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199 Cards in this Set
- Front
- Back
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what is the difference between bacteristatic and bactericidal?
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bacteristatic antibiotics do not kill the organism, rather they inhibit a metabolic pathway required for growth making it more susceptible to the immune system. bactericidal antibs kill the organism outright via lysis.
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can an antibiotic cause resistance? why or why not?
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NO, antib resistance is due to a mutation in the bacteria the antib is targeting. this mutation would have occured no matter what. the bacteria's mutation may create an enzyme which metabolizes the antib.
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why is antib resistance dangerous? what should the course of drug treatment be?
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if the antib has selective resistance, it will only kill the bacteria which are still susceptible to it. the bacteria that resisted the antib will overgrow in population. begin tx with a broad spectrum antib then choose a more specific rx once the pathogen is known.
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define synergism in regards to antibiotics.
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using two drugs in conjunction will give a greater effect than using each separately.
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how are frequencies of resistance related?
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they are additive.
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is fever always related to an infection?
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no, it can be due to a pyrogen (foreign substance altering the thermoregulatory system).
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what types of drugs are sulfonamides, generally?
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broad spectrum STATIC against g+/g-
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what is the mechanism for sulfonamides?
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inhibit dihydropteroate synthase, the first step of folic acid synthesis.
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name the enzyme required for this rxn:
PABA + pteridine -> dihydropteroic acid |
dihydropteroate synthase
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what is N5, N10 methylene THF?
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the 1 carbon carrier which transfers a methyl group to dUMP in the synthesis of thymidine.
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at what stage is glutamate involved in folic acid synthesis?
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it is added to dihydropteroic acid to form FH2 which is reduced by DHFR to FH4.
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why are sulfonamides ultimately succesful?
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they are able to inhibit DNA synthesis.
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why don't the sulfonamides affect human DNA synthesis?
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b/c humans don't make folic acid, they take it in pre-formed as green veggies, etc.
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what are DHFR inhibitors used with? why?
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they are used with sulfa drugs for a synergistic affect.
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what is the function of DHFR?
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it reduces FH2 to FH4 to be reused in thymidine synthesis.
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why does a DHFR inhibitor provide synergism with a sulfonamide?
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because together they inhibit two steps in the synthesis of TH4.
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name three DHFRIs
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trimethoprim
pyrimethamine methotrexate |
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which DHFRI is antimalarial? which DHFR does it inhibit?
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pyrimethamine
it inhibits protozoal DHFR |
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which DHFRI inhibits mammalian, bacterial and protozoal DHFR? what else is it used to treat?
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methotrexate. it's also used for psoriasis and various cancers.
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which DHFRI may cause blood dyscrasius? which DHFR does it inhibit?
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trimethoprim. it inhibits bacterial DHFR.
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what must you consider when treating women with sulfonamides?
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pregnancy. sulfonamides can cross the placenta and cause unwanted side effects in fetus and antibacterial effects. it is pregnancy category B (animals = no risk)
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what are two common oral sulfonamides?
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sulfisoxazole and sulfamethoxazole
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what antib should be used in kids with acute otitis media? recurrent?
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acute: amoxicillin or an 2nd/3rd generation cephalosporin.
recurrent: sulfisoxazole |
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what are the main causes of UTIs in community? in hospitals?
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community:
e.coli 80% s.saph. 10% nosocomial: e.coli 50% klebsiella, proteus,enterobacter, serratia 40% enterococcus faecalis, s.saph & s.aures 10% |
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what is an alternative antib for an uncomplicated UTI?
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sulfisoxazole.
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what is sulfamethoxazole often offered with? why?
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it's often available with trimethoprim, aka Co-trimoxazole. it's a DHFRI, which provides synergism.
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how is co-trimoxazole given? what is another name for it?
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oral and IV
TMP-SMZ trimethoprim-sulfamethoxazole |
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what are some uses for trimethoprim-sulfamethoxazole?
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1.UTI if local e.coli rez to TMP-SMZ is < 20%.
