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PDA Block 3 > Antibiotics 2 > Flashcards

Antibiotics 2 Flashcards

1
Q

Quinolones

A

-Norfloxacin, ciprofloxacin, moxifloxacin

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2
Q

Drugs that target nucleic acids

A
  • Quinolones: Norfloxacin, ciprofloxacin, moxifloxacin
  • Nitrofurantoin
  • rifampin
  • metronidazole
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3
Q

Mechanism of action quinolone

A
  • inhibits alpha and possibly beta subunit of DNA gyrase, thereby interfering with control of DNA winding (replication and repair)
  • bactericidal
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4
Q

what kind of killing are wuinolones

A

AUC24/MIC

-desired is over 125 for gram negatives, and over 40 for gram positives

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5
Q

Ways to increase AUC24

A
  • more frequent doses
  • more drug per dose
  • longer half life
  • drugs with better MICs
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6
Q

Norfloxacin uses

A

-UTIs was the number one but NOW, it is not.

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7
Q

Ciprofloxacin uses

A
  • useful for infections at many sites
  • UTIs
  • infectious diarrhea
  • bone and joint infections
  • skin infections
  • not the best choice for gram positives when prescribed alone
  • other quinolones have better gram positive and respiratory activity (eg moxifloxacin)
  • uncomplicated gonorrhea
  • chlamydia
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8
Q

how do the other quinolones compare to ciprofloxacin when it comes to treating gram positive bacteria

A

-Moxifloxacin and levofloxacin are much better against gram positives than ciprofloxacin

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9
Q

Moxifloxacin uses

A
  • better for gram positives than many quinolones (eg ciprofloxacin)
  • Strep pneumoniae , MSSA
  • respiratory infections
  • community acquired pneumonia
  • acute exacerbation of bacterial bronchitis
  • not approved for strep throat
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10
Q

Distribution of quinolones

A
  • some (eg norfloxacin) and the non fluorinated agents achieve therapeutic concentrations only in the urinary tract.
  • but fluorinated drugs are well distributed
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11
Q

quinolones side effects

A
  • nausea, vomiting, abdominal pain, enterocolitis
  • dizziness, headache, restlessness, depression
  • seizures (esp those with seizure history)
  • rashes
  • EKG irregularities, arrhythmias (prolonged QT interval)
  • peripheral neuropathy
  • arthropathy (tendone rupture)
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12
Q

precautions with Quinolones

A
  • those with seizure disorders
  • pregnancy (category C)
  • use in children (possible cartilage damage)
  • 2nd line agents for certain serious infections in children, but CAUTION USE IN CHILDREN FOR LES SERIOUS NFECTIONS
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13
Q

tell me about the use of quinolones in children

A
  • not a good idea bc can cause cartilage damage
  • is 2nd line drug for very serious infections in children (ex: pyelonephritis), BUT use is VERY CAUTIONED for less serious infections in children. Aka don’t use it in children unless you absolutely HAVE to
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14
Q

what side effect of quinolones is increased in patients over the age of 60

A

Arthropathy (10-1550

-but incidence varies with specific quinolones, and there is a higher incidence in the elderly

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15
Q

Should Quinolones be the 1st line drug for UTIs?

A

NO nor should it be first line for sinusitis, bronchitis

-it should be reserved for very serious infections

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16
Q

Nitrofurantoin

A

-M: nitroreductase enzyme converts these drugs to reactive compounds (including radicals) which can damage DNA

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17
Q

uses for nitrofurantoin

A

-urinary tract infections (UTI only, not renal)

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18
Q

side effects nitrofurantoin

A

-nausea, vomiting, diarrhea
-hypersensitivity, fever, chills
-peripheral neuropathy
-acute and chronic pulmonary reaction
acute and chronic liver damage so contraindicated in those with prior hepatic dysfunction
-granulocytopenia, leukopenia, megaloblastic anemia
-acute hemolytic anemia (in those with glucose-6-P-dehydrogenase deficiency)

