevirapine toxicity
|
rash
fever fatigue nausea liver toxicity |
|
|
efavirenz
|
non-nucleoside reverse transcriptase inhibitor
oral administration OK |
|
|
efavirenz toxicity
|
CNS: impaired concentration, abnormal dreams, HA, dizziness, rash
|
|
|
True or False: Efavirenza plus 2 of 3 nucleosides was superior to the use of 3 nucleoside reverse transcriptase inhibitors
|
True
|
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protease function
|
cleave initially synthesized viral proteins to active anzymes
|
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protease inhibitors
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block viral maturation
antimetabolites - mimic peptide structure |
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what kind of anti-HIV drug is indinavir
|
protease inhibitor
|
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indinavir toxicity
|
GI upset
liver toxicity hyperglycemia onset or worsening of diabetes fat redistribution & hyperlipidemia |
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enfuvirtide
|
36 residue polypeptide
binds to HIV viral envelope & inhibits fusion of HIV with CD4+ cells $20,000/year |
|
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Maraviroc
|
binds to CCR5 co-receptor on surface of CD4+ T cell
blocks HIV from entering target cell will not be effective against HIV that targets the CXCR4 receptor oral administration |
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maraviroc toxicity
|
HA
dz/wk nausea |
