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anti bacterials Flashcards

1
Q

bactericidal vs bacteriostatic

MIC vs MBC

A 
bactericidal= kills the bacteria
bacteriostatic= stops the active growth of the bacteria but they remain viable
MIC= minimal inhibitory concentration, ie bacteriostatic
MBC= minimal  bactericidal concentration
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2
Q

time dependent killing vs concentration dependent killing

A

time dependent killing: best clinical effect when remain 4-fold above the MIC for >50% of total time, Beta lactams (penicillins, cephalosporins)

Concentration-dependent kiling: maximize the peak concentration (Cmax), Aminoglycosides (gentamicin, tobramycin)

peak conc= Cmax/MIC

Killing dependent of concentrationX time (aka Area under curve dependent killing)

AUC24hr/MIC expressed in hours (quinolones, ma

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3
Q

classes of resistance mechanism

A

Intrinsic resistance- fundamental properties of a given microbe (cell wall structure)

non-inherited resistance- cells not actively replicating

mutations- mutations that alter cell susceptibility to antimicrobial agent

Plasmid-mediated resistance (extrachromosomal genes that encode resistance mechanisms) Can potentially be transferred to other microbes, concept of multiple-resistance (many examples)

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4
Q

Beta lactams, genreal information

A

cell wall agents
most of the time=bactericidal
kill gram positive and gram negative
activity is maximal on actively growing bacteria

MOA: inhibit transpeptidases (penicillin-binding proteins or PBPs) which catalyze cell wall crosslinks (B-lactams covalently bind to PBPs) competitive, irreversible

bacterial resistance to B-lactams: most prevalent is B lactamase (cleaves B lactam ring). S.aureus to ampicillin and penicillin G; B-lactamases also produced by many gram negative

Altered PBP will not bind to B-lactam effectively, methicillin resistance of staphylococci

B-lactam agent cant reach PBPs- problem with many gram negative organisms whose Outer membrane is impermeable to B-lactams)

B- lactams are time-dependent killers: their short T.5 implies the need for shorter dosing intervals. need to keep the drug 4-fold above the MIC for >50% of treatment time

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5
Q

Penicillins general

A

Beta lactams
well distributed to most areas of body (low penetration into CSF but increases during meningitis), oral and IV admin. Short t.5 (30 mins to a few hours, renal elimination- anion transport) all B- lactams are time dependent killers (keep 4 fold above MIC for >50% of time)

all end in cillin

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6
Q

penicillin G and V

A

V is more acid stable than G, for gram pos and gram neg cocci (Non- B lactamase producing) effective against:

gram-pos anaerobes, not Bacteroides fagilis
Streptococcus pneumoniae (20-30% show resistance)
Streptococci (strep throat)
Neisseria meningitidis
Syphilis- IM penicillin G benzathine

good activity against anthrax, listeria, actinomyces

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7
Q

oxacillin

A

for B-lactamase producing staphylococci methicillin-susceptible Staphylococcus aureus (MSSA)

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8
Q

ampicillin/amoxicillin

A

various B-lactamase negative gram positive (listeria, streptococcus) and some gram neg (Haemophilus, Neisseria, Escherichia, Salmonella)

Alternate choice for lyme disease

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9
Q

ticarcillin

A

broad gram neg
Pseudomonas, some enterobacter and proteus

Some anaerobes (when combines with a B-lactamase inhibitor)

often used with B-lactamase inhibitor

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10
Q

piperacillin

A

broad gram neg
Some psuedomonas and klebsiella

often used with B-lactamase inhibitor

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11
Q

excretion/metabolism of penicillins

SE of penicillins
Admin of penicillins

A

Excretion/metabolism of penicillins: 30% hepatic metabolism, mostly renal (20% GF/ 80% tubular anionic excretion)

Some adverse reactions to penicillins: allergic rarely but severe, anaphylaxis, rash, fever
diarrhea, entrocolitis, nausea, vomiting

All antibacterials can cause diarrhea and enterocolitis

elevated liver enzymes, hemolytic anemia, seizures

Admin of penicillins: some IV or IM or oral, generally well distributed, short half lives

Procaine and benzathine penicillin are slow release IM forms that substantially increase the duration over which effective drug levels are maintained
increased CNS distribution with inflamed meninges

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12
Q

beta lactamase inhibitors

A

limit hydrolytic cleavage of B-lactams by some types of B-lactamses

Clavulanic acid, tazobactam: B-lactam analogs that bind irreversibly to B-lactamase

not all b-lactam resistance is due to B-lactamase

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13
Q

Cephalosporins

A

well distributed to most areas of the body, only some reach the CSF

majority require injection, short half lives (at best only a few hours), MOA similar to B-lactam,

resistance mechanism same as penicillins

Start with CEF

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14
Q

1st generation cephalosporin

A

mostly effective against gram positive (MSSA and streptococcus)