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19
Q

RIfampin

-mechanism

A
  • binds to and inhibits bacterial RNA polymerase B
  • this inhibits RNA synthesis
  • bactericidal
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20
Q

uses rifampin

A
  • tuberculosis
  • meningitis prophylaxis
  • neisseria meninigitidis
  • Haemophilus influenzae
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21
Q

side effects rifampin

A
  • serious hepatotoxicity
  • rifampin strongly induces many enzymes (eg CYP3A, 2C9, 2C19, aA, 2A, 2B) that inactivate other drugs-orange color to urine, salivia, sweat, tears
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22
Q

effect of rifampin on other antibiotics

A

it strongly induces most CYP enzymes which means rapid inactivation of most other drugs

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23
Q

Fidaxomicin

  • mechanism
  • administration
A

-non-competitive inhibitor of RNA polymerase inhibits RNA synthesis
-bactericidal
oral administration, poorly absorbed

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24
Q

uses of fidaxomicin

A

-clostridium difficile infection, as of March it is the first line drug!!!!

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25
Q

Fidaxomicin side effects

A
  • GI upset

- GI bleeding

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26
Q

Metronidazole mechanism

A
  • anaerobes reduce the nitro group of metronidazole (to a radical reactive species) ; the resulting product damages/disrupts DNA
  • bactericidal
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27
Q

Metronidazole uses

A
  • anaerobes
  • clostridium difficile enterocolitis: alternate choice for mild/moderate cases of C diff only
  • Helicobacterpylor in combination with other antibacterials and an acid blocker
  • Gardnerella vaginalis (bacterial vaginosis)
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28
Q

Metronidazole side effects

A
  • nausea, vomiting, anoerexia, diarrhea
  • transient leukopenia, neutropenia
  • thrombphlebitis after IV infusion
  • bacterial and fungal superinfections (esp Candida)
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29
Q

C. difficile enterocolitis

A

-can be caused by all antibacterial
-consider in all patients with antibacterial drugs in last 2 months
-therapy
*1st line= Vancomycin or Fidaxomicin
*alternative=metronidazole (for mild to moderate only)
or vancomycin and metronidazole for very severe cases

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30
Q

aminoglycosides

A
  • freeze initiation (premature release of ribosome from mRNA)
  • cause misreading of mRNA
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31
Q

tetracycline and chloramphenicol

A

-prevent tRNA from binding

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32
Q

chloramphenicol

A

blocks peptide bondformation (peptidyl transferase)

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33
Q

-Erythromycin and clindamycin

A

block translocation step

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34
Q

List the classes of protein synthesis inhibiting antibiotics

A
  • aminoglycosides
  • tetracyclines
  • macrolides
  • glycycycline: Tigecycline
  • Oxazilidinones: linezolid
  • Misc:chloramphenicol, clindamycin
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35
Q

aminoglycoside drugs

A

-gentamicin, tobramycin, amikacin

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36
Q

tetracycline drugs

A

-doxycycline, minocycline

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37
Q

glycylcycline drugs

A

tigecycline

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38
Q

macrolides

A

-erythromycin, clarithromycin, azithromycin

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39
Q

Oxazilidinones drugs

A

linezolid

40
Q

Misc drugs protein synthesis inhibitors

A

-chloramphenicol, clindamycin

41
Q

general properties aminoglycosides

  • static vs cidal
  • administration
A
  • bactericidal ( only protein synthesis inhibitors that are cidal)
  • IV, IM, topical
42
Q

Mechanism aminoglycosides (gentamicin, tobramycin, amikacin)

A
  • transported into bacteria by energy requiring aerobic process
  • bind to several ribosomal sites (30s/50s interface)
  • stops initiation, and cause premature release of ribosome from mRNA
  • causes mRNA misreading

-binds extremely tight to the ribosome, it isn’t irreversible, but once it binds it is stuck for a long time, this is why it is concentration dependent killing not time dependent killing

43
Q

uses for aminoglycosides

A
  • primarily for gram negative aerobic bacilli
  • Enterobacteriaceae (E coli, Klebsiella, Enterobacter, Serratia etc)
  • pseudomonas aeruginosa
  • often used in combination (with cell wall inhibitors or quinolones)–synergism

