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Pharmacology > Lecture 3 (ID)- Exam 2 > Flashcards

Lecture 3 (ID)- Exam 2 Flashcards

1
Q

Cross tolerance:
* When does it happen?
* When switching to another opioid, what must happen with the starting dose of the new opioid?

A
  • Development of tolerance to the effects of pharmacologically related drugs, particularly those that act on the same receptor site.
  • When switching to another opioid, the starting dose of the new opioid must be reduced by at least 25% of the calculated equianalgesic dose to prevent overdosing
  • Monitor clinical response and adverse effects
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2
Q

What are ways to classify and group bacteria? (3)

A
  • Aerobic/anaerobic
  • Gram negative/positive
  • Atypicals
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2
Q

What are common gram negative bacteria (10)?

A
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3
Q

What are the most common gram positive bacteria (10)?

A
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4
Q

What are the gram + cocci?

A
  • Staphylococcus spp (purple clumps)- aureus or epidermidis
  • Streptococcus spp (purple chains)- viridian, pyogenes, pneumoniae
  • Enterococcus spp
  • Peptococcus
  • Peptostreptococcus

Highlighted: anaerbic mouth flora

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5
Q

What are the gram (-) cocci?

A
  • Moraxella catarrhalis (common for URI)
  • Neisseria spp (dicocci) -gonorrhea, meningitidis
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6
Q

What are the gram + rods?

A
  • Listeria
  • Bacillus
  • Corynebacterium
  • Propionibacterium
  • Clostridium spp-perfringens, difficile
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7
Q

What are the gram - rods that are aerobes?

A
  • Hemophilus Influenzae
  • Escherichia Coli
  • Proteus spp
  • Klebsiella spp
  • Pseudomonas spp
  • Enterobacter spp
  • Gardnerella vaginalis
  • Legionella
  • Pasteurella multocida
  • Salmonella
  • Shigella
  • Campylobacter
  • Yersinia
  • Helicobacter
  • Vibrio
  • Bartonella
  • Bordetella
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8
Q

What are the gram - anaerobes?

A
  • Bacteroides fragilis
  • Fusobacterium spp
  • Prevatella spp
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9
Q

What are the atypical bacteria?

A
  • Mycoplasma pneumoniae
  • Chlamydia spp-pneumoniae, trachomatis
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10
Q

What is the mycobacteria bacteria?

A

Tuberculosis

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11
Q

What are the spirochetes bacteria?

A
  • Treponema pallidum
  • Borrelia burgdorferi
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12
Q

What are the beta lactam antibiotics? (4) What type of agents are they?

A

Cell wall active agents
* Penicillins
* Cephalosporins
* Carbapenems
* Monobactams

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13
Q

What are the glycopeptide antibiotics? What type of agent are they?

A

vancomycin-Cell wall active agent

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14
Q

What is the MOA for penicillin?

A

Inhibits bacterial cell wall synthesis
* Target bacterial penicillin binding protein (PBP)
* Interfere with transpepiation
* Creates an unstable cell wall-> cell death

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15
Q
  • For penicillin, what needs to happen for renal impairment?
  • What penicillin goes through hepatic elimination?
A
  • Most required dose reduction for renal impairment
  • Nafcillin – hepatic elimination
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16
Q

What are the adverse effects? of penicillin

A
  • GI effects: Nausea / vomiting / diarrhea
  • Allergic reactions
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17
Q

What are the penicillins? Aminopenicillins?

A

Penicillins
* Penicillin (IV, PO, IM)

Aminopenicillins
* Amoxicillin (PO)
* Ampicillin (IV)

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18
Q

What are the Penicillinase Resistant (antistaphylococcal)? Extended spectrum (antipseudomonal)?

A

Penicillinase Resistant (antistaphylococcal)
* Oxacillin (IV)
* Nafcillin (IV)
* Dicloxacillin (PO)

Extended spectrum (antipseudomonal)
* Ticarcillin (IV)
* Piperacillin (IV)

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19
Q

What are the b-lactamase combos?

A
  • amoxicillin / clavulanate (Augmentin) (PO)
  • ampicillin / sulbactam (Unasyn) (IV)
  • piperacillin / tazobactam (Zosyn) (IV)
  • ticarcillin / clavulanate (Timentin) (IV)
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20
Q

Penicillin:
* What bacteria does penicillin treat (gram +, anaerobes and other)

A
  • Gram (+): Steptococcus spp
  • Anaerobe: Mouth flora-> Peptococcus and Peptostreptococcus
  • Other: T. pallidum
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21
Q

For ampicillin, amoxicillin, what bacteria do they treat (gram +, gram-, anerobe_?

A
  • Gram(+): Streptococcus spp (same as PCN), listeria, enterococcus
  • Gram (-): E. Coli, Proteus spp, H. influenzae, M. catarrhalis, N. meningitidis, Salmonella, Shigella, Helicobacter
  • Anaerobe: Peptococcus and Peptostreptococcus (same as PCN)
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22
Q

For oxacillin, nafcillin (methicillin), what bacteria do the meds treat?

A
  • Streptococcus spp
  • Staphylococcus spp but Not MRSA

Do not use methicillin because of renal toxity

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23
Q

For Ticarcillin and Piperacillin, what bacteria do they treat (gram +, gram - and anaerobe)?

A
  • Gram (+): Streptococcus spp (same as penicillin)
  • Gram (-): same as ampicillin and amoxicillin Including Pseudomonas
  • Anaerobe: B.fragilis

Amp and amox: E. Coli, Proteus spp, H. influenzae, M. catarrhalis, N. meningitidis, Salmonella, Shigella, Helicobacter

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24
Q

For Ampicillin/sulbactam and Amoxicillin/ clavulanat, what bacteria does it treat (gram +, Gram - and anaerobe?

A
  • Gram (+): Staphylococcus, Streptococcus, Enterococcus
  • Gram (-):Good vs most including B. Including beta-lactamase producing organisms
  • Anaerobe: B. fagilis

  • BROADEST
  • beta lactamase inhibitors
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25
Q

For Ticarcillin / clavulanate and Piperacillin /tazobactam, what bacteria do they treat? (gram +, gram - and anaerobe)

A
  • Gram (+): Staph, strept and enterococcus (Same as ampicillin / sulbactam)
  • Gram (-): Good vs most including beta lactamase producing organisms and Pseudomonas
  • Anaerobe: B. fragilis

  • BROADEST
  • B lactamase inhibitors
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26
Q

Cephalosporins:
* What is the MOA?
* What are the pharmokinetics?

A
  • MOA: inhibits bacterial cell wall synthesis
  • PK: most require adjustment for renal impairment; not ceftriaxone
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27
Q

What cephalosporin drug does not need to be adjusted for renal impairment ?

A

ceftriaxone

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28
Q

What are the adverse rxns of cephalosporins?

A
  • Mild GI effects
  • Rash
  • Leukopenia (rare)
  • PCN cross-reactivity
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29
Q

What are the 1st gen of cephalosporins?

A
  • Cefazolin (Ancef) IV
  • Cephalexin (Keflex) PO

Fa+pha rule

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30
Q

What are the 2nd gen cephalosporins?

A
  • Cefuroxime (Zinacef-IV, Ceftin-PO)
  • Cefprozil (Cefzil) PO
  • Cefotetan (Cefotan) IV
  • Cefoxitin (Mefoxin) IV

FURry FOXes TAN like PROs

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31
Q

What are the 3rd gen cephalosporins?

A
  • Cefotaxime (Claforan) IV
  • Ceftriaxone (Rocephin) IM/IV
  • Cefpodoxime (Vantin) PO
  • Cefdinir (Omnicef) PO
  • Ceftazidime (Fortaz) IV

-ime,-one, -ir

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32
Q

What is the 4th gen cephalosporin?

A

Cefepime (Maxipime) IV

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33
Q

What is the 5th gen cephalosporins?

A

Ceftaroline (MRSA)

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34
Q

What generations of cephalosporins are for anerobic activity?

A

1st and 2nd generation

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35
Q

For the cephalosporins, how do they treat gram + or -?

A
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36
Q

For first gen (Cefazolin (Ancef) IV and Cephalexin (Keflex) PO), what bacteria does the drugs treat? (gram pos, negative and anaerobe)

A
  • Gram (+): Staphylococcus spp (not MRSA), Streptococcus spp (not Strep pneumoniae) and Not Enterococcus spp
  • Gram (-): Moderate because better than PCN or ampicillin
    * E. Coli
    * Klebsiella spp
    * Proteus spp
  • Anaerobe: poor
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37
Q

For 2nd gen (Cefuroxime (Ceftin) PO Cefprozil (Cefzil) PO), what bacteria does the drugs treat? (gram pos, negative and anaerobe)

A

Gram (+): Staphylococcus spp (not MRSA), Streptococcus spp (not Strep pneumoniae) and Not Enterococcus spp
* SAME AS FIRST GEN
* Gram (-): Same as first (E. Coli, Klebsiella spp, Proteus spp) plus H.influenza and M.catarrhalis
* Anaerobe: Poor

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38
Q

What does 2nd gen (cefotetan and cefoxitin) treat?

A

Anaerobe: B. fragilis

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39
Q

For third gen,
* Cefotaxime
* Ceftriaxone (Rocephin) IV/IM
* Cefpodoxime (Vantin) PO
* Cefdinir (Omnicef) PO
* Cefixime (Suprax)

What do they treat? (gram pos, Gram neg and anerobes)

A
  • Gram (+): Good Strep spp – including S. pneumoniae and Moderate Staph spp (MSSA)
  • Gram (-): Good->N. gonorrhea
  • Anaerobes: poor
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40
Q

What 3rd generation cephalosporin is great for pseudomonas?

A

Ceftazidime (Fortaz) IV plus limited staph/strep

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41
Q

For 4th gen, Cefepime(IV), what bacteria do they treat (gram pos, neg and anaerobes?
* What are they more of?

A

More resistant to beta lactamase
* Gram (+): good strep spp., moderate Staph spp but not MRSA
* Gram (-): Similar to ceftriaxone (n.gonorrhea)
* Anerobes: poor

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42
Q

What are the carbapenems?

A

Imipenem, meropenem, ertapenem, doripenem (IV only)->DEMI needs CARBs

THE PENEMs!!!

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43
Q

What is the moa of carbapenems?

A

MOA: inhibit bacterial cell wall synthesis
* Still have beta-lactam ring but slight structure change including substitution from sulfur with carbon makes them more resistant to beta lactamases

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44
Q

Carbapenems:
* What type of antibiotic is it
* Which one does not cover pseudomonas or acinetobacter?
* What is doripenem approved for and not approved for?

A
  • Very broad spectrum including most gram positives, gram negatives and anaerobes
  • Ertapenem – does NOT cover Pseudomonas or Acinetobacter
  • Doripenem
    * Approved for complicated intra-abdominal and urinary tract infections only
    * Not approved for the treatment of pneumonia (because it does not get into the lungs)
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45
Q
  • Carbapenems should be reserved for what?
  • What are the adverse reactions of carbapenems?
A
  • Reserved for resistant infections only

ADR:
* Nausea / vomiting (worse with imipenem)
* Seizures (worse with imipenem)

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46
Q

Monobactam:
* What is the drug name?
* What is the MOA?
* What is the structure of the drug?

A

Aztreonam
* MOA: inhibit bacterial wall synthesis
* Beta-lactam ring is not fused – very resistant to beta lactamases

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47
Q

Aztreonam (monobactams):
* For are they great for? What activity do they not have?
* What are they reserved for?
* SE?

A
  • Excellent gram-negative coverage including Pseudomonas spp
  • No gram-positive activity
  • Reserved for the treatment of resistant infections or patients with severe allergy to other beta lactam antibiotics
  • Well tolerated with few side effects
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48
Q

PENICILLIN ALLERGY:
* Est. on how many ppl say they are allergic and how many actually are?
* What needs to be obtained with someone who reports pen allergy? Why?

A
  • Estimated that 10% of the U.S. population labeled as penicillin allergic and < 1% actually are
  • A detailed history should be obtained in patients who report a penicillin allergy
    * Not an allergy – intolerance; correct chart
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49
Q

What are the delayed type rxns for pencillin allergies? Should you give them the med anyways?

A

Delayed-type reaction (e.g., Stevens Johnson Syndrome, Toxic Epidermal Necrolysis, serum-sickness, etc)
* Avoid penicillins, cephalosporins, carbapenems

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50
Q

What is a mild, without history of IgE mediated features or unverified patient, patient cannot recall reaction to penicillin getting? (recommended and considered)

A

Mild, without history of IgE mediated features or unverified (maculopapular rashes with or without pruritis, not hives), patient cannot recall reaction
* Minimal risk of IgE mediated reaction
* Recommend any generation cephalosporin or carbapenem
* Consider penicillin de-labeling with amoxicillin oral challenge

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51
Q

patients with past reaction with IgE medicated features should get what?

A

Past reaction with IgE medicated features (angioedema, anaphylaxis, wheezing, laryngeal edema, hypotension, hives/urticaria)
* Some risk of serious IgE mediated reaction
* Recommend:

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52
Q

What is the moa of vancomycin?

A
  • MOA: inhibits bacterial wall synthesis
  • Glycopeptide antibiotic – binds tetrapeptide chains and prevents linking
  • Do not bind PBPs – bypass PBP mutations
  • Resistance secondary to bacterial changes in the tetrapeptide chains – vancomycin can no longer bind
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53
Q

What are the indications of vancomycin?

A
  • Treatment of gram-positive organisms resistant to other antibiotics
  • Commonly incorporated into empiric regimens
  • Treatment of Clostridium difficile enterocolitis
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54
Q

How do you give vancomycin and why?

A

Not absorbed from the GI tract – must be given IV for systemic infections

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55
Q

What are the adverse reactions to vancomycin?

A
  • ­ Ototoxicity
  • ­ Nephrotoxicity
  • ­ Thrombophlebitis
  • ­ “Red-man’s syndrome
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56
Q

Vanco

Dose and frequency determined and monitored via what?

A

Via drug levels
* ­ Troughs – adjust per clinical pharmacy
* ­ Goal trough levels usually 15 to 20; depends on infection and MIC of bacteria

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57
Q

What are the different protein synthesis inhibitors?

A
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58
Q

What is the moa of aminoglycosides?

A

Inhibits bacterial protein synthesis
Irreversibly binds to 30s subunit and prevents protein synthesis
* Must enter through the cell wall to the nucleus
* Cannot penetrate the thick gram-positive cell wall
* Requires and oxygen-dependent co-transporter – not effective for anaerobic infections

59
Q

What are the different aminoglycosides?

A
  • Gentamicin
  • Tobramycin
  • Amikacin
  • Streptomycin
60
Q

For the aminoglycosides, what bacteria do they treat? (gram pos, neg, and other ones)

A
  • Gram (+): Only in combination with cell active agent
    * Strep spp, Entercoccus spp, Listeria
  • Gram (-): Combination with cell active agents recommended
    * Good against most including Pseudomonas spp
  • Other: Anerobes are poor, and Mycobacteria TB, MAI best (amikacin, streptomycin)

Not staph gram (+), good gram (-), use with other drugs

61
Q

What are the adverse effects of aminoglycosides?

A
  • Ototoxix and Nephrotoxic
  • Entirely renally eliminated; dose reduction required
  • Contraindicated in pregnancy
  • Monitoring: Drug levels and Serum creatinine

GET LEVELS

62
Q

Tetracyclines:
* What are the different drugs?
* What is the MOA?

A

Tetracycline, doxycycline, minocycline, tigecycline

MOA: inhibit bacterial protein synthesis
* Binds to A-site of 30S subunit
* Inhibits binding of tRNA to mRNA ribosome complex

63
Q

Tetracyclines:
* What is the coverage?
* What is no longer used and why?

A

Broad spectrum gram-positive and gram-negative coverage

Parent drug (tetracycline) no longer used
* Less convenient dosing
* Less active
* More drug interactions

64
Q

For doxycyline, what bacteria does it treat? (gram pos, neg and others?

65
Q

What is the first line for tick borne diseases like rickettsia (RMSF) and borrelia (lyme)?

A

Doxycyclin

66
Q

What are the adverse effects for tetracyclines?

A
  • Phototoxicity
  • Deposition in teeth – permanent yellow-grey-brown discoloration in children / fetus (worst with tetracycline)
  • Nausea, vomiting, diarrhea -> do not take on empty stomach
  • Erosive esophagitis (same as biphosphates)
  • Minocycline – lupus like reaction
  • Minocycline – pseudotumor cerebri-> increase intracranial pressure
  • Tinnitus, vestibular symptoms (minocycline)-> dizzy and ringing of ears
67
Q

What does american academy of pediatrics say about tetracyclines?

A

American Academy of Pediatrics (AAP) – doxycycline can be safely
administered for short durations (≤ 21 days) regardless of age

68
Q

What are unique SE of minocyclines?

A
  • lupus like reaction
  • pseudotumor cerebri
69
Q

What are the different macrolides?

A

Erythromycin, clarithromycin, azithromycin

70
Q

What is the moa of macrolides?

A
  • ­ Inhibits bacterial protein synthesis
  • ­ Bind to 50s subunit and prevent translocation; ribosome can’t slide to the next codon on the mRNA
71
Q

Macrolides:
* What is the coverage?
* What drug is not used a lot and why?

A

Broad spectrum gram-positive and gram-negative coverage

Parent drug (erythromycin) minimal use as antimicrobial
* Less convenient dosing
* More adverse effects
* More drug interactions

72
Q

For Erythromycin (PO, IV), Azithromycin (PO, IV) Clarithromycin (PO), what bacteria does it treat (gram pos, neg and others)?

73
Q

What are the interactions of macrolides?

A

Avoid concomitant administration with magnesium or aluminum-
containing antacids

74
Q

What are the adverse reactions of macrolides?

A

GI: nausea, vomitingE, diarrhea
* ­ Erythromycin > clarithromycin > azithromycin

Prolongation of QTc – interval
* Avoid in patients with known prolonged QT or history of arrythmias
* Caution with other drugs that prolong QTc interval

Hepatotoxicity

Drug interactions CYP3A4 (erythromycin, clarithromycin)

Hearing loss (erythromycin)

75
Q

What macrolides has the most SE?

A

Erythromycin

76
Q

Clindamycin:
* What is the MOA?
* What does it inhibit in vitro

A

MOA
* ­ Inhibits bacterial protein synthesis
* ­ Bind to 50s subunit and prevent translocation; ribosome can’t slide to the next codon on the mRNA

Inhibits in vitro the production of the streptococcus superantigen pyrogenic exotoxins A (SPEA) and B (SPEB)-> used with cell wall active agent to neutralize the endotoxin (toxic shock)

77
Q

For clindamycin, what bacteria does it treat? (gram pos, neg and anaerobes)

78
Q

linezolid:
* What is the MOA?

A
  • Inhibits bacterial protein synthesis
  • Bind to 50s subunit and prevents it from binding to the 30S subunit to form initiation complex; stops protein synthesis before it begins
79
Q

What are the SE of linezoid?

A
  • Nausea, vomiting, diarrhea, rash – short term
  • Bone marrow suppression (leukocytopenia, thrombocytopenia)
  • Peripheral neuropathy and optic neuropathy – long term
  • Inhibits monoamine oxidase – may interact with other medications that increase serotonin (MAOIs, SSRIs, SNRIs)
    * Serotonin syndrome – fever, agitation, mental status changes, muscle rigidity, tremor, seizures
80
Q

What drug can cause serotonin syndrome when taken with a monoamine oxidase drugs?

81
Q

For linezolid, what bacteria can be treated? (gram pos, neg and others)

A
  • Gram (+): Excellent; including MRSA and VRE
    * Used in locations where MRSA cannot be penetrated
  • Gram (-): poor
  • Other: poor
82
Q

What are the different DNA synthesis inhibitors?

83
Q

Fluoroquinolones:
* What are the different drugs?

A

Ciprofloxacin, levofloxacin, moxifloxacin, delafloxacin

84
Q

Fluoroquinolones:
* What is the MOA?
* What is it metabolized via what?
* Should not be taken with what and why?

A
  • Inhibits bacterial replication by inhibition of DNA gyrase (topoisomerase I) and topoisomerase IV)
  • Metabolized via CYP450; also inhibitor
    * Many drug interactions
  • Should not be taken with calcium, iron, zinc – bind quinolones and cause chelation and decreased absorption
85
Q

Fluoroquinolones:
What are the adverse effects?

A
  • Tendonitis – achilles tendon MC (avoid in athletes or elderly)
  • Cartilage damage
  • GI distress
  • CNS headache, agitation dizziness, insomnia, peripheral neuropathy, seizures
  • Prolong QT interval: monitor QTc in patients on concomitant drugs that prolong QT interval
  • Hyper / hypoglycemia (MC moxifloxacin)

Need to be careful with elderly

86
Q

For ciprofloxacin, levofloxacin, and moxifloxacin, what bacteria can be treated (gram pos, neg and anaerobe)?

87
Q

For delafloxacin, what bacteria does it treat? (gram pos, neg and anaerobe)

A

Gram (+): s. aureus including MRSA
Gram (-): Excellent including Pseudomonas (ciprofloxacin superior)
Anaerobe: Moderate including b.fragilis

88
Q

What is the black box warning for fluoroquinolones?

A
  • Serious, potentially irreversible adverse effects including tendinopathy and CNS effects. Avoid use / discontinue in any patients experiencing these side effects.
  • Risks > benefits for chronic bronchitis, sinusitis, uncomplicated cystitis
89
Q

What is the MOA of metronidazole?

A

inhibits DNA synthesis; produces free radicals which damage bacterial DNA; bacteria cannot produce nucleic acids

90
Q

What are the adverse effects of metronidazole

A
  • Anorexia
  • ­ Nausea
  • ­ Stomach cramps
  • Disulfiram-like effect (nausea, vomiting and headaches if taken with alcohol-> 24hr to 48hrs)
91
Q

For metronidazole, what bacteria does it treat (Gram pos, neg and others)?

A
  • Gram (+): poor
  • Gram (-): poor, H.Pylori (in combination)
  • Anerobic: Bacteroides fragilis and Clostridium difficile
  • Other: Entamoeba histolytica, Gardnerella spp, Trichomonas
  • Giardia
92
Q

Sulfamethoxazole/trimethoprim (SMX/TMP):
* What is the MOA?

A

inhibit bacterial DNA synthesis; each inhibit different steps in bacterial folate synthesis; no folate = no nucleic acids = no DNA

93
Q

Sulfamethoxazole/trimethoprim (SMX/TMP):
* Dosing based on what?
* What is the strength dose?
* What can happen if Allergic reaction to sulfonamide group?

A
  • Dosing based on TMP component
  • One double strength tablet = 160 mg TMP/ 800mg SMX
  • Allergic reaction to sulfonamide group: can cross react with other drugs with sulfonamide group including hydrochlorothiazide and glyburide
94
Q

⭐️

Sulfamethoxazole/trimethoprim (SMX/TMP):
* What is the CI?
* What type of inhibitor? what does this cause?

A
  • CI: pregnancy, infants < 2 months dt leukopenia and binds to albumin and kicks off billy rubin
  • CYP450 2C9 inhibitor - increases warfarin levels
95
Q

Sulfamethoxazole/trimethoprim (SMX/TMP):
* What are the adverse effects?

A
  • Nausea, vomiting
  • Skin rash, photosensitivity, erythema multiforme, Stevens-Johnson syndrome
  • Bone marrow suppression
  • Hemolytic anemia – patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency
  • Crystalluria / nephritis
  • Kernicterus in neonates
96
Q

For Sulfamethoxazole / trimethoprim (Bactrim / Septra), what bacteria does it treat (gram pos, neg and other)?

A
  • Gram (+): staph spp including MRSA
  • Gram (-): good versus most, not pseudomonas
  • Other: poor anaerobic and DOC for pneumocystis jirovecii
97
Q

What is the DOC for Pneumocystis jirovecii

A

Sulfamethoxazole / trimethoprim (Bactrim / Septra) (IV/PO)

98
Q

Rifampin:
* What is the MOA?
* Never use as what?
* Inducer of what?

A
  • MOA: inhibits bacterial RNA synthesis; inhibits RNA polymerase
  • NEVER us as monotherapy – rapid development of resistance
  • Inducer of CYP3A4 – many significant drug interactions * Monitor closely
99
Q

What are the adverse effects of rifampin?

A
  • Nausea, vomiting, diarrhea
  • Red-orange discoloration of tears, sweat, urine, etc-> any body fluid
    * Stains contact lenses
  • Flu-like syndrome – rash, fever, abdominal pain
  • Hepatitis – rare but can be life-threatening
100
Q

For rifampin, what bacteria does it treat? (gram pos, neg and other)

A
  • Gram (+): Staph and Strep spp including MRSA
  • Gram (-): Poor->H. influenzae, N. Meningitidis (post exposure prophylaxi)
  • Other: M.tuberculosis
101
Q

Daptomycin:
* What is the MOA?

A

binds to and depolarizes the bacterial cell wall membrane; intracellular inhibition of DNA, RNA, and protein synthesis

102
Q
  • What is the pharmokinetics of daptomycin? What is it not recommended for?
  • What does it penetrate?
A

PK: not absorbed orally, 90% protein bound, 80% eliminated unchanged in the urine
* Pulmonary surfactant inactivates daptomycin not recommended for treatment of pneumonia

Penetrates biofilm of gram-positive organisms

103
Q

What are the adverse effect of daptomycin?

A

Myopathy and rhabdomyolysis
* Monitor weekly creatine phosphokinase (CPK); more frequent with renal failure or patients on statins
* Eosinophilic pneumonia
* Peripheral neuropathy

104
Q

For daptomycin, what bacteria does it treat (gram pos, neg and others)?

A
  • Gram (+): Excellent including MRSA and VRE
  • Gram (-): none
  • Anaerobe: none
105
Q

Mechanism of resistance

What happens when there is an antibioic modification or inactivation?

A
  • ­ Bacteria develop enzymes that inactivate and destroy antibiotics
  • ­ E.g. – beta lactamase destroys beta lactam ring
106
Q

Mechanism of resistance

What happens when there is Alteration of target or binding site – antibiotic can’t bind to target

A

­ E.g. – MRSA modifies its penicillin binding proteins

107
Q

Mechanism of resistance

what happens when there is a bypassing metabolic inhibition?

A

E.g., sulfonamides inhibit folic acid synthesis; bacteria find ways to scavenge folic acid from the environment

108
Q

What happens when there is a prevention antibiotic accumulation – decrease intra- bacteria abx conc

A

­ E.g., preventing cell membrane permeation, creation of efflux pumps

109
Q

What are the different antimicrobial resistance mechanisms?

110
Q

What is a bactericidal antibiotics? What are the examples?

A

Antibiotics that kill bacteria without help from patient’s immune system
* Penicillins
* Cephalosporins
* Carbapenems
* Vancomycin
* Fluoroquinolones
* Daptomycin
* Metronidazole
* Sulfamethoxazole/trimethoprim

111
Q

Are bacteriostatic drugs? what are the examples?

A

Antibiotics that inhibit the growth of bacteria – utilize the patient’s immune system to kill the bacteria
* Tetracyclines
* Clindamycin
* Macrolides
* Linezolid

112
Q

What are some caveats about bacteriostatic and bactericidal drugs?

A
  • Some drugs are static at low concentrations and cidal at high concentrations
  • Some drugs are static against certain bacteria and cidal against others
  • Some drugs are static on their own but cidal when combined with other antibiotics
113
Q

When is bactericidal necessary?

A
  • Patient’s immune system is not functioning
  • Serious infections that require early bacterial killing to preserve life or function (sepsis, meningitis)
  • Site of infection is poorly accessible to antibiotics
114
Q

When is bacteriostatic appropriate?

A
  • Antibiotic targets a specific bacteria
  • Only drug available to treat a specific bacteria due to resistance
  • When it is used with another drug for synergistic effects
116
Q

What are imidazoles? What are triazoles?

A
  • Imidazoles: Clotrimazole, Miconazole and Ketoconazole
  • Triazoles: Itraconazole, Fluconazole, Voriconazole, Posaconazole, Isavuconazole
117
Q
  • For clostrimazole and micronazole, what is the MOA, route and SE?
  • Ketoconazole?
118
Q

For the triazoles: What is the MOA, route and SE?

119
Q

What does fluconazole treat?

120
Q

What does itraconazole treat?

121
Q

For Voriconazole, Posaconazole,Isavuconacole what do they treat?

122
Q

Echinocandins:
* What is the spectrum of activity?

A
  • Candida spp = +++
  • Aspergillosis = ++
123
Q

Echinocandins

For caspofungin, micafungin and anidulafungin, what is the MOA, route and SE?

124
Q

Nystatin:
* What is the fungals treated, MOA, Route and SE?

A

Candida only
* MoA: Increases cell permeability causing cell death
* Route: topical/PO-> diapers or for thrush and diapers
* SE: GI distress

125
Q

Amphotericin:
* What are the fungals that can be treated, MOA, route and SE?

126
Q

Flucytosine:
* What fungals can be treated, MOA, Route and SE?

127
Q

Acyclovir:
* Pharmcokinetics, MOA, Spectrum and SE?

128
Q

Valacyclovir:
* PK, MOA, Spectrum and SE?

129
Q

For Famciclovir (PO), Ganciclovir (IV) and valganciclovir (PO):
* What is the MOA, spectrum and SE?

131
Q

What anti-influenza agents are M2 channel blockers, neuraminidase inhibitors, and endonuclease inhibitors?

A
  • M2: Amandtadine and rimantidine
  • Neuraminidase inhibitors: Oseltamivir and zanamivir
  • endonucleases inhibitor: Baloxavir marboxil
132
Q

Amantadine and rimantidine:
* What is the MOA, Spectrum and SE?

133
Q

For Oseltamivir and Zanamivir, what is the MOA, spectrum and SE?

134
Q

For Baloxavir marboxil (Xofluxa), what is the MOA, spectrum and SE?

135
Q

Neuraminidase inhibitors MC:
* What drug is approved for all age groups including preg woman?

A

Oseltamivir MC
* oral tablets and suspension

136
Q

What diseases should you have Treatment and post-exposure prophylaxis for influenza?

A
  • Chronic lung disease (COPD, asthma)
  • Organ dysfunction (heart, kidney, liver)
  • Neurologic disorders
  • Immunocompromised
  • Obese
  • Extremes of age (> 65 years or < 2 years)
  • Pregnancy
137
Q
  • For the anti-influenza agents, when must treatment start?
  • Hospitalized patients may benefit if started when?
  • What is the effect of starting meds early?
A
  • Treatment must start within 48 hours of symptoms onset – modest symptom reduction in healthy patients
  • Hospitalized patients may benefit if started within 5 days of symptom onset
  • Decrease in duration of symptoms (avg: 1 day) and severity of disease
138
Q

What si the recommendion for seasonal vaccine?

A

Seasonal vaccine recommended for all patients > 6 months of age without vaccine contraindications

139
Q

antimicrobial selection:
* what do you need to confirm?
* What do you need to identify?
* What do you need to start?

140
Q

For empiric therapy, what