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104 Cards in this Set
- Front
- Back
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Theory applied to antibiotic treatment
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-Selective toxicity to the bacteria but not so much to the host
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History of Antibiotics
-3 main events |
-Sulfa drugs developed in the 1930s
-Penicillin discovered in 1929 but useful amounts available in 1940s -Streptomycin discovered in 1940s |
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Things to know to properly prescribe antibiotics
(3 main) |
-Likely/known infecting organism(s)
-Likely/known antibiotic susceptibilities of infecting organism(s) Relevant host factors: -Age -Pregnancy -Renal/hepatic impairment -Site of infection -Previous drug allergies (and rxns) -Other genetic/metabolic abnormalities |
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Goal of antibiotics?
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-Achieve a dose of the drug in blood/body site that is greater than the MIC
-MIC = minimum inhibitory concentration |
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Concentration Dependent Killing Agents
-Defn? |
-Agents eliminate bacteria when their conc is above the MIC
-When ratio of antibiotic conc to MIC increases --> more killing of bacteria -More is better -Correlates to C(max) or peak |
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Time-dependent Killing agents
-Defn? -Correlates to? |
-Kills bacteria when the conc is higher than the MIC but depends on the TIME above MIC
-Further increases above the MIC does NOT give more killing -Correlates to time above the MIC |
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General consideration for intracellular pathogens?
(1) |
-Drug has to get inside the host cell
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General adverse reactions with antibiotics?
(2) -Reasons for this rxn? (2) |
-Nausea
-Diarrhea -Seen in most antibiotics and will only be mentioned if it is severe -Due to action of the drug -Due to alteration of normal flora by drug |
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Special considerations for CNS antibiotic penetration?
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-Several only penetrate if there is CNS inflammation
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Special consideration for urinary tract antibiotic penetration?
-Esp for which condition? (1) |
-Must be excreted and concentrated in an active form in the urine
-Especially for treatment of cystitis |
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Bactericidal versus Bacteriostatic?
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-Bactericidal = kills bacteria
-Bacteriostatic = stops bacterial growth |
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List of Bactericidal agents
(6) |
-Beta-lactams
-Aminoglycosides -Fluoroquinolones -Vancomycin -Rifampins -Metronidazole |
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List of Bacteriostatic agents
(5) |
-Chloramphenicol
-Clindamycin -Macrolides -Tetracyclins -Sulfa drugs |
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When are bactericidal agents preferable?
(2) |
-If host is compromised (esp. neutropenic--cancer pts)
-If host defense mechanisms do not operate well (pts w/ bacterial endocarditis or meningitis) |
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Components necessary for agents to be active intracellularly?
(3) |
-Must enter cell at adequate levels
-Penetrate into microenvironment that contains the bacteria (phagosome) -Be stable to the conditions in microenvironment of the cell (low pH, lytic enzymes) |
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Fluoroquinolones
(2) |
-Ciprofloxacin
-Levofloxacin |
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Fluoroquinolones
-Drugs in class (2) -MOA? -Basis for selective action? |
Drugs
-Ciprofloxacin -Levofloxacin MOA -Inhibit Type II topoisomerases -Inhibit DNA gyrase (supercoiling) -Inhibit TopoIV (decatenation) -Blocks DNA replication and transcription Selectivity -These do NOT exist in eukaryotic cells -Bactericidal |
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Fluoroquinolones
-Mechanisms of Resistance? (4) |
Resistance mechanisms
-Target modification in gyrase or topoIV genes* -Altered uptake or efflux (drugs blocked from being transported into cells) -Reduced permeability* -Plasmid-mediated drug modification by quinolone transacetylase (evolved from aminoglycoside transacetylase) |
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Fluoroquinolones
-Pharmacokinetics (2) -Administration? (1) |
Kinetics
-Absorbed well from oupper GI tract -Tissue distribution is good Administration -Can be given either orally or IV |
