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70 Cards in this Set

  • Front
  • Back
Penicillin
-Class?
-Drugs to know? (5)
-MOA?
-Mechanism of Resistance (3)
Class
-Beta Lactam antibiotics

Drugs to know
-Ampicillin
-Amoxicillin
-Penicillin
-Nafcillin
-Dicloxacilin

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
Penicillin
-Pharmacokinetics (4)
-SEs? (4)
-Administration
-Penicillin Allergies can also have allergies to which other drugs? (2)
-No allergies seen with? (1)
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

Allergy possible with:
-Cephalosporins (5-10%)
-Carbapenems

Not with:
-Monobactams
Beta-lactamase inhibitors
-MOA
-Used with?
-Uses? (1)
Drugs to know in penicillin w/ beta-lactamase inhibitor class
(3)
-Administration? (2)
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

Drugs to know:
-Amoxicillin-clavulanate (PO or IV)
-Ampicillin-sulbactam
-Pipericillin-tazobactam (IV)
Cephalexin
-Class
-MOA?
-Mechanism of Resistance (3)
Class
-1st Gen. Cephalosporin class

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*
Cephalexin
-Pharmacokinetics (4)
-SEs? (4)
-Reaction seen with?
Kinetics
-Good bioavaliability
-Cross BBB if inflammation present
-Short half lives

SEs
-Allergic reactions
-Nausea, vomiting, diarrhea
-Hives, asthma, shortness of breath or other systemic reactions

Reaction with:
-Pencillin (5-10%)
Ceftazidime
-Class
-MOA?
-Mechanism of Resistance (3)
Class
-3rd Gen. Cyclosporin

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
Ceftazidime
-Pharmacokinetics (4)
-SEs? (4)
-Reaction seen with?
Kinetics
-Good bioavaliability
-Cross BBB if inflammation present
-Short half lives

SEs
-Allergic reactions
-Nausea, vomiting, diarrhea
-Hives, asthma, shortness of breath or other systemic reactions

Reaction with:
-Pencillin (5-10%)
Cefotaxime
-Class
-MOA?
-Mechanism of Resistance (3)
Class
-3rd Gen. cyclosporin

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
Cefotaxime
-Pharmacokinetics (4)
-SEs? (4)
-Reaction seen with?
Kinetics
-Good bioavaliability
-Cross BBB if inflammation present
-Short half lives

SEs
-Allergic reactions
-Nausea, vomiting, diarrhea
-Hives, asthma, shortness of breath or other systemic reactions

Reaction with:
-Pencillin (5-10%)
Ceftriaxone
-Class
-MOA?
-Mechanism of Resistance (3)
Class
-3rd Gen. Cylcosporin

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
Ceftriaxone
-Pharmacokinetics (4)
-SEs? (4)
-Reaction seen with?
Kinetics
-Good bioavaliability
-Cross BBB if inflammation present
-Short half lives

SEs
-Allergic reactions
-Nausea, vomiting, diarrhea
-Hives, asthma, shortness of breath or other systemic reactions

Reaction with:
-Pencillin (5-10%)
Imipenem/cilastatin
-Class
-MOA
-Role of cilastatin
Class
-Carbapenems class

MOA
-Inhibit transpeptidases or penicillin binding proteins
-Stop cross-linking and weaken cell wall

Role
-Cilastatin = No antibacterial action but prolongs half-life
Imipenem and prevents nephrotoxic effects
Aztreonam
-Class
-MOA
-Mechanism of Resistance (3)
Class
-Monobactams

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*
Vancomycin
-MOA?
-Mechanism of Resistance? (2)
-Pharmacokinetics
-Administration
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

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
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
Bacitracin
-MOA?
-Mechanism of resistance?
-Administration
-Used with? (2)
-Uses (1)
-SEs (1)
MOA
-Inhibits dephosphorylation of the lipid carrier
-Blocks transfer of cell wall components thru the bacterial membrane by binding to the carrier molecule
- Gram+ and anaerobic cocci

Resistance
-Unclear

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
- frequent use can give allergic contact dermatitis
Quinupristin/dalfopristin
-Class
-MOA
-Mechanism of Resistance (3)
-SEs? (3)
Administration?
Class
-Streptogramins

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

SEs
-Athralgias
-Myalgias
-Dose needs adjustment if pts have liver problems

Administration
-IV
Linezolid
-Class
-MOA?
-Mechanisms of resistance (1)
-Administration?
Class
-Oxazolidinones

MOA
-Block protein synthesis
-Bind to 50s subunit

Resistance
-Mutation of 23s rRNA

Administration
-IV or PO
Linezolid
-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
Erythromycin
-Class
-MOA?
-Mechanisms of Resistance (2)
-Used when?
-Pharmacokinetics?
Class
-Macrolides

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

Kinetics
-Reasonable oral bioavailability
-Good tissue distribution
Erythromycin
-Administration
-Differences from other Macrolides? (2)
-SEs? (2)
-Additional use? (1)
Administration
-IV or PO

Differences
-New, extended release version now available
-Topical form available

SEs
-More nausea
-Greater risk of QT prolongation
- topically can get burning and irritation

Use
-Acne
Clarithromycin
-Class
-MOA?
-Mechanisms of Resistance (2)
-Used when?
-Pharmacokinetics?
-Administration
Class
-Macrolides

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

Kinetics
-Reasonable oral bioavailability
-Good tissue distribution

Administration
-IV or PO
Azithromycin
-Class
-MOA?
-Mechanisms of Resistance (2)
-Used when?
Class
-Macrolides

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
Azithromycin
-Pharmacokinetics?
-Administration
-Differences from other Macrolides
-Given to? (2)
Kinetics
-Reasonable oral bioavailability
-Good tissue distribution

Administration
-IV or PO

Differences
-Longer half life
-Taken less often

Given to:
-Children
-Pregnant women
Clindamycin
-Class
-MOA
-Mechanisms of resistance (4)
Class
-Lincosamines

MOA
-Block protein synthesis
-Binding to 50s subunit of ribosome

Resistance
-Ribosome RNA methylation
-Alterned ribosomal proteins
-Adenylation
-Both chromosomal and plasmid resistance genes
Clindamycin
-Pharmcokinetics?
-Administration?
-SEs? (1)
Kinetics
-Well absorbed
-Good tissue penetration but NOT in CNS

Adminstration
-IV, PO or topically

SEs
-Some allergic rnxs
Streptomycin
-MOA?
-Transport into bacteria
-Transport inhibition? (4)
MOA
-Block protein synthesis
-Bind to 30S subunit
-Bactericidal

Transport
-Disrupt Mg2+ bridges btw LPS molecules
-Transported across membrane in energy dependent manner

Transport inhibition
-Divalent cations
-Increase osmolality
-Acidic pH
-Anaerobic environment
Streptomycin
-Mechanisms of Resistance (7)
-Pharmacokinetics
-Used in combo with?
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**
Point mutation in:
-rpsL gene, encoding S12 ribosomal protein gene
-rrs gene, encoding 16S ribosomal rRNA

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
Streptomycin
-SEs
-Contraindications
-Administration
-Additional SE? (1)
-Uses? (3)
SEs
-Nephrotoxicity
-Ototoxicity

Contraindications
-Pts with impaired renal function
-Pts taking other nephrotoxic drugs

Administration
-IV or IM*
- muti drug regime for TB

Additional info
-High ototoxicity

Use
-First line drug for several bioterriorism agents
-M TB, mainly Extracellular
-Resistant TB Strains
-M avium complex
-M kansaii
-Other M species are resistant to it
Gentamicin
-Class
-MOA?
-Transport into bacteria
-Transport inhibition? (4)
Class
-Aminoglycosides

MOA
-Block protein synthesis
-Bind to 30S subunit
-Bactericidal

Transport
-Disrupt Mg2+ bridges btw LPS molecules
-Transported across membrane in energy dependent manner

Transport inhibition
-Divalent cations
-Increase osmolality
-Acidic pH
-Anaerobic environment
Gentamicin
-Mechanisms of Resistance (5)
-Pharmacokinetics
-Used in combo with?
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**

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
Gentamicin
-SEs
-Contraindications
-Administration
SEs
-Nephrotoxicity
-Ototoxicity

Contraindications
-Pts with impaired renal function
-Pts taking other nephrotoxic drugs

Administration
-IV or IM*
Tobramycin
-Class
-MOA?
-Transport into bacteria
-Transport inhibition? (4)
Class
-Aminoglycosides

MOA
-Block protein synthesis
-Bind to 30S subunit
-Bactericidal

Transport
-Disrupt Mg2+ bridges btw LPS molecules
-Transported across membrane in energy dependent manner

Transport inhibition
-Divalent cations
-Increase osmolality
-Acidic pH
-Anaerobic environment
Tobramycin
-Mechanisms of Resistance (5)
-Pharmacokinetics
-Used in combo with?
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**

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
Tobramycin
-SEs
-Contraindications
-Administration
SEs
-Nephrotoxicity
-Ototoxicity

Contraindications
-Pts with impaired renal function
-Pts taking other nephrotoxic drugs

Administration
-IV or IM*
Tetracycline
-Class
-MOA?
-Mechanisms of Resistance (3)
-Kinetics?
Class
-Tetracyclines

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*

Kinetics
-Good absorption
-Reasonable tissue distribution, including CNS
Tetracycline
-Administration?
-Not given with? (1)
-SEs? (3)
-Contradictions (2)
-Exception to Contraindications? (1)
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
Doxycycline
-Class
-MOA?
-Mechanisms of Resistance (3)
-Kinetics?
Class
-Tetracyclines

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*

Kinetics
-Good absorption
-Reasonable tissue distribution, including CNS
Doxycycline
-Administration?
-Not given with? (1)
-SEs? (3)
-Contradictions (2)
-Exception to Contraindications? (1)
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
Tigecycline
-MOA?
-Resistance?
-Kinectics?
-Administration?
MOA
-Block protein synthesis by ribosomes
-Bind 30S subunit

Not affected by resistance
-Tigecycline

Kinetics
-Good absorption
-Reasonable tissue distribution, including CNS

Administration
-IV or PO
Tigecycline
-Not given with? (1)
-SEs? (3)
-Contradictions (2)
-Exception to Contraindications? (1)
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
Chloramphenicol
-MOA?
-Mechanism of Resistance? (2)
-Administration?
MOA
-Block protein synthesis
-Binds to 50s subunit

Resistance
-Acetyltransferases*
-Efflux pumping

Administration
-IV or PO
Chloramphenicol
-SEs? (4)
SEs
-Aplastic anemia
-Bone marrow suppression
-Gray syndrome (circulatory collapse, coma, death)
-Dose adjustment if patient has liver problems
Mupirocin
-MOA
-Mechanism of Resistance? (1)
-Adminstration
- Vehicle
MOA
-Blocks protein synthesis
-Inhibits isoleucine tRNA synthetase

Resistance
-Target site mutation

Administration
-Topical on skin or mucosal surface
- intranasal

Vehicle
- polyethylene glycol
Mupirocin
-Uses? (2)
-SEs?
Uses
-Elimination of nasopharyngeal carriage of S. aureus
-Skin infections (Gram+)
- impetigo

SEs
-Unclear
- some irritation of mucous membranes
Sulfamethoxazole
-Class
-MOA?
-Specificity?
-Given with? (1)
Class
-Sulfonamides

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
Sulfamethoxazole
-Do not work in which situation?
-Problems due to?
-Mechanism of Resistance? (4)
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

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
Sulfamethoxazole
-Pharmacokinetics
-Administration
-Addition fact for sulfa drugs (1)
-SEs? (3)
-Contraindications? (3)
Kinetics
-Both act synergistic (given together)
-Good bioavailability

Administration
-IV or PO
-Sulfa--can be given along w/ silver ions in a topical cream

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
Sulfadiazine
-Class
-MOA?
-Specificity?
-Given with? (1)
Class
-Sulfonamides

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
Sulfadiazine
-Do not work in which situation?
-Problems due to?
-Mechanism of Resistance? (4)
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

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
Sulfadiazine
-Pharmacokinetics
-Administration
-Addition fact for sulfa drugs (1)
-SEs? (3)
-Contraindications? (3)
Kinetics
-Both act synergistic (given together)
-Good bioavailability

Administration
-IV or PO
-Sulfa--can be given along w/ silver ions in a topical cream

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
Dapsone
-Class
-MOA?
-Useful against? (2)
-Mechanism of Resistance? (4)
Class
-Sulfonamides

MOA
-Folic acid blocker
-Analog of PABA

Useful against
-Mycobacteria (esp leprosy)
-Pneumocytis jiroveci/carinii (fungus)

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
Dapsone
- Metabolism
-SEs? (3)
-Contraindications? (3)
-Administration
-Addition fact for sulfa drugs (1)
Metabolism
- kidney eliminated (dose adjust in kidney failure)
SEs
-HIV pts can develop neutropenia and exfoliative dermatitis
-HIV pts given these drugs prophylaxically
-Allergic rxns including anaphylaxis

Contraindications
-Glucose-6-phosphate deficiency (get hemolysis)
-Folic acid deficiency
-Pregnant

Administration
-IV or PO
-Sulfa--can be given along w/ silver ions in a topical cream
- w/ rifampin and clofazimine for leprosy (better result, less resistance)
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
-Produced sequential block of folic acid synthesis
-Synergistic
Trimethoprim
-Mechanisms of resistance? (2)
-Pharmacokinetics
-Administration
-Addition fact for sulfa drugs (1)
Resistance
-Altered targets/bypass*
-Metabolic bypass is most common as new enzymes are provided**
-Reduced permeability*

Kinetics
-Both act synergistic (given together)
-Good bioavailability

Administration
-IV or PO
-Sulfa--can be given along w/ silver ions in a topical cream
Trimethoprim
-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
Ciprofloxacin
-Class
-MOA?
-Basis for selective action?
-Administration? (1)
Class
-Fluoroquinolones

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

Administration
-Can be given either orally or IV
Ciprofloxacin
-Mechanisms of Resistance? (4)
-Pharmacokinetics (2)
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)

Kinetics
-Absorbed well from oupper GI tract
-Tissue distribution is good
Ciprofloxacin
-Contraindications? (2)
-Due to?
-Adverse reactions? (2)
-Do not use in which pts? (2)
Contraindications
-Pregnant patients
-Under 18 yrs old

Due to
-Anthropathy (joint problems) observed in animals

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
Levofloxacin
-Class
-MOA?
-Basis for selective action?
-Administration? (1)
Class
-Fluoroquinolones

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

Administration
-Can be given either orally or IV
Levofloxacin
-Mechanisms of Resistance? (4)
-Pharmacokinetics (2)
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)

Kinetics
-Absorbed well from oupper GI tract
-Tissue distribution is good
Levofloxacin
-Contraindications? (2)
-Due to?
-Adverse reactions? (2)
-Do not use in which pts? (2)
Contraindications
-Pregnant patients
-Under 18 yrs old

Due to
-Anthropathy (joint problems) observed in animals

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
Metronidazole
-MOA?
-Mechanism of resistance?
MOA
-Produces compounds that are toxic to DNA
-Exact mechanism is unclear

Resistance
-Rare and mechanism is not clear
Metronidazole
-Pharmacokinetics
-Administration?
-Uses (4)
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
- acne rosacea
Metronidazole
-Adverse reactions? (2)
-Contraindications? (1)
SEs
-Promote renal retention fo Li+
-Decreased elimination of ergot derivatives

Contraindications
-Pts. should not drink alcohol
- pregnant/lactating women
Nitrofurantoin
-MOA?
-Mechanism of resistance? (1)
-Administration
MOA
-Unclear
-Attacks bacterial metabolism
-Mimics radiation damage
-Drug must be reduced inside bacteria

Resistance
-Altered levels of reduction enzymes

Administration
-PO
Nitrofurantoin
-Pharmacokinetics?
-Use (1)
-SEs (2)
Kinetics
-Drug concentrated in urine

Use
-Uncomplicated UTIs

SEs
-Turns urine brown (harmless)
-Lung problems in pts on prolonged or prophylaxis treatment
Polymixins
-MOA?
-Mechanism of Resistance?
-Administration?
MOA
-Disrupts bacterial membranes by charge alternation

Resistance
-Unclear

Administration
-Topical
-IV or IM
Polymixins
-Used with? (2)
-SEs?
-Uses (1)
Used with:
-Neomycin
-Bacitracin (Neosporin)

SEs
-Few if used topically

Uses (neosporin)
-Prevention of infection in minor cuts, scrapes, burns
- Gram+ organisms
Daptomycin
-MOA?
-Mechanisms of resistance?
-Administration? (1)
-SEs?
MOA
-Cyclic lipopeptide interferes w/ bacterial membrane function and pore formation

Resistance
-Unclear

Administration
-IV

SEs
-Elevated liver function tests and creatine phosphokinase
-Muscle weakness and pain w/ elevated creatine phosphokinase (discontinue drug)