Limited gram negative activity
uncomplicated outpatient skin infections
Surgical prophylaxis for skin flora

Cefazolin: best gram positive activity of 1st gen cephalosporins

Cephalexin: oral

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15
Q

2nd generation cephalosporins

A

increased gram negative activity, less active against staphylococci

Cefuroxime: only 2nd generation to penetrate CSF, best of 2nd generation against Haemophilus

Cefoxitin: also good for some anaerobes

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16
Q

3rd generation cephalosporins

A

more active against gram negatives
good for klebsiella, enterobacter, proteus

Ceftriaxone: therapy of choice for gonorrhea with azithromycin or doxycycline) empiric therapy for meningitis long t.5 (6-9 hours)

Ceftazidime: effective againsts many Pseudomonas aeruginosa

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17
Q

4th generation cephalosporins

A

cefepime: IV admin
spectrum like ceftazidime, except more resistant to type 1 B lactamases, empirical treatment of serious inpatient infections

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18
Q

excretion/ metabolism SE of cephalosporins

A

Excretion/metabolism of cephalosporins: renal clearance by glomerular filtation and tubular secretion, some are deacetylated to less potent metabolites

SE: allergic reactions, nausea vomiting, diarrhea, enterocolitis, hepatocellular damage

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19
Q

imipenem

A

B-lactam
administered IV, well distributed
broad spec, not degraded by most B-lactamases including ESBLs), not effective against MRSC

given with cilastatin bc susceptible to hydrolysis by renal dipeptidases

Used for mixed or ill-defined infections
those not responsive to other drugs

SE: hypersensitivity, some cross allergies with penicillin/cephalosporins. Seizures, dizziness, confusion, nausea, vomiting, diarrhea, pseudomembranous colitis, superinfection

20
Q

aztreonam

A

used against gram neg aerobic rods

not useful against gram positive and anaerobes
not degraded by several B-lactamases, can be used in those with known hypersensitivities to penicillins

not indicated for meningitis

SE: seizures, cramps, nausea, vomiting, enterocolitis, anaphylaxis, transient EKG changes

21
Q

Vancomycin

A

glycopeptide antibiotic, not a B-lactam

MOA: bactericidal, inhibits cell wall synthesis, binds free carboxyl end of D-Ala-D-Ala of the pentapeptide. interferes with transpeptidation (cross linking) and transglycosylation (elongation)

Used for gram positives only including MRSA, hemolytic streptococcus, S. pneumoniae, Enterococcus, C diff enterocolitis (1st line choice!) empirical meningitis treatment Vancomycin +ceftriaxone

Must be given IV for systemic infections
Oral for C. diff
used in serious infections

SE: red man or red neck syndrome, nephrotoxic, phlebitis, ototoxicity

22
Q

fosfomycin

A

MOA: inhibits synthesis of peptidoglycan building blocks by by inactivating enolpyruvyl transferase, an early stage cell wall synthesis enzyme

Uses: uncomplicated UTIs caused by E. coli, enterococcus

toxicity: headache, diarrhea, nausea, vaginitis

23
Q

bacitracin

A

polypeptide, not a b-lactam

MOA: interferes with cell wall synthesis by interfering with lipid carrier that exports early wall components through the cell membrane

Use: topical use only, very nephrotoxic, gram positive cocci and bacilli

toxicity: allergic dermatitis

24
Q

polymyxins general

A

cell membrane agents

MOA: act as cationic detergents that bind LPS in the outer membrane of gram negatives

uses: polymyxin B: topical use, esp for pseudomonas and other gram negative infections. Systemic use-potential for serious nephrotoxicity and neurotoxicity

25
Q

daptomycin

A

cell membrane, cyclic lipopeptides
MOA: binds to bacterial cytoplasmic membrane, causing rapid membrane depolarization, bactericidal

Uses: complicated skin and skin structure infections. Staph aureus (MSSA, MRSA), streptococcus pyogenes and agalactiae, enterococcus, also for staphylococcus bacteremia, NOT FOR PNEUMONIA

Iv admin, renal elimination

SE: nausea, diarrhea, GI flora alteration, muscle pain and weakness.