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Fluoroquinolones
-Contraindications? (2) -Due to? |
Contraindications
-Pregnant patients -Under 18 yrs old Due to -Anthropathy (joint problems) observed in animals |
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Fluoroquinolones
-Adverse reactions? (2) -Do not use in which pts? (2) |
SEs
-Arthropathy (joint pain esp in Achilles tendon) -Levofloxacin --> Prolonged QT interval Should NOT be used in pts. -Receiving class I or III antirrhythmics -Known conduction abnormalities or taking other drugs that prolong the QT interval or induce bradycardia |
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Rifampin
-MOA? -Selectivity? -Used in? (2) |
MOA
-Inhibit RNA Polymerase of bacteria -Bactericidal Selectivity -Not present in mammalian cells so it is selective Used in: -Mycobacterial infections commonly -Increasingly used due to increase in resistant gram positive bacteria |
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Rifampin
-Mechanism of Resistance? (1) |
Resistance
-Target site mutation in the gene for the rpoB subunit of RNA polymerase* (altered RNA polymerase) |
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Rifampin
-Pharmacokinetics -Adminstration? |
Kinetcs
-Rapid oral absorption -Excellent tissue penetration including the CNS -Excellent penetration intracellularly Administration -Can be given IV or PO |
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Rifampin
-Adverse reactions? (4) |
SEs
-Can turn pts bodily fluids reddish-orange -Liver problems --> Esp if given with other mycobacterial drugs (isoniazid) -Induces CP450 enzymes -Special problem w/ pts. taking inhibitors of HIV protease (hepatotoxcity)** |
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Metronidazole
-MOA? -Mechanism of resistance? |
MOA
-Produces compounds that are toxic to DNA -Exact mechanism is unclear Resistance -Rare and mechanism is not clear |
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Metronidazole
-Pharmacokinetics -Administration? -Uses (3) |
Kinetics
-Excellent tissue penetration, including CNS -Reduction of metronidazole creates conc gradient --> drives uptake of more drug -Then promotes formation of intermediate compounds and free radicals that are toxic to cell Administration -IV or PO administration -Topical Uses (w/ topical) -Inflammatory pustules -Papules -Bacterial vaginosis |
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Metronidazole
-Adverse reactions? (2) -Contraindications? (1) |
SEs
-Promote renal retention fo Li+ -Decreased elimination of ergot derivatives Contraindications -Pts. should not drink alcohol |
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Sulfa drugs
-Drugs in class? (1) -MOA? -Specificity? -Given with? (1) |
Drugs in class
-Sulfanilamide MOA -Analog of para-aminobenzoic acid (PABA) that binds to dihydropteroate synthetase -Results in a fall of folic acid levels -Bacteria stop growing as folic acid levels fall Specificity -Humans do not have this enzyme (we obtain folate acid in diet) Given with: -Trimethoprim |
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Sulfa drugs
-Do not work in which situation? -Problems due to? |
Problematic situations
-Problems with sites of tissue destruction -Purulent exudate -Wounds Problems due to: -Enough of the final products made with folate acid are still available -Growth can then resume |
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All sulfa drugs have what in common? (1)
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-All derivatives of para-aminobenzene sulfonamide
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Trimethoprim
-MOA? -Specificity? -Given with? (1) |
MOA
-Analog of dihydrofolic acid --> binds to bacterial dihydrofolic acid reductase -Blocks formation of folic acid Selectivity -Does not readily inhibit mammalian dihydrofolic acid reductase Given with? -Sulfa drugs |
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Which two drugs are normally given together? (2)
-MOA? -Mechanisms of resistance? (2) |
-Trimethoprim + sulfa drug
-Produced sequential block of folic acid synthesis -Synergistic -Called "TMP-SMX" combo Resistance -Altered targets/bypass* -Metabolic bypass is most common as new enzymes are provided** -Reduced permeability* |
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Dapsone
-MOA? -Useful against? (2) |
MOA
-Folic acid blocker -Analog of PABA Useful against -Mycobacteria (esp leprosy) -Pneumocytis jiroveci/carinii (fungus) |
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Sulfa Drugs
-Mechanism of Resistance? (4) -Resistance found on? (2) |
Resistance
-Mutated genes for target enzymes -High levels of expression of enzymes -Newly transferred genes with resistant enzymes -Altered uptake and efflux -Major problems with this class Resistance found on: -Both chromosomes and plasmids |
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Sulfa drugs and trimethoprim
-Pharmacokinetics -Administration -Addition fact for sulfa drugs (1) |
Kinetics
-Both act synergistic (given together) -Good bioavailability Administration -IV or PO -Sulfa--can be given along w/ silver ions in a topical cream |
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Sulfa Drugs
-SEs? (3) -Contraindications? (3) |
SEs
-HIV pts can develop neutropenia and exfoliative dermatitis -HIV pts given these drugs prophylaxically -Allergic rxns including anaphylaxis Contraindications -Glucose-6-phosphate deficiency -Folic acid deficiency -Pregnant |
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Classes that inhibit bacterial cell wall growth (6)
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-Natural penicillins
-Artificial penicillins -Artificial penicillins w/ beta-lactamase inhibitors -Monobactams -Cephalosporins -Carbapenems |
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Antibiotics that inhibit cell wall growth
-MOA? |
-Bactericidal for growth bacteria
-W/o cell wall --> osmotic pressure causes bacteria to burst -If osmotic pressure is eliminated (with right buffer) then cell do not lyse but become spheroplasts or protoplasts |
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Bacitracin
-MOA? -Mechanism of resistance? |
MOA
-Inhibits dephosphorylation of the lipid carrier -Blocks transfer of cell wall components thru the bacterial membrane by binding to the carrier molecule Resistance -Unclear |
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Bacitracin
-Administration -Used with? (2) -Uses (1) -SEs (1) |
Administration
-Topical Used with -Neomycin -Polymixin B -All = neosporin Uses (neosporin) -Prevention of infection in minor cuts, scrapes, burns SEs -Very few -Rarely allergic reaction giving anaphylaxis |
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Vancomycin
-MOA? -Mechanism of Resistance? (2) |
MOA
-Bind to D-alanine dimer at the end of the crosslinking peptide in the peptidoglycan of the bacteria Resistance -Set of genes on a transposon that encode enzymes that make a cell wall w/ D-serene or D-lactate instead of D-alanine* -Altered targets/bypass |
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Vancomycin
-Pharmacokinetics -Administration -Monitoring |
Kinetics
-Good tissue availability but not to CNS w/o inflammation and not to bone Administration -Usually IV* -Can be given orally but not really absorbed there (remains in lumen) --therefore can only treat GI tract infections w/ oral administration Monitor -Conc of vancomycin are monitored to determine time above MIC |
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Vancomycin
-Use (1) -SEs? (3) |
Use
-MRSA SEs -Rapid IV administration --> can cause Red Man Syndrome (histamine mediated rxn w/ flushing and redness of upper body) -Anaphylaxis -Nephrotoxicity esp if given with aminoglycosides |
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Beta Lactam antibiotics
-Drugs in class -MOA? -Mechanism of resistance? (4) |
Drugs in class
-Penicillins -Cephalosporins -Monobactams -Carbapenems MOA -Inhibit transpeptidases or penicillin binding proteins -Stop cross-linking and weaken cell wall Resistance -Altered transpeptidases or altered penicillin binding proteins* -Reduced permeability* -Beta-lactamases-hydrolysis* -Extended spectrum beta lactamases(ESBLs) -->hydrolyze 3rd generation cephalosporins and many synthetic penicillins |
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Penicillin
-MOA? -Mechanism of Resistance (3) |
MOA
-Binds transpeptidases and prevent cross linking -Inhibit growth of bacterial cell wall Resistance -Mutations in the genes encoding penicillin binding proteins or transpeptidases -Beta-lactamases which hydroxyze the beta-lactam ring -Altered uptake |
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Penicillin
-Pharmacokinetics (4) -SEs? (4) -Administration |
Kinetics
-Good bioavaliability -Cross BBB if inflammation present -Short half lives -Can be desensitized to drug (only pregnant women w/ syphilis) Administration -Given several times a day -IV, PO or both SEs -Allergic reactions -Nausea, vomiting, diarrhea -Hives, asthma, shortness of breath or other systemic reactions |
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Pt w/ Pencillin Allergies can also have allergies to which other drugs? (2)
-No allergies seen with? (1) |
Allergy possible with:
-Cephalosporins (5-10%) -Carbapenems Not with: -Monobactams |
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General info about cyclosporins
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-Come in 'generations' (4)
-Successive generations have broader spectrum of activity -Also are more resistant to beta-lactamases |
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Drugs to know in penicillin class
(5) |
-Ampicillin
-Amoxicillin -Penicillin -Nafcillin -Dicloxacilin |
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Drugs to know in penicillin w/ beta-lactamase inhibitor class
(3) -Administration? (2) |
-Amoxicillin-clavulanate (PO or IV)
-Ampicillin-sulbactam -Pipericillin-tazobactam (IV) |
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Drugs to know in cephalosporin class
(4) |
-Cephalexin
-Cefotaxime -Ceftazidime -Ceftriaxone |
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Drugs to know in Monobactams class
(1) |
-Aztreonam
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Drugs to know in Carbapenems class
(1) |
-Imipenem/cilastatin
-Cilastatin = No antibacterial action but prolongs half-life Imipenem and prevents nephrotoxic effects |
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Tetracyclines
-Drugs in class to know (3) -MOA? -Mechanisms of Resistance (3) -Not affected by resistance (1) |
Drugs to know
-Tetracycline -Doxycycline -Tigecycline MOA -Block protein synthesis by ribosomes -Bind 30S subunit Resistance -Found on plasmids and transposons -Efflux pumping** -Produce proteins that binds ribosome and blocks tetracylines* Not affected by resistance -Tigecycline |
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Tetracyclines
-Kinectics? -Administration? -Not given with? (1) -SEs? (3) -Contradictions (2) -Exception to Contraindications? (1) |
Kinetics
-Good absorption -Reasonable tissue distribution, including CNS Administration -IV or PO Not given with: -Beta-lactams since they are antagonists SEs -Nausea -Photosensitivity -Sun exposure --> rash Contraindications -Children under 8 b/c of long lasting discoloration of teeth -Pregnancy Exception -Rocky mountain spotted fever |
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Macrolides
-Drugs to know in class (4) -MOA? -Mechanisms of Resistance (2) -Used when? |
Drugs to know:
-Erythromycin -Azithromycin -Clarithromycin -Telithromycin MOA -Block protein synthesis -Binds 50S subunit of ribosome Resistance -Methylation of ribosomes (block drug binding)* -Efflux pumping Used when: -Pts are allergic to penicillin |
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Macrolides
-Pharmacokinetics? -Administration |
Kinetics
-Reasonable oral bioavailability -Good tissue distribution Administration -IV or PO |
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Azithromycin
-Differences from other Macrolides -Given to? (2) |
Differences
-Longer half life -Taken less often Given to: -Children -Pregnant women |
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Erythromycin
-Differences from other Macrolides? (2) -SEs? (2) -Additional use? (1) |
Differences
-New, extended release version now available -Topical form available SEs -More nausea -Greater risk of QT prolongation Use -Acne |
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Telithromycin
-Addition SE? (1) |
SE
-Severe Hepatotoxicity |
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Aminoglycosides
-Drugs from class to know? (3) -MOA? -Transport into bacteria |
Drugs to know
-Streptomycin -Gentamicin -Tobramycin MOA -Block protein synthesis -Bind to 30S subunit -Bactericidal Transport -Disrupt Mg2+ bridges btw LPS molecules -Transported across membrane in energy dependent manner |
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Aminoglycosides
-Transport inhibition? (4) -Mechanisms of Resistance (5) |
Transport inhibition
-Divalent cations -Increase osmolality -Acidic pH -Anaerobic environment Resistance -Found on plasmids and transposons -Altered binding by ribosome* -Efflux pumping -Decreased uptake by outer membrane changes--altered permeability* -Enzymatic inactivation by acetylation, phosphorylation or adenylation** |
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Aminoglycosides
-Pharmacokinetics -Used in combo with? |
Kinetics
-Post-antibiotic effect --> suppress bacteria growth after drug is gone -Concentration dependent --> higher conc induced more rapid, complete killing Combo with -Beta-lactams (cell wall active agents) --synergistic effect |
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Aminoglycosides
-SEs -Contraindications |
SEs
-Nephrotoxicity -Ototoxicity Contraindications -Pts with impaired renal function -Pts taking other nephrotoxic drugs Administration -IV or IM* |
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Streptomycin
-Additional info? (1) -Uses? (1) |
Additional info
-High ototoxicity Use -First line drug for several bioterriorism agents |
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Lincosamines
-Drugs to know in class? (1) -MOA -Mechanisms of resistance (4) |
Drugs to know
-Clindamycin MOA -Block protein synthesis -Binding to 50s subunit of ribosome Resistance -Ribosome RNA methylation -Alterned ribosomal proteins -Adenylation -Both chromosomal and plasmid resistance genes |
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Lincosamines
-Pharmcokinetics? -Administration? -SEs? (1) |
Kinetics
-Well absorbed -Good tissue penetration but NOT in CNS Adminstration -IV, PO or topically SEs -Some allergic rnxs |
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Oxazolidinone
-Drugs to know in class? (1) -MOA? -Mechanisms of resistance (1) -Administration? |
Drugs to know
-Linezolid MOA -Block protein synthesis -Bind to 50s subunit Resistance -Mutation of 23s rRNA Administration -IV or PO |
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Oxazolidinone
-Pharmacokinetics -SEs -Need to monitor? (4) -Contraindications? (1) |
Kinetics
-Good absorption SEs -Thrombocytopenia Monitor -Platelets -CBC -Creatinine -LFT (liver function test) Contraindications -Pts on SSRIs |
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Chloramphenicol
-MOA? -Mechanism of Resistance? (2) -Administration? |
MOA
-Block protein synthesis -Binds to 50s subunit Resistance -Acetyltransferases* -Efflux pumping Administration -IV or PO |
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Chloramphenicol
-SEs? (4) |
SEs
-Aplastic anemia -Bone marrow suppression -Gray syndrome (circulatory collapse, coma, death) -Dose adjustment if patient has liver problems |
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Streptogramins
-Drugs to know in class (2) -MOA -Mechanism of Resistance (3) |
Drugs to know
-Quinupristin/Dalfopristin combo (synercid) MOA -Both block protein synthesis -Binds to 50s ribosomal subunit Resistance -Target alteration by ribosome methylation -Efflux pumping -Resistance readily occurs in only 1/2 is given |
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Streptogramins
-SEs? (3) Administration? |
SEs
-Athralgias -Myalgias -Dose needs adjustment if pts have liver problems Administration -IV |
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Mupirocin
-MOA -Mechanism of Resistance? (1) -Adminstration |
MOA
-Blocks protein synthesis -Inhibits isoleucine tRNA synthetase Resistance -Target site mutation Administration -Topical on skin or mucosal surface |
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Mupirocin
-Uses? (2) -SEs? |
Uses
-Elimination of nasopharyngeal carriage of S. aureus -Skin infections SEs -Unclear |
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Retapamulin
-MOA? -Mechanism of Resistance? (1) -Adminstration? |
MOA
-Blocks protein synthesis -Binds to 50s ribosomal subunit Mechanisms of Resistance -Target site mutataion Administration -Topical on skin surface |
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Retapamulin
-Uses? (1) -SEs? |
Uses
-Treat impetigo with MRSA* SEs -Unclear |
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Daptomycin
-MOA? -Mechanisms of resistance? -Administration? (1) |
MOA
-Cyclic lipopeptide interferes w/ bacterial membrane function and pore formation Resistance -Unclear Administration -IV |
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Daptomycin
-SEs? |
SEs
-Elevated liver function tests and creatine phosphokinase -Muscle weakness and pain w/ elevated creatine phosphokinase (discontinue drug) |
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Polymixins
-MOA? -Mechanism of Resistance? -Administration? |
MOA
-Disrupts bacterial membranes by charge alternation Resistance -Unclear Administration -Topical -IV or IM |
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Polymixins
-Used with? (2) -SEs? |
Used with:
-Neomycin -Bacitracin (Neosporin) SEs -Few if used topically |
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Nitrofurantoin
-MOA? -Mechanism of resistance? (1) -Administration -Pharmacokinetics? |
MOA
-Unclear -Attacks bacterial metabolism -Mimics radiation damage -Drug must be reduced inside bacteria Resistance -Altered levels of reduction enzymes Administration -PO Kinetics -Drug concentrated in urine |
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Nitrofurantoin
-Use (1) -SEs (2) |
Use
-Uncomplicated UTIs SEs -Turns urine brown (harmless) -Lung problems in pts on prolonged or prophylaxis treatment |
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Antibiotic Formulary
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-Many hospitals do not carry all antibiotics
-Carry subset and hospital will send up equivalent if a doctor prescribes a different one |
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Empiric use of antibiotics
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-Physicians may begin treatment before organism is identified
-Requires treatment matched to disease and not organism -Selections often give broader spectrum of coverage -May not be drug of choice once organism is identified |
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Summary on antibiotics
(4) |
-Many different drugs with many mechanisms --> only universal principle is selective toxicity
-Many antibiotics are products of other microbes (some are not--sulfa and fluoroquinolones) -Antibiotics are used before organisms are identified sometimes -Mechanisms of resistance vary |
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Measurement of antibiotics sensitivities
-Done for? -Always done for which species? (4) |
-Done especially for nosocomial infections but increasing need
Species tested -Enterococcus -Staphylcoccus aureus -Pseudomonas aeruginosa -Streptococcus pneumoniae |
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Antibiotic Resistance
-Measured? |
-Measured in terms of MIC
MIC measured by -Inoculation of living bacteria in a series of tubes with growth media and varying drug levels -Inocolation of living bacteria on agar plate + disks w/ antibiotics in them --> measure inhibition of growth |
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Etest Determination
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Determination of MIC
Similar to disk diffusion test |
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Laboratory Reporting of MICs
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Most clinical lab report MICs
Also give a reference so that the strain is indicated as resistant, intermediate or sensitive |
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Mutations in Bacteria
-Ways (2) -Expressed |
Ways
-Induced -Spontaneous Rare mutation expressed -Bacteria are haploid -Rapid growth rate Selective advantage enriches for mutations Gene transfer transfer occurs in bacteria between species and within species |
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Types of resistance genes
(5) |
-Mutations in target gene (chromosomal)
-Transport mutations (chromosomal) -Gene for an efflux pump that actively transports an antibiotic out of the bacteria (chromosome and plasmid) -Gene that chemically alters or degrades the antibiotics (plasmid and chromosome) -Genes that biochemically bypasses the block provided by the antibiotic (plasmid and chromosome) |
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Clindamycin
-Administration? -Uses? (2) |
Administration
-Topical antibiotic Uses -Acne -Bacterial vaginosis |
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Clindamycin-benzoyl peroxide
-Administration? -Uses (1) |
Administration
-Topical antibiotic Uses -Acne |
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Elegy
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A lament for someone's death or the passing of a love or concept.
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Mafenide (sulfa)
-Administration -Use (1) |
Administration
-Topical antibiotic Use -Burns |
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Probiotics
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-Normal flora contributes to health
-Can be disrupted/altered in disorders -Research in therapeutic value |
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Ways to alter the microbial flora therapeutically
(4) |
-Antibiotics
-Prebiotics = dietary supplements that promote growth of good bacteria -Probiotics = administration of live, benefical bacteria -Combo of pre- and pro- biotics |
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Probiotics
-Source -Organisms used? (3) |
Source
-Derived from food sources, especially cultured milk products Organisms - Lactobacilli are common used -Other bacteria/yeasts |
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Commonly recommended as a source of probiotics
(1) -Disadvantages (2) |
Yogurt
Disadvantage -Do not survive well in an acidic environment -They don't colonize the microflora efficiently |
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Probiotics
-MOA? -Conditions treated? (1) |
MOA
-Unclear -Inhibit growth or epitheilial binding/invasion by pathogenic bacteria -Improvement in intestinal barrier function -Modulation of the immune system, esp. suppression of inflammatory cytokines Conditions treated -Diarrhea -Antibiotic-associated diarrhea -Ulcerative colitis -Pouchitis(complication of IPAA-proctocolectomy w/ ileal pouch-anal anastomosis) -IBS |
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Clavulanic acid and
other beta-lactamase inhibitors -MOA -Used with? -Uses? (1) |
MOA
-Bind strongly to beta lactamases (which hydrolyse the beta-lactam rings) -Inactivate these beta-lactamase Used with: -Beta-lactams Uses -Given so that other antibiotics are not inactivated |
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Beta-Lactamase inhibitors?
(3) |
Inhibitors
-Tazobactam -Sulbactam -Clavulanate |
