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Pharm II > (3-22-17) Antibiotics > Flashcards

(3-22-17) Antibiotics Flashcards

1
Q

who is most guilty for the emerging resistance of antibiotics?

A

agriculture

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2
Q

why are bacterioCIDAL drugs preferred to bacterioSTATIC?

A
  • rely less on host immune system
  • take effect more quickly
  • maintain their effect longer, making exact dosing interval less critical
  • very important for prophylaxis

***post antibiotic effects: seen with static drugs that may change its thinking

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3
Q

what is the post antibiotic defect?

A

persistent suppression of bacterial growth after a brief exposure (1-2 hrs) of bacteria to an antibiotic even in the absence of host defect mechanisms
*may be related to DNA alteration

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4
Q

which spectrum (narrow vs broad) is better and why?

A

NARROW

  • often more effective
  • less alteration of normal flora, therefore, less super infection
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5
Q

what is the dosage of a drug determined by?

A
  • MIC minimum inhibitory conc
  • -too much = toxicity
  • -to littler = resistance
  • -host function may alter
  • -inc evidence that “loading dose” is helpful
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6
Q

what is the MIC?

A

minimum inhibitory conc

-minimum conc of a drug that will prevent visible growth of bacteria in culture after an overnight incubation

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7
Q

is rebound of infection common in oral/facial infection of odontogenic infection?

A

no

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8
Q

what is the general rule of thumb for termination of antibiotic?

A

when sure pt is on the way to recover based on clinical eval.

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9
Q

what are the 3 adverse effects of antibiotics?

A
  • toxicity
  • allergy
  • superinfection
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10
Q

what are some examples of toxicity for antibiotics?

A
  • GI distress
  • hepatotoxicity (antifungals)
  • nephrotoxicity (penicillin, aminoglycosides)
  • neurotoxicity (aminoglycosides)
  • blood and blood forming organs (choramphenicol, destruciton of normal flora needed for vit K absorption)
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11
Q

what are often confused with true allergies?

A

toxicities or side effects

*multiple allergies may severely limit critical therapy

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12
Q

in what circumstances are superinfections more common?

A
  • young and old

- broad spectrum therapy

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13
Q

what do superinfections sometimes cause?

A

inc or dec in effectiveness of other drugs

ie birth control pills

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14
Q

what is pseudomembranous colitis?

A
  • caused by C. difficile
  • cephs, ampicillin, clindamycin
  • frequent, watery/bloody diharrea and cramps
  • stop drug immediately
  • oral vancomycin is no longer accepted tx
  • METRONIDAZOLE is now used to treat
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15
Q

what is an optimal antibiotic?

A
  • active against pathogen
  • reaches effective conc
  • low toxicity
  • not cause resistance
  • desirable route
  • economical
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16
Q

T/F oral bacteria are commonly primary pathogens?

A

FALSE

gererally several organisms not just one
*resistnace is no longer a “non-issue” as it has been in the past

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17
Q

widest spectrum of all antibacterials

A

beta lactam antibiotics

from narrow to broad range spec:

  • PENICILLINS
  • CEPHALOSPORINS
  • carbapenems
  • monobactams
  • carbacephems
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18
Q

what is the mechanism of action of penicillins?

A

cell wall synthesis

  • prevents cross linking
  • low toxicity in general
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19
Q

Pen V

A
  • combine with potassium or sodium to make a salt (Pen VK)
  • stable in gastric pH (orally effective)
  • low toxicity
  • narrow spectrum specific to oral microbes
  • CIDAL
  • inexpensive
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20
Q

Pen G

A
  • IV or IM only
  • unstable in gastric contents
  • formulated as: aqueous, procaine, benzathine
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21
Q

what is the drug of choice for most odontogenic infections?

A

Penicillin

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22
Q

what is the dosing rule for penicillin?

A

may load up to 2 grams followed by 500 mg every 6 hrs

*parenteral dosage given as “units”

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23
Q

in what circumstances should you dec dose for penicillin?

A
  • renal compromised

- infants

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24
Q

B-lactamase resistant penicillins

A
  • “anti-staph” penicillins
  • methicillin was prototype (MRSA)
  • less activity against oral bacteria
  • expensive
  • indicated for ONLY STAPH infections
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25
Q

Extended spectrum penicillins (Amoxicillin group)

A

amoxicillin is the one that is used orally

26
Q

is amoxicillin B-lactamase resistant?

A

no

27
Q

why is amox better for SBE prophylaxis than PCN VK?

A
  • more predictable
  • longer half life
  • higher plasma conc
  • is NOT USED bc it is broader spectrum
  • *these properties along with better dosage regimen may make amox an acceptable alternative to PCN for odontogenic infections
28
Q

Extended spectrum penicillins

anti-pseudomonas penicillins

A
  • carbenicillin, ticarcillin, piperacillin, and others
  • less activity against oral bacteria
  • NOT INDICATED for any head and neck infection as DOC
29
Q

beta lactamase

A
  • cleave the B-lactam ring
  • 100’s described
  • transferred to bacteria by infective process
  • combated by inc “R” chains or by competitive inhibition
30
Q

beta-lactam inhibitors

A

3 available:

  • clavulonic acid
  • sulbactam
  • tazobactam

*bind active site of B-lactamase action

31
Q

Augmentin

A
  • amox + clavulonic acid
  • augmentin XR
  • oral
  • improved staph and H. flu coverage
32
Q

what are the indications for augmentin?

A
  • otitis (ear)
  • bite wounds
  • sinusitis (non-odontogenic)
  • UTI
33
Q

Unasyn

A
  • ampicillin + sulbactam
  • parenteral
  • similar spectrum as augmentin
  • due to inc resistance to PCN, it is the DOC for serious infections being treated in a HOSPITAL SETTING
34
Q

what are the adverse effects of penicillins?

A
  • allergy (1-10% occurence)(2% average)(usually not fatal)
  • antagonized by bacteriostatic drugs
  • dec excretion in very young, old, or compromised renal function
35
Q

most frequent DOC for odontogenic infection

A

PCN V

36
Q

DOC for hospital infection

A

unasyn

37
Q

if significant anerobic component of infection, what is the DOC?

A

metronidazole

38
Q

DOC for bites, non-odontogenic sinusitis, otitis?

A

B-lactamase inhibitiors such as augmentin

39
Q

DOC for prophylaxis?

A

amox

40
Q

cephalosporins

A
  • 5 generations
  • beta-lactam configurations
  • inc resistnace to B-lactamase by addition of R groups
  • “custom” antibiotics
41
Q

cephalosporin pharmacology

A
  • cidal- cell wall inhibition
  • low toxicity
  • extended spectrum in comparison to PCN
  • oral and parenteral forms
  • expensive in comparison to PCN
42
Q

first generation ceph

A

-parenteral

steph, staph, e coli, MSSA not MRSA

43
Q

second generation ceph

A

-oral

44
Q

what are the indications for a first generation cephalosporin

A
  • community aquired staph infection
  • surgical wound prophylaxis with skin incision
  • odontogenic infection in pen allelrgic pt
45
Q

what is the incidence of a PCN allergy?

A

5-8%

46
Q

what % of PCN allergics will have ceph allergy as well?

A

1-10%

*ceph allergy predisposes to unknown incidence of PCN allergy

47
Q

if pt has severe PCN allergy, should you avoid ceph?

A

yes, if severe

*should be fine if the allergy is mild

48
Q

if pt has ceph allergy, should you avoid PCN?

A

yes ALWAYS, even if it is mild

49
Q

what is the mechanism of action for macrolides

A
  • irreversibly bind 50s ribosomal units
  • inhibit RNA dependent protein synthesis
  • selective uptake by phagocytic cells which serve as repository. leads to high levels at infection relative to blood levels
  • significant post-antibiotic effect
50
Q

clarithromycin

A
  • similar to erythromycin
  • less resistance
  • better H. influenza coverage
  • BID dosing (250mg)
  • less GI distress
  • 1 hr before or 2 hr after eating
  • expensive
51
Q

what are the indications for clarithromycin?

A
  • sinus infection
  • Mild to moderate odontogenic infection in PCN allergic pt
  • SBE prophylaxis in PCN allergic pt as alternate to clindamycin
  • pneumonia/ bronchitis
52
Q

azithromycin

A
  • similar to clairithromycin but better for strep and g- anerobes
  • 3 day course as effective as 7-10 days of augmentin
  • pneumonia/ bronchitis
  • SBE prophylaxis
  • daily dosing/ improved compliance
  • not require dosing around meals
  • less GI distress
  • expensive
53
Q

what are the adverse effects of macrolides?

A
  • GI distress, worse with erythromycin
  • ototoxicity
  • cholestatic jaundice
  • long Q-T interval/Torsades de pointes
  • inc activity of digitalis
  • potentiation of oral anticoagulants such as coumadin
  • myopathy in pts taking statins for elevated cholesterol
54
Q

lincosamides

A
  • bind 50s ribosome leading to bacteriostatic inhibition of protein synthesis
  • clindamycin- currently the only one in use in US
55
Q

what is the spectrum of clindamycin?

A
  • strep
  • staph
  • actinomyces
  • anaerobes
56
Q

what is the pharmacology of clindamycin?

A
  • static except at high doses
  • bone penetration
  • higher toxicity than some
  • expensive
57
Q

what are the indications of clindamycin?

A
  • chronic recurrent infection
  • osetomyelitis
  • odontogenic infection in immunocompromised pt with severe PCN allergy
  • inc use in routine odontogenic infection due to inc resistance to PCN by oral anearobes
58
Q

metronidazole

A
  • CIDAL
  • oral dose equivalent to parenteral
  • mild toxicity
  • disulfuram effect
  • inexpensive
  • disrupts DNA in anaerobic environment
59
Q

what are the indications for metronidazole?

A
  • chronic anaerobic infection
  • any need for bone penetration
  • in combo with PCN or ceph in serious odontogenic infection
60
Q

tetracyclines

A
  • static - 30s ribosomal inhibition
  • broad spectrum
  • high resistance
  • inexpensive
61
Q

what are the indications for tetracyclines?

A
  • early adjunctive tx of peri-implantitis
  • resistant hospital aquired infections
  • helobactor related gastric and peptic ulcer due to inc resistance to metronidazole
  • topical therapy
  • dry socket prevention
  • NO INDICATION FOR ODONTOGENIC INFECTION
  • may result in deformity of developing teeth

Pharm II (16 decks)

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