-poor activity against anaerobes

44
Q

Aminoglycosides are primarily for use against gram negatives, but sometimes can be used against gram positives explain

A
  • in order to work for gram positive bacteria the aminoglycosides must be used in combination with another drug
  • often the cell wall inhibitors (B-lactams, vancomycin) enhance permeability of aminoglycosides
  • although it is good to use them together, it is NOT good to mix them up in the same bag or give them at the same time because the chemical reaction between the two inactivates aminoglycosides, so you should space them out
45
Q

Aminoglycosides post-antibiotic effect

A
  • sustained activity for several hours after aminoglycosides concentration has dropped below ‘effective’ levels
  • because they are also concentration-dependent killers allows for less frequent dosing
  • narrow therapeutic window
  • use restricted to serious infections (due to side effects)
46
Q

aminoglycosides are concentration killers

A
  • Cmax/MIC ratio more than 8 is ideal
  • problem: toxicity is dose-related
  • Cmax killing and post antibiotic effect allows for less frequent dosing

**half life is about 3 hours, but it can be dosed every 12 or 24 hours!! this lowers toxicity

47
Q

a lot pf pseudomonas aeruginosa are becoming resisitant to gentamicin, but what are they not resistant to

A

-approximately 50% gentamicin strains remain sensitive to tobramycin

48
Q

Aminoglycosides side effects

A
  • narrow therapeutic window
  • nephrotoxicity: usually reversible
  • ototoxicity: mostly irreversible and deafness is delayed
  • neuromuscular blockade
49
Q

Tetracyclines

  • mechanism
  • resistance
A

-transported into the cells by a protein carrier system
-prevent attachment of aminoacyl-tRNA bind to 30S ribosomal subunits
-bacteriostatic
-resistance:
most common is the drug efflux pump
resistance to one tetracycline often implies resistance to them all

50
Q

uses of tetracyclines

A
  • preferred agents for unusual bugs
  • Rickettsial disease
  • lyme disease
  • chlamydia, Mycoplasma, Ureaplasma
51
Q

doxycycline

A
  • alternative for penicillin G sensitive syphilis
  • uncomplicated N gonorrhea (however CDC says that doxycycline is not adequate on its own)
  • half life is 24 hours
  • less affinity for calcium
52
Q

minocycline

A
  • alternative for penGsensitive syphillis
  • uncomplicated gonorrhea
  • calcium binding is more than doxycycline but less than tetracycline
53
Q

tetracyclines and calcium

A

-bind calcium, inhibits tetracycline absorption

54
Q

side effects of tetracyclines

A
  • gastrointestinal disturbances, including enterocolitis
  • candida superinfection in colon
  • photosensitization with rash
  • teeth discoloration
  • avoid use in children especially under 8 years old
  • contraindicated in pregnancy
55
Q

Tigecycline

A
  • novel drug class
  • like the tetracyclines but also binds additional unique sites in the ribosomes
  • resistance: no cross resistance with other antibacterials including tetracyclines
56
Q

Tigecycline uses

A
  • skin/skin structure infections
  • complicated intra-abdominal infections
  • CAP (community acquired pneumonia)
  • gram negatives:
  • E coli, citrobacter, klebsiella, enterobacter, NOT pseudomonas
  • gram positives
  • staphylococcus (MSSA, MRSA)
  • streptococcus
  • Anaerobes
  • bacteroides
  • clostridium perfringens
57
Q

adverse reactions Tigecycline

A
  • nausea vomiting enterocolitis
  • other side effects similar to tetracyclines including calcium binding
  • increased risk of death esp those with serious infections-considered last line agent when there are no other good choices
58
Q

Chloramphenicol

A
  • interferes with binding of aminoacyl-tRNA to 50s ribosomal subunit and inhibits peptide bond formation
  • were originally broadspectrum
  • but very serious side effects restrict its use only when no other agents suitable
  • generally bacteriostatic
59
Q

current indications for chloramphenicol

A
  • by type of infection
  • meningitis: alternative in those with serious cephalosporin allergy
  • brain abscesses (often anaerobes)
  • generally bacteriostatic
60
Q

Chloramphenicol side effects

A
  • bone marrow depression
  • fatal aplastic anemia, not necessarily dose related, can be delayed

-gray baby syndrome

  • optic neuritis and blindness
  • GI effects including enterocolitis
61
Q

Macrolide drugs list

A
  • erythromycin
  • clarithromycin
  • azithromycin
62
Q

macrolid (erythromycin, clarithromycin, azithromycin) mechniasm of action

A

-bind to 50s subunit, blocks translocation along ribosomes

63
Q

erythromycin uses

A
  • primarily against gram positive
  • alternative for strep throat in penicillin allergies

-many gram negatives are resistant

  • also effective against “unusual” or “atypical” bugs
  • chlamydia, mycoplasma
  • legionella
  • campylobacter, bordetella
64
Q

Erythromycin side effects

A
  • nausea, vomiting (20-40%)
  • directly enhances GI motility
  • inhibits CYP3A metabolism/excretion of many drugs
  • increases QT interval on EKG
65
Q

Clarithromycin

A
  • mechanism similar to erythromycin but more expensive
  • differences from erythromycin:
  • better kinetics: less frequent dosing
  • less GI motility
  • somewhat wider antibacterial spectrum

-also some CV risk: prolongs QT interval

66
Q

Clarithromycin uses

A
  • same as erythromycin plus:
  • Haemophilus influenzae, Moraxella
  • penicillin resistance strep pneumoniae
  • atypical mycobacteria
  • licensed for helicobacter pylori
  • **3 drug combos have been started for helicobacter, it is two antibiotics and an acid blocker
67
Q

Helicobacter pylori treatment

A

2 antibacterials (maybe even 3) and a proton pump inhibitor

  • clarithromycin + amoxicillin + omeprazole (or other PPI)
  • clarithromycin + metronidazole +omeprazole (or other PPI)
  • metronidazole + tetracycline +bismuth subsalicylate +PPI
68
Q

Azithromycin

A
  • very common for outpatient respiratory tract infections
  • genital infections:-chlamydia

(note gonorrhea is ceftriaxone and azithromycin or doxycyline)

  • GI infections (off label uses)
  • campylobacter pylori, shigella salmonella

-not approve for H pylori

69
Q

rank the GI and drug metabolism and adverse reactions of the macrolides

A

erythromycin
clarithromycin
azithromycin

*azithromycin has a few effects on CYP 3A4

70
Q

azithromycin side effects

A
  • a few effects on CYP3A4
  • Cardiac QT prolongation

*although incidence is lower than for erythromycin

71
Q

clindamycin-mechanism

A
  • bind to 50s ribosomal subunit, blocks translocation along ribosomes
  • significant cause of enterocolitis
72
Q

clindamycin use

A
  • gram positive cocci (ex strep and MSSA)
  • *suppress bacterial toxin production (strep and staph)
  • many anaerobes including bacteroides fragilis
  • not for C difficile
73
Q

clindamycin side effects

A
  • GI irritation
  • antibiotic associated enterocolitis
  • hepatotoxicity
74
Q

Linezolid-mechanism

A
  • inhibits protein synthesis
  • binds 50s ribosomal subunit, interfering with formation of 70s initiation complex
  • bacteriostatic for staph and enterococcus
75
Q

linezolid uses

A
  • gram positive spectrum
  • skin:
  • VRE (vancomycin-resistant enterococcus faecium)
  • staphylococcus aureus: MRSA and MSSA
  • streptococcus grp A and B
  • nosocomial pneumonia
  • strep pneumoniae (including multidrug resistant)
  • staphylococus
76
Q

linezolid side effects

A
  • non-selective inhibitor of MAO
  • many possible drug interactions
  • avoid foods with tyramine
  • contraindicated with MAO inhibitors
  • possible serotonin syndrome if given with SSRIs, tricyclics, triptans, buspirone
  • diarrhea, superinfection including enterocolitis
  • headache nausea/vomiting
  • bone marrow suppression
77
Q

antifolates

A
  • inhibit folate synthesis (we get folate from our diet but bacteria have to make it on their own)
  • Sulfonamides: Sulfamethoxazole, Sulfadiazine

-Trimethoprim

78
Q

Sulfonamides MOA

A
  • bacteriostatic

- sulfonamides are competitive analogs of p-aminobenzoic acid, a precursor in folate synthesis

79
Q

sulfonamide use

A

-today most commonly used sulfonamides are combines with other antibacterial (like trimethoprim)

80
Q

sulfamethoxazole

A
  • used with trimethoprim as part of synergistic combination

- best pharmacokinetic match to trimethoprim

81
Q

silver sulfadiazine

A

-used topically for infection prevention in burn patients

82
Q

side effects of sulfonamides

A
  • hypersensitivity
  • rashes, serum sickness: sunlight (UV) makes rash worse)

-GI disturbances

  • renal damage (crystalluria)
  • drug metabolites crystallize (precipitate) in renal tubules

-potentiate action of other drugs
*inhibit CYP2C9
ex warfarin

83
Q

Trimethoprim

A
  • inhibits folate synthesis in bacteria by competitively inhibiting dihydrofolate reductase
  • it is a dihydrofolate analog
84
Q

Trimethoprim uses

A

-usually in combination with sulfamethoxazole
*synergistic effect
*2 static drugs=1 cidal combination
Trimethoprim+sulfamethoxazole can be called TMP/SMX or sulfamethoprim

85
Q

TMP/SMX uses

A

-first choice empiric therapy for uncomplicated UTTIs (cysctitis)

  • upper respiratory tract, ear infections
  • H. infleunzae, Moraxella, strep pneumoniae

-Pneumocystitis jiroveci (carnii) first line choice for treatment and prophylaxis

86
Q

TMP/SMX side effects

A
  • all of the sulfonamide side effects
  • but also:
  • nausea, vomiting, diarrhea, rashes
  • bone marrow suppression

-trimethoprim side effects especially pronounced with long term use ie AIDS patients

87
Q

Prophylactic

  • description
  • drug selection
A
  • description: prevent surgical wound infections

- drug selection: based on predominant flora at site of interest

88
Q

Empiric

  • description
  • drug selection
A
  • description: organism unknown but syndrome known

- drug selection: which drugs have good activity against most common pathogens

89
Q

pathogen-directed

  • description:
  • drug selection: `
A
  • description: pathogen known, but not susceptibility not yet known
  • drug selection: which drugs likely target this pathogen
90
Q

susceptibility guided

A
  • description: both pathogen and susceptibility known

- drug selection: susceptibility results

91
Q

diagnostic vs non-diagnostic approach

A
  • diagnostic:
  • obtain culture/diagnostic test
  • empiric therapy
  • diagnostic results, sensitivity profile
  • modify therapy as needed
  • cure

vs non diagnostic is just empiric therapy (guess) and then if it stry try again over and over again

-Froedtert pharmacy stops empiric therapy after 72 hours unless order is rewritten to dicourage non-diagnostic approach

92
Q

one common use of empiric therapy

A
  • uncomplicated cystitis in non-pregnant women
  • 1st line drugs (IDSA guidelines)
  • TMP-SMX
  • Nitrofurantoin
  • fosfomycin
93
Q

reasons for antibacterial failures

A

-drug choice
*susceptibility of pathogen
site of infection: drug penetration
*emergence of resistance
*superinfection with another organism

  • host factors:
  • do abcesses need draining
  • is host immune response ok
  • are there foreign bodies, implants, mechanical device, indwelling lines
94
Q

N gonorrhoeae treatment

A

-Ceftriaxone with doxycyline or azithromycin

95
Q

Drugs for MRSA Hospital acquired

A
  • vancomycin (IV)
  • linezolid (IV, oral)
  • daptomycin (IV)
  • tigecycline (IV)
96
Q

community acquired MRSA

A
  • linezolid (oral)
  • doxycycline, minocycline (oral)
  • clindamycin (oral)
  • TMP-SMX (oral)

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