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57 Cards in this Set
- Front
- Back
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strep and taph
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gram pos cocci
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enterococci
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gram pos cocci
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neisseria
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gram neg cocci
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e coli
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gram neg rod
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pseudomonas aeruginosa
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gram neg rod
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clostridia
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gram pos rod ANAEROBE
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bacteroides fragilis
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gram neg rod ANAEROBE
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stages of inhibition of synthesis or damage to cell wall
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1- alanine racemase
2- D-ala-D-ala pentapeptide 3 - transpeptidase |
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stage 2 inhibitors (-pentapeptide)
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vacomycin
bactoprenol lipid carrier bacitracin |
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stage 3 inhibitors (-transpeptidase)
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PCN
CEPH Monobactams Carbapenems |
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rifampin
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moifies synthesois / metabolism of nucleic acids through RNA polymerase
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inhibition or modification of protein synthesis via
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30S ribosome
50S ribosome isoleucyl-tRNA synthetase |
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which antimicrobials bind to the 30S ribosome
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aminoglycosides
tetracyclines |
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which antimicrobials bind to the 50S ribosome
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clindamycin
macrolides chloramphenicol streptogramins |
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which antimicrobials modify intermediary metabolism (folate metabolism)
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sulfonamides (modify dihydropteroate synthase)
trimethoprim (modify dihydrofolate reducase) |
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prokaryotes have which ribosomal subunits
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50S and 30S
humans have 40 and 60S |
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whats the diff in nucleic acid synthesis between prok and euk
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prokarotes have DNA gyrase
humans have topoisomerase RNA polymerase is tructurally distinct in bacteria |
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macromolecular structure difference between microbes and humans
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ergosterol = fungal membrane
cholesterol = mammalian membrane |
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why are fungii and mycoplasma resistant to PCN
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fungus lack peptidoglycans
mycoplasma do not have cell walls at all pseudomonas aeruginosa is resistant because PCN cannot cross outer membrane |
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how do microbes esacape antibiotic consequences
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- purines , thymidine, serine, methionine released from purulent infections (sulfonamide resistance)
OR -failure to lyse due to lack of osmotic pressure difference |
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acquired resistance
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-mutational chromosomal resistance
-plasmid mediated resistance |
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-antibiotic resistance
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--altered targets (ab cannot bind anymore)
--enzymatic destruction or inactivation of antibiotic --increased efflux --alternative resistant metabolic pathway --decreased entry |
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exchange of genetic material among bacteria occurs by what mechanisms:
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1) conjugation
2) transduction 3) transformation |
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conjugation
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between 2 physically attached bacteria
exchange of plasmid DNA containig resistant determinant |
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transduction
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with virus (bacteriophage) carrying resistance determinant R to bacteria
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transformation
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ability of certain bacteria to pickup free from the environment
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altered targets / receptors to which the antibiotic CANNOT bind
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PCN
DNA gyrase peptidoglycan side chain 50S ribosome methylation |
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MRSA, S pneumoniae, enterococci alter tragets / receptors to prevent binding via which proteins and become resistant to which Antibiotics
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alter penicillin binding proteins
and resistant to beta lactam antibiotics (PCN, ceph, carba) |
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fluoroquinolones become resistant to which microbe species
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s. aureus, pseudomonas
altered DNA gyrase --> resistance |
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altering the peptidoglycan side chain prevents which entibiotic from binding
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vancomycin
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50S ribosome methylation prevents which antibiotics from binding
(when treating staph, strep, enterococci) |
erythromycin, clindamycin
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bactericidal mechanisms
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-inhibition of cell wall synth
-disrupt cell membrane -interfere with DNA function / synth |
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bacteriostatic mechanisms
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-inhibition of protein synthesis (exception = aminoglycosides which are -cidal)
-inhibiton of intermediary metabolic pathways |
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if you have a patient with impaired host defense, which type of antibacterial agent would you use? - cidal or -static
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bacteriocidal
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to get to locations of infections that re inaccessible, which type of agent would you use
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bacteriocidal
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when would you recommend taking an antibiotic on an empty stomach
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when antibiotic is unstable then dont want lots of gastric (acid) secretions to break down the drug too fast.
if drug is stable then can take with food |
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which antibiotics get into the CSF readily
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chloramphenicol
sulfonamides trimethoprim rifampin metronidazole |
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which antibiotics enter with inflammation
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PCN
CEPH cipro (used in meningitis bc crosses BBB) vancomycin |
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which antibiotics enter CSF poorly
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aminoglycosides
ceph (1 & 2) erythromycin clindamycin tetracycline |
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which types of antibiotics should be avoided in pregnant women
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oral antibiotics can cross placental barrier (gastric mucosal barrier) so can harm fetus
e.g. dont use aminoglycosides, chloramphenicol, metroidazole, tetracyclines |
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what selective distribution benefit does clindamycin have
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tends to accumulate in bone so advantageous for treatmnet of osteomyelitis
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what selective distribution benefit do macrolides provide
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tend to concentrate into pulmonary cell so advantageous in upper respiratory infections
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what selective distribution benefit do tetracyclines provide
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tend to accumulate into gingival crevicular fluid and sebut so advantageous in periodotitis and acne
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what aspect of aminoglycosides in terms of selective accumulation causes toxicity
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AG binds cells of inner ear and renal brush border --> increase ototoxicity and nephrotoxicity
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what aspect of tetracyclines in terms of selective accumulation causes toxicity
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TET binds to calcium in developing bone and teeth --> abnormal bone growth and brownish tooth discoloration in the fetus / young children
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renal excretion
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SCr and CrCl (creatinine clearance) measurements --> renal status
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hepatic metabolism
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no lab value gives a good estimate of the livers ability to metabolize antibiotics.
*avoid antibiotics metabolized by liver in patients with liver dysfxn |
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post antibiotic effect
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some antibiotics (AG and fluoroquinolones) can continue to kill bacteria for hrs after concentration of drug falls below MIC
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concentration dependent killing
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some antibiotics kill bacteria faster when given in doses that result in higher plasma concentrations
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narrow spectrum
extended spectrum broad spectrum |
narrow : effective only against + OR -
extended : gram + AND - broad: gram +, - AND atypical |
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names some narrow spectrum drugs
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aminoglycosides
bacitracin clindamycin vancomycin metrondiazole PEN G and V penicillinase resistant penicillins monobactams |
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examples of extended antibiotics
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good against + and -
extended spectrum PCNs Ceph fluoroquinolones (cip, levo) carbapenems |
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name some broad spectrum antibiotics
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macrolides
chloramphnicol fluoroquinolones sulfonamides tetracyclines trimethoprim |
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direct toxicity usually involves
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GI tract
liver kidney nervous system blood and blood forming system |
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indirect toxicity
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1. allergic reactions, hypersensitivity
2. salt efects. (due to salt administered with antibiotic, NOT the antibiotic itself 3. drug-drug interactions. (antibiotics can alter ativity of CYP450 drug metabolizing enzymes) |
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disturbance of host microflora (superinfection)
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1. disturbances of ecological balance of microbial community. this allows overgrowth of normally suppressed pathogenic organisms
2. pseudomembranous colitis due to clostridium dificile overgrowth 3. commonly assoc with broad spectrum antibiotics. |
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host factors (toxicity)
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1. age
2. preg 3. drug hypersensitivity |