26
Q

quinolones general

A

moa: inhibits alpha and beta subunit of DNA gyrase, thereby interfering with control of bacterial DNA winding (replication and repair)

bactericidal, killing dependent on AUC/MIC

Resistance: altered DNA gyrase, combination of decreased permeability and altered DNA gyrase will result in resistance to the newer fluorinated compounds

Uses: nonfluorinated compounds- in urinary tract
Fluorinated quinolones (end in floxacin)
27
Q

norfloxacin and ciprofloxacin

A

norfloxacin/ciprofloxacin

UTIs: enterobacteriaceae
fluoroquinolones not first line for UTIs

28
Q

Ciprofloxacin

A

UTIs, infectious diarrheam skin infections, bone and joint infections, chlamydia, there are better quinolones for respiratory and gram -pos infections

29
Q

moxifloxacin

A

better gram positive activity than many quinolones
respiratory infections but not for strep throat
community acquired pneumonia, bacterial bronchitis

30
Q

excretion and metabolism and side effects of quinolones

A

excretion/metabolism: GF and active tubular secretion for many, and bile

SE: nausea, vomiting, abdominal pain, enterocolitis
dizziness, headache, restlessness, depression

rare seizures
Contraindicated in those with seizures disorders, preganancy, children

Rashes

EKG irregularities, arrhythmias
peripheral neuropathy

arthropathy and tendon rupture

IV admin, oral, well distributed

31
Q

nitrofurans

A

MOA: nitroreductase enzyme converts them to reactive compounds (including free radicals) which can damage DNA

not common in resistance

Uses- inhibit gram positive and negative bacteria
Nitrofurantoin for lower UTI (e coli, enterococcus, staphylococcus)

Excretion/metabolism: biliary, GF and tubular secretion

SE: nausea, vomiting, diarrhea, peripheral neuropathy, hypersensitivity, fever, chills, acute and chronic pulmonary reactions, acute and chronic liver damage, granulocytopenia, leukopenia, megablastic anemia, acute hemolytic anemia

Oral admin

32
Q

rifampin

A

MOA: inhibits bacterial RNA synthesis by binding RNA polymerase B, bactericidal

Uses: pulmonary TB, prophylaxis of meningococcal meningitis, prophylaxis of Haemophilus influenza type B meningitis

Excretion: liver, biliary
Admin: oral and IV

SE:serious hepatotoxicity, induction hepatic enzymes (CYPs) that inactivate other drugs, orange color in bodily fluids

33
Q

fidaxomicin

A

MOA: noncompetitive inhibitor of RNA polymerase, so inhibits RNA synthesis, bactericidal

Uses: C. diff infection (1st line choice)

Excretion: fecal elim
ADmin: oral, poorly absorbed

SE: GI upset, GI bleeding, neutropenia

34
Q

Metronidazole

A

MOA: anaerobes reduce the nitro group of metronidazole, resulting product disrupts DNA and inhibits nuclei acid synthesis, bactericidal

Resistance: anaerobes lose ability to reduce

Use: some parasites, anaerobes, C diff enterocolitis, therapy for Helicobacter pylori in combination with other antibacterials and acid blocker, Gardnerella vaginalis (bacterial vaginosis)

SE: nausea, vomiting, anorexia, diarrhea, transient leukopenia, neutropenia, thrombophlebitis after IV infusion, bacterial and fungal superinfections

Admin: oral or IV

35
Q

Bacterial protein synthesis and points where antibacterials act

A

1) aminoglycosides freeze initiation (premature release of ribosome from mRNA)
2) tetracycline and chloramphenicol prevent tRNA from binding
3) Chloramphenicol blocks peptide bond formation (peptidyl transferase)
4) erythromycin and clindamycin block translocation step
5) aminoglycosides cause misreading of mRNA

36
Q

aminoglycosides

A

Bactericidal, not absorbed orally (given IV or IM or topically)
MOA: penetrate pores of outer membrane of gram negatives or the water filled matrix of the cell wall of gram positive, bind to transport molecule on outer surface of cytoplasmic membrane, transported into bacteria by an energy-requiring aerobic process, binds to several ribosomal sites, stops initiation causes premature release of ribosome from mRNA and mRNA misreading, post-antibiotic effect, concentration-dependent killing

Resistance: enzymatic modification of the aminoglycosides

Uses: effective against gram negative, poor activity against anaerobes, used for gram neg aerobic bacilli, gram-pos activity requires combination with cell wall inhibitors, uses restricted to serious infections, streptomycin

Gentamicin, tobramycin, amikacin

Excretion/ metabolism: glomerular filtation

SE: narrow therapeutic window, nephrotoxic, ototoxicity, neuromuscular blockade

Admin: not absorbed GI, given IV or IM, poor penetration in CSF, often combined with other antibiotics for serious bacterial infection

37
Q

tetracyclines

A

MOA: modern ones minocycline, doxycycline have longer t.5 and are more lipophilic. Transported into the cells, bind to 30S ribosomal subunits, prevent attachment of aminoacyl-tRNA to the acceptor site on the mRNA-ribosomal complex, AAs cannot be added to the protein being synthesized, bacteriostatic

Resistance: most common- increased transport of the drugs out of the bacterial cells, resistance to one tetracycline often implies resistance to them all

Uses: resistance has increased, preferred agents for (rickettsial diseases, chlamydia, mycoplasma, ureaplasma, borrelia lyme disease)

admin: oral admin, Ca binds to tetracyclines inhibiting their absorption (antacids and Ca and Mg decrease absorption), can also be given parenternally

SE: GI disturbances, pseudomembranous enterocolitis, Candida superinfection in colon, photosensitization with rash, teeth discoloration in kids, CX in pregnancy

38
Q

tigecycline

A

MOA: bacteriostatic, binds 30 S ribosomal subunit and blocks aminoacyl-tRNA entry, also binds additional unique sites in the ribosomes

Resistance: no cross-resistance with other antibacterials including tetracyclines

Uses: skin/skin structure infection, complicated intraabdominal infections, community acquired pneumonia (CAP). By pathogen: e. coli, citrobacter, klebsiella, enterobacter, staphylococcus (MSSA and MRSA), bacteroides, C. perfringens, S pneumoniae, Haemophilus

SE: nausea, vomiting, enterocolitis, others similar to tetracyclines including calcium binding, higher death rate than with other antibacterials

39
Q

chloramphenicol

A

MOA: interferes with binding of aminoacyl-tRNA to 50S subunit and inhibits peptide bond formation, usually bacteriostatic

Uses: originally had broad spectrum, very serious side effects so use as alternate agent for treatment of meningitis and brain abscesses

SE: bone marrow depression, can progress to a fatal aplastic anemia, grey baby syndrome, optic neuritis and blindness, GI effects

40
Q

Macrolides general

A

Erythromycin, Clarithromycin, Azithromycin
MOA: all bind to the 50S ribosomal subunit, blocking protein synthesis by blocking the translocation step, bacteriostatic

resistance: common

41
Q

erythromycin

A

uses: oral/IV, primarily against gram positive, used as alternative in B-lactam allergic patients

also effective against: chlamydia, mycoplasma, legionella, bordetella, campylobacter

Toxicity: nausea/vomiting, inhibits CYP3A4 metabolism/excretion of many drugs, increases risk of arrhythmias and cardiac arrest

42
Q

Clarithromycin

A

mechanims: similar to erythromycin

Uses: alternative to erythromycin for treatment of: pharyngitis, respiratory infections, same as erythromycin plus expanded spectrum (haemophilus, moraxella, penicillin-resistant strep pneumonia)

Helicobacter pylori (in combination with other antibacterials and an acid suppressant) treatment of atypical mycobacterial infections

SE: Cv risk prolonged QT interval, GI distrubances, hearing loss

43
Q

Azithromycin

A

MOA: similar to erythromycin
Uses: respiratory infections, GI pathogens, genital (chlamydia, with ceftriaxone for N. gonorrhoeae)

SE: fewer GI disturbances, few drug interactions, cardiac QT prolongation)

44
Q

Clindamycin

A

macrolide-like, binds to 50s ribosomal subunit, blocks translocation along ribosomes

uses: most gram positive cocci and many anaerobes including bacteroides fragilis, cause of C. diff, can suppress bacterial toxin production

SE: antibiotic-associated enterocolitis, GI ittitation, diarrhea, hepatotoxicity, neuromuscular transmission

45
Q

linezolid

A

interferes with protein synthesis, binds to 50 S ribosomal subunit, interfering with formation of 70 S initiation complex, bacteriostatic

uses: Vancomycin resistant enterococcus faecium, Staphylococcus aureus, MRSA and MSSA, streptococcus group A and B, streptococcus pneumoniae

Admin: iv, oral

SE: non selective inhibitor of MAO (drug and foods with tyramine interactions), CX: SSRI tricyclics, triptans, buspirone, GIT stuff, bone marrow suppression

46
Q

Sulfonamides

A

antifolate, bacteriostatic

MOA: folate is needed and produced by the bacteria

sulfonamides: inhibit folate synthesis in bacteria by competitive inhibition of dihydropteroate synthase.

Uses: UTI, sulfamethoxazole f]given with trimethoprim, UTI, nocardiosis, ulcerative colitis

Silver sulfadiazine used topically for burn patients

SE: hypersensitivity, rashes, serum sickness, GI disturbances, renal damage from crystalluria, inhibit CYP2C9: potentiates action of various other drugs

47
Q

trimethoprim

A

MOA: inhibits folate synthesis in bacteria by competitvely inhibiting dihydrofolate reductase

Uses: in conjuction with sulfamethoxazole, the synergistisic effects are bactericidal, urinary infections, upper respiratory and ear infections, also for pneumocystis jiroveci carinii,

Some adverse reactions: nausea, vomiting diarrhea, rashes, eosinophils, neutropenia, bone marrow suppression

pharm 3 (11 decks)

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