2. respiratory and GI infections 3. high doses for pneumocystis carinii in AIDS |
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if resistance to e.coli is greater than 20%, what can be used to treat a UTI?
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nitrofurantoin or phosphomycin
alternate: a flouroquinalone (ie ciproflaxin) |
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what are some topical sulfonamides?
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sulfacetamide
silver sulfadiazine mafenide |
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why is sulfacetamide given with phenylephrine? what is this combination called?
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sulfacetamide is given in eye infections. the phenylephrine is a vasoconstrictor and helps with bloodshot eyes. VASOSULF
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how do vasopressers work? give an example of one.
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vasopressers stimulate the alpha 1 adrenergic receptors on vasculature. this constricts the smooth muscle.
PHENYLEPHRINE |
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what is glucocorticoid given with a sulfonamide? what is the fxn of this combination?
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sulfacetamide + prednisolone = BLEPHAMIDE
it treats a bacterial eye infection, the glucocorticoid is anti-inflammatory. |
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what does a drug like blephamide treat?
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it is for bacterial eye infections, but it also treats the inflammatory component of the infection.
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what is blephamide an alternate for? what would be a better/preferable choice?
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it's an alt. for ulcerative blepharitis, an inflammatory condition cause by bacteria.
ideally it would be treated with polysporin ointment. |
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what are common bacterial causes of ulcerative blepharitis?
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s.aureus and s.epidermidis
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what is polysporin ointment composed of? what sort of coverage does it offer? is it rx?
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it's composed of bacitracin and polymyxin B. bacitracin gives g+ coverage, plymyxin B gives g- coverage. it is an OTC ointment.
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how would you 'up' your gram negative coverage in the case of ulcerative blepharitis.
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use the aminoglycoside antibiotic GENTAMICIN ophthalmic ointment.
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what are the most common bacterial culprits of bacterial conjunctivitis?
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s.aureus
strep pneumonia h.influenza moraxella catarrhalis |
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when suffering from bacterial conjunctivitis, which drug is preferrable? why?
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vasosulf (sulfacetamide + phenylephrine). vasodilation is common in bacterial conjunctivitis, causing red sclera. this rx will remove the infxn and the redness.
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in the case of bacterial conjunctivitis with NO VASODILATION, what is the drug of choice?
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polysporin (bacitracin + polymyxin B).
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what provides better gram negative coverage for a bacterial conjunctivits? (than polysporin)
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ophthalmic form of flouroquinolone ciprofloxacin
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if a newborn presents with bacterial conjunctivitis, how will you proceed?
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it is important to know how soon after birth the symptoms appeared, this will determine the causative organisms and tx.
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what are two sulfonamides used for burn tx? what is specific about them?
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silver sulfadiazine
mafenidine BOTH TOPICAL |
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which sulfonamide helps prevent sepsis in burn victims? how does it work?what caution must be taken?
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silver sufadiazine. the silver released is toxic to microorganisms. caution must be taken not to use the drug over too large a surface area, or the sulfa can be absorbed.
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what are the general side effects of sulfonamide drugs?
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1.crystalluria
2.kernicterus 3.blood dyscrasias 4.hypersensitivity |
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which side effect of sulfonamides is preventable with drinking lots of water with oral dose?
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crystalluria
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which side effect demands that sulfonamides not be given to newborns and infants under 2 mos old?
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kernicterus
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which side effect of sulfonamides causes generalized CNS depression and neonatal jaundice? how does it happen?
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kernicterus.
it's a form of jaundice where the bilirubin gets displaced from plasma proteins. free bilirubin then enters the CNS and deposits in the basal ganglia and other areas. |
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what is a rare but potentially fatal side effect of sulfonamides? what does it cause?
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blood dyscrasius. acute hemolytic anemia, agranulocytosis, aplastic anemia.
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what is stevens-johnson syndrome?
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a form of hypersensitivity and a side effect to sulfonamides. 'erythema multiforme major'. it's characterized by bullous eruptions on the skin and mucous membranes. ****can cause suffocation***
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what is rx fever?
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another sensitivity side effect to sulfonamides.
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name a group of broad spectrum cidal agents used mostly for gram negative (SOME gram positives).
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flouroquinolones
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what is the fq g- mechanism? g+?
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g-: inhibit DNA gyrase (cuts and reanneals DNA). get ds DNA fragmentation.
g+: inhibits topoisomerase IV which is involved in separation of daughter cells during replication. |
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list 9 flouroquinolones
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1.ciprofloxacin
2.gatifloxacin 3.moxifloxacin 4.gemifloxacin 5.levofloxacin 6.lomefloxacin 7.norfloxacin 8.ofloxacin 9.sparfloxacin |
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which flouroquinalones are for ophthalmic use?
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ciprofloxacin = ciloxan
gatifloxacin = zymar (oral + ophthalmic) moxifloxacin = vigamox |
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what flouroquinalone has an otic version?
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ciprofloxacin = cipro hydrocortisone otic
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which flouroquinalone is for mild comm.acquired pneumonia and exacerbations of chronic bronchitis?
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gemifloxacin
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which flouroquinalone is for UTIs and lower RTIs?
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lomefloxacin
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which flouroquinalone is NOT good for systemic infxn? what is it used for?
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norfloxacin. use for UTI.
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what is ciprofloxacin known for?
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it has the best gram negative activity. (and a ophthalmic and otic version)
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a patient suffers peritonitis in a perforated colon. what is the most likely bacteria and some of it's characteristics? what is the first choice tx?
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b.fragilis, a gram negative rod (part of colon's normal flora). weak endotoxic activity.
1st choice tx: ampicillin and sulbactam |
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what is an alternative rx for b.fragilis?
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moxifloxacin
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which potential rx for b.fragilis has increased gram negative activity?
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ampicillin + sulbactam = an aminoPCN with a beta-lactamase inhibitor.
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how do piperacillin and tazobactam work? what other bacteria, besides b.fragilis are they helpful towards?
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you have an antipseudomonas PCN with a beta lactamase inhibitor. P.aeruginosa is another common pathogen in peritonitis. it's gram positive spectrum is similar to PCN.
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what are the major side effects of flouroquinalones? what bacterial infxn are they often responsible for?
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nausea, vomiting and diarrhea. they cause c.difficle-induced diarrhea and psuedomembranous colitis.
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what is the pathogenesis of c.difficile?
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it survives as spores until the antib is discontinued. it then grows w/o competition for nutrients. it makes toxin A and B, which cause fluid production and cell lysis. it causes psuedomembranous plaques to form on the colon wall.
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how do flouroquinolones cause c.difficile?
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they disrupt normal bowel flora.
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how can c.difficile be treated?
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1st choice: metronidazole (forms reactive anion which damages bacterial DNA, kills c.difficile)
2nd: vancomycin |
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name five side effects of flouroquinolones.
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1.phototoxicity (red rash)
2.increased QTc (conduction) 3.arthropathy (cartilage dmg) 4.tendon rupture 5.CNS stimulation (convulsions, psychoses) |
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a patient suffering an ear infxn is carrying an rx for moxifloxacin/gatifloxacin/ sparfloxacin AND one for altered cardiac conduction. what do you do?
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take them OFF flouroquinolones! they can cause increased QTc.
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which part of the PCN structure is required for activity? which part determines the property/spectrum?
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thiozolidine and beta-lactam rings make the nucleus and are required for activity. side chains determine property and spectrum.
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what are two beta-lactamase inhibitors?
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sulbactam and tazobactam.
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what do gram positive bacterial cell walls contain? how does PCN work on this?
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the walls are made of pep-g, made of two alternating sugars, NAG & NAM. they are CROSS-LINKED. NAM has a D-aa which has to be removed by transpeptidase before this cross-linking can occur. PCN INHIBITS THE TRANSPEPTIDASE.
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what does inhibition of the transpeptidase by PCN cause? what sort of antibiotic are PCNs?
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inhibition of cell wall synthesis and, ultimately, lysis. therefore PCNs are CIDAL.
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what is the main mechanism of resistance to PCN?
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development of beta-lactamases.
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why is PCN-G given paraenterally? in which case will it distribute to the the CNS?
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it's given via IV/IM b/c it is unstable in the stomach. it'll distribute to the CNS only if the meninges are inflamed.
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how is the activity of PCN expressed?
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UNITS. 1 unit = 0.6 micrograms
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what are the three forms of PCN G?
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1.aqueous (IV/IM) Na+/K+ salts
2.procaine (suspension IM only) + anasthetic 3.benzathine (suspension IM) |
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which PCN G is the longest acting?
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benzathine
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the g+ spirochete treponema pallidum causes what dz? what is the rx? what is an alternative if allergic?
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syphilis. benzathine is given ideally.
if allergic: doxycycline or tetracycline (orally) or 3rd gen.cephalosporin ceftriaxone (IV/IM) |
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what is another name for PCN G?
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benzyl PCN
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what is the difference between PCN G and PCN V?
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V is an acid stable form for oral use. G is not stable in the stomach. V is dosed in mgs, G is dosed in units.
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what is PCN V also knowns as? how is it prescribed?
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phenoxymethyl PCN. food interferes with it's absorption, so give 1hr pre meals a.c. or 1hr p.c.
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what are three drugs only to be used against resistant staph (not against microbes sensitive to PCN G or V)?
what is another name for them? |
1.dicloxacillin (oral)
2.oxacillin (oral sol & inject) 3.nafcillin (injection) penicillinase resistant PCNs |
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what does MRSA mean?
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methicillin resistant staph aureus.
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how are dicloxacillin, oxacilin, and nafcillin eliminated? when is this an advantage?
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50% biliary and 50% renal excretion. this is an advantage in liver or kidney dz.
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what are 'extended spectrum PCNs?' how are they similar to PCN? different?
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aminopenicillins. they are still susceptible to PCNases and strains that resist PCN resist aminoPCNs. BUT they have MORE gram negative coverage.
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what are some aminopenicillins?
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ampicillin & amoxicillin
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what is ampicillin often given with? what is it given for? how is it administered?
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it's often given with sulbactam/unasyn for peritonitis due to b.fragilis. it's administered IV/IM.
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what is sulbactam?
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it's a beta lactamase inhibitor.
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what is augmentin? what are it's uses?
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clavulanate (beta lactamase inhibitor) + amoxicillin.
1.alt for UTI if TMP/SMZ or fq fails. 2.otitis media ** 3.prophylaxis pre dental procedure if mitral valve prolapse. |
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why isn't amoxicillin available for peritonitis? how is it administered?
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it's not available paraenterally.
it's administered with oral caps and pediatric drops. |
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what are the major causes of otitis media? what guidelines must be kept in mind when prescribing?
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strep pneumonia (g+) causes 50%
h.influenza(g-) causes 25% rule: NO antib in past month use amoxicillin YES antib in past month, augmentin. |
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a child suffering from otitis media is allergic to PCN. what's the rx? for his mom with the same problem?
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kid:
pediazole (sulfisoxizole + macrolide erythromycin) mom: macrolide (clarithromycin) |
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an RTI from s.pyogenes, s.pneumonia (g+) and h.flu (g-rod) can all be treated with what aminopenicillin?
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either ampicillin and amoxicillin.
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what forms of sinusitis can either aminopenicillin treat?
what are other first line agents for these infections? |
from strep pneumoniae, h.influenzae and moraxella catarrhalis.
other agents: 3rd generation cephalosporins, cefdinir, cefpodoxime. |
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what is unique about antipseudomonas PCNs? name two.
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they are active against some pseudomonas (modest v. P.aeruginosa) and some resistant proteus but still susceptible to PCNases.
1.ticarcillin 2.piperacillin (+tazobactam always) |
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what is ticarcillin available with? what is this combination active against?
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clavulanate (beta lactamase inhibitor) as timetin. it's active vs some pseudomonas and some resistant proteus. still susceptibile to PCNases!
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what are the general side effects of PCNs as a group?
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1.hypersensitivity
2.diarrhea 3.superinfxn 4.increase seizure risk |
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what is an example of 'superinfection'?
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overgrowth of c.difficile produces toxins which cause psuedomembranous colitis.
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what is the hypersensitivity to PCNs due to?
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it's from metabolites acting as haptens and is IgE mediated. it's characterized by rashes, fever, bronchospasms, serum sickness, steven-johnson syndrome, anaphylaxis.
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which PCN side effect does decreased renal function adversely affect?
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it increases the chance that the PCN will cross the BBB, increasing seizure likelihood.
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what is the structure of cephalosporins? what is the mechanism?
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beta lactam + dihydrothiazine ring with side chains. they act by the same mech as PCNs (inhibits transpeptidase enzyme).
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what is the advantage to using a cephalosporin?
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they resist many beta lactamases.
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what organisms do the 1st generation cephalosporins work on?
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PEcK:
proteus mirabilis (enteric) e.coli (enteric) klebsiella pneumoniae (RTI/UTI) |
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which organism, which can be treated by 1st generation cephalosporins, is urease +, promoting stones?
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proteus mirabilis
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when does proteus mirabilis infect? what does it generally cause?
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it infects when it leaves the intestinal tract. it generally causes UTIs.
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what are two 1st gen. cephalosporins? how are they given?
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cephalexin and cefadroxil. both given orally.
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what coverage do first generation cephalosporins have? what kind of PCNase do they resist?
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they have good g+ coverage and PEcK g-. they resist staph PCNases.
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what kind of coverage do second generation cephalosporins have?
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less g+ but more g-.
HNPEck: H.influenzae N.meningitidis Proteus mirabilis E.coli Klebsiella pneumoniae |
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what are some 2nd generation cephalosporins? include dosage.
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1.cefaclor (oral q.8hrs) *serum sickness*
2.loracarbef (oral q.12h) 3.cefuroxime q.12hr (oral = ceftin, IV = zinacef) |
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what is a 2nd generation cephalosporin active against bacteroides fragilis?
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the cephamycins, specifically cefoxitin (IV/IM)
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what differentiates the 3rd generation cephalosporins? name four.
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they have much less g+ and much MORE gram negative coverage. also best v. meningitis.
1.ceftriaxone (IV/IM) 2.cefotaxime (IV/IM) 3.cefpodoxime (oral) 4.cefdinir (oral) |
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which 3rd generation cephalosporin should not be given to children under 3 mos due to kernicterus risk? what is the exception to this?
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ceftriaxone should not be given (it's HIGHLY protein bound, can displace bilirubin easily) UNLESS as single does for gonorrheal conjunctivitis.
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how is ceftriaxone a good drug in case of renal failure?
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1/2 is excreted in bile, 1/2 in kidneys.
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what is the best 3rd generation cephalosporin aganist n.gonorrhea?
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ceftriaxone. SAME RX AS FOR MENINGITIS
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which 3rd generation cephalosporin will also cover bacteroides?
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cefotaxime (IV/IM)
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an infant develops reddened feces after meningitis tx. what is the cause?
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an rx of cefdinir. it binds Fe and decreases it's absorption of Fe. infants fed formula high in Fe can suffer reddened feces.
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name two 4th generation cephalosporins.
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cefepime & cefditoren
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how is cefepime administered? what is it effective against? what are it's side effects?
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IV/IM
it's good for gram negative rods resistant to 3rd generation cephalosporins. it has good CNS penetration, but neurological side effects: myoclonus EEG changes with increase risk if epileptic. disorientation. |
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what is the most common side effect of cephalosporins? what other abnormalities may present?
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hypersensitivity is most common.
coagulation abnormalities may result due to interference with vitamin K, which increases prothrombin time. caution with warfarin/heparin or bleeding disorder. |
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with which drug must you use caution with a patient on warfarin or with a bleeding disorder?
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cephalosporins.
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what are carbapenems?
name 3. |
they are the broadest spectrum beta lactams available. includes anaerobes and some MRSA.
1.imipenem 2.meropenem 3.ertapenem |
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what is cilastatin?
what is it given with? |
Cilastatin is a chemical compound which inhibits the human enzyme dihydropeptidase. Dihydropeptidase is found in the kidney and is responsible for degrading the antibiotic imipenem.
it's given with imipenem. |
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which carbapenem causes fewer seizures? what is it not metabolized by?
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meropenem. it's not metabolized by dipeptidase.
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which carbapenem is only dosed once a day?
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ertapenem.
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what are common uses of carbapenems?
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1.UTIs
2.lower RTIs (s.aureus, e.coli, klebsiella, enterobacter, h.influenzae) 3.intra-ab & gyn infxns, bacterial septicemia. 4.bone, joint & skin infxns(enterococcus faecalis, s.aureus & epidermidis, p.aeruginosa) |
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what is vancomycin used for?
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IV for MRSA or for nonresistant staph if allergic to beta lactams. the oral form is not absorbed but is an alternate for psuedomembranous colitis.
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what causes psuedomembranous colitis? how does it become a problem?
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c.difficile.
it makes 2 toxins, one causes fluid production and the other lyses epithelium to form plaques. |
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what is the first drug of choice for c.difficile?
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metronidizone b/c it produces an anion which ruins the DNA of c.difficile
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b.cereus is a spore forming g+rod which causes food poisoning. what is a good rx for it?
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vancomycin
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what is red man syndrome? what causes it?
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due to IV of vancomycin. get flushed upper body, hypotension, tachycardia and shock. it's caused by the release of histamine from basophils and mast cells.
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what are some other vancomycin side effects?
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ototoxicity and nephrotoxicity.
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what drug is not a beta lactam antibiotic, but still inhibits cell wall synthesis? it is useful against UTIs from e.coli and enterococcus faecalis in women.
what is it's mechanism? |
fosfomycin. it inhibits enolpyruvate transferase.
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how does fosfomycin inhibit cell wall synthesis?
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it blocks addition of phosphoenolpyruvate to UDP-N-acetylglucosamine (2nd step in park peptide synthesis).
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what is an injectable lipopeptide for skin infxns from g+ and MRSA organisms? what is it's side effect?
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daptomycin. it's side effect is increased creatine kinase.
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what type of anti-b is bacitracin? what is it's mechanism?
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it's cidal vs. various g+ cocci and bacilli.
bactoprenol transports NAG/NAM outside cell, where it can be attached to pep-g. the bactoprenol must be de-pho'd before combining with NAM. bacitracin + pho, preventing de-pho of bactoprenol. NO CELL WALL SYNTHESIS. |
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what is bactoprenol? how does bacitracin affect it?
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it's a lipid carrier molecule involved in cell wall synthesis. bacitracin prevents it from being de-phosphorylated and therefore keeps it inactive.
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what staph infxn is bacitracin useful for?
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ulcerative blepharitis from s.aureus and s.epidermidis
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what causes bacterial conjunctivitis?
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s.aureus
strep pneumonia h.influenzae moraxella catarrhalis |
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what is the structure of aminoglycosides? how are they used synergistically?
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amino sugars attached in glycosidic links to an aminocyclitol ring. mostly for g- organisms. used with beta lactams for synergistic effect for g+ coverage.
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what drugs are aminoglycosides used with in synergy?
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carbapenems: broadest spectrum of all beta lactams. no nephro or ototoxicity.
cephalosporins: 3rd and 4th gen. give best g- coverage flouroquinalones: no nephrotox. |
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how are aminoglycosides usually given? what is an exception to this?
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they are polycations, v.polar and usually given by IV. sometimes they are given orally to clean out the bowel.
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what are side effects to aminoglycosides?
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they are nephrotoxic and ototoxic. all are excreted by kidney!
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what is the antibiotic mechanism of aminoglycosides?
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they enter the periplasmic space of G-bacteria thru porin channels. they pass thru inner membrane by flowing down the electrochemical gradient.
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what are the static effects of aminoglycosides? how is this altered by does?
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at low levels: mRNA is misread, giving faulty proteins. some insert into membrane = lysis.
at high levels: inhibit initiation of pr- synthesis. |
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at which levels are aminoglycosides cidal?
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at LOW levels. the faulty proteins produced cause leaky membranes.
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where can aminoglycosides attain their highest levels?
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renal cortex = nephrotoxicity
(in proximal tubules the drug accumulates in lysosomes, ruptures) endolymph = ototoxicity |
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what is the ultimate effect of ototoxicity?
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irreversible damage b/c sensory hair cells cannot regenerate.
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what can cause ototoxicity in neonates? why?
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aminoglycosides, b/c the drugs accumulate in the fetal plasma.
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name three IV administered aminoglycosides:
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1.gentamicin
2.tobramycin 3.amikacin |
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what aminoglycoside is topical, used for burns, wounds; ophthalmic prep. AND is interchangeable with tobramycin?
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gentamicin
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what is an ophthalmic rx for conjunctivitis and blepharitis with g- organisms?
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tobradex (tobramycin + dexamethasone *glucocorticoid*)
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what is a nosocomial "big gun" aminoglycoside?
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amikacin
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name three oral aminoglycosides.
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kanamycin
neomycin paromomycin |
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what are kanamycin and neomycin both used for? which is also a topical disinfectant?
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both are oral for bowel prep. neomycin is also a topical antiinfectant.
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what is the number one choice for amoebic dysentary (entamoeba histolytica)?
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paromomycin
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which aminoglycoside can be given orally and by IV?
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kanamycin
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name two ways to adjust dose for renal fxn.
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1.change dose amt.
2.manipulate dose interval |
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what is the formula for creatine clearance?
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(140-age)x(lean wt in kg)/
72 x serum creatine (mg/dl) women: x 0.85 |
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where do aminoglycosides distribute? why?
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in lean body mass b/c they are polycations.
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how is lbw calcuated for men? women?
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men: 50 kg + 2.3kg for each inch over 5ft
women: 45.5kg + 2.3kg for each inch over 5ft |
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what is the aminoglycoside dose formula?
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max daily dose x est CLcr/normal CLcr
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what is normal CLcr for a typical 70kg male?
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120-125 ml/min
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when should peak levels be drawn after the dose?
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30-60 minutes
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what are some other side effects of aminoglycosides? what is the mechanism?
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neuromuscular block causing respiratory paralysis. Ach release is blocked.
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how can you treat Ach inhibition?
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IV of Ca2+ or neostigmine
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what kind of rx is neostigmine?
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it's a cholinesterase inhibitor. it metabolizes Ach, so if inhibited, Ach levels rise.
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what is the mechanism of tetracyclines?
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they inhibit the binding of aminoacyl tRNA to acceptor site of ribosome. STATIC. inhibit protein synthesis.
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why can levels of tetracycline persist?
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they undergo enterohepatic recycling.
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what type of tetracycline is tetracylcine? what is it given for? what might be better?
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it's a short acting (6-8hr t1/2). it's an alternate oral or topical for inflammatory acne.
1st choice: topical erythromcin (a macrolide) + benzoyl peroxide w or w/o oral antib |
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what symptom of syndrome of inappropriate ADH secretion can be treated by this sort of tetracycline?
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chronic dilutional hyponatremia. tx with demeclocycline, an intermediate acting tetracycline (t1/2 = 12hrs)
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this tetracycline can tx rickettsia, chlamydia trachomatis and lyme dz. how is it administered?
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doxycycline. oral and IV.
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what can rickettsia cause? what does chlamydia trachomatis cause?
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rocky mountain spotted fever.
nongonococcal urethritis and most nongonococcal cervicitis. |
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the spirochete borrelia burgdorferi causes this dz which results in skin lesions, joint pain, maybe cardiac and neuro issues. what drug can treat it?
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lyme dz. doxycycline.
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a pt with syphilis AND vibrio cholerae is allergic to PCN. what should you give them?
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doxycycline
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what would be the first choice drug for the pt with cholera?
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flouroquinalone b/c better g- coverage.
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what decreases absorption of tetracyclines? by what mechanism?
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dairy products and antacids.
via chelation |
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what are side affects to tetracyclines?
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1.GI upset (take with food)
2.photosensitivity (esp demeclocycline) 3.brown discoloration of teeth. |
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what rx is structurally similar to tetracyclines? what is it's mechanism?
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tigecycline. it inhibits pr- synthesis by blocking entry of aminoacyl t-RNA to the acceptor site.
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what is tigecycline good for?
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it's active v.tetracycline sensitive g+/g- organisms and MRSA. it's used for complicated skin and intraabdominal infections.
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what is the structure of the macrolides? what are they effective against?
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lactone ring + 1 or more deoxy-sugars. effective against methicillin sensitive s.aureus, moraxella catarrhalis, h.influenzae
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what is the macrolide mechanism?
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they inhibit translocation from acceptor site to donor site (near where tetracycline acts)
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what is an example of a macrolide? what was it historically effective against? is it still used for that?
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erythromycin (enteric coated). it was first used against legionanaire's dz, now azithromycin is preferred b/c of better lung penetration. paraenteral flouroquinalone is also useful.
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what sort of macrolide is used for otitis media?
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erythromycin + sulfisoxazole = pediazole! *RECURRENT*
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how is erythromycin coated?
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with estolate salt (causes cholestatic hepatitis, but best absorbed)
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what is erythromycin first choice for?
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1.pneumonia by various organisms
2.camyplobacter jejuni 3.corynebacterium diptheriae 4.bordetella pertussis |
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what does campylobacter cause? what does it look like?
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a comma shaped g- rod which causes diarrhea.
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what is a g+ rod which produces exotoxin to damage respiratory mucosa? it is treated with erythromycin.
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c.diphtheriae
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what bacteria causes whooping cough? what does it allow for?
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bordetella pertussis. a g- organism, makes pertussis toxin. the coughing and necrosis can allow for staph or influenza invasion.
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how does erythromycin inhibit it's own metabolism?
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it's metabolites complex with cytochrome heme Fe2+ and inhibit CYP3A (the P450 which metab. erythromycin).
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what is torsades? how can it be caused by erythromycin?
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torsades is an arrhythmia. erythromycin can prolong repolarization. the risk is increased with any other rx that inhibits cyp3a b/c that increases your levels of erythromycin.
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what are diltiazem and verapamil? how are they related to erythromycin?
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they are also metabolized by CYP3A. taking one of these with erythromycin increases risk of sudden death five-fold. (they are Ca2+ channel blockers)
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what are the uses of azithromycin?
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1.community acquired pneumonia
2.legionnaires 3.chlamydia trachomitis 4.bordetella pertussis 5.mycobacterium avium complex |
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how is azithromycin metabolized?
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it's t1/2 is 70 hrs and it concentrates intracellularly. it does NOT inhibit P450 and is excreted unchanged in the bile.
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what rx can cause hypoglycemia (a macrolide)? what is it used for?
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clarithromycin. it's used for community acquired pneumonia and mycobacterium avium complex. it does inhibit CYP3A.
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what is a macrolide derivative with increased gram positive activity?
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ketolide
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which macrolide concentrates in pulmonary tissue and WBCs? what is it for?
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telithromycin.
it's for community acquired respiratory infections. it's active v.beta lactam and macrolide rez organisms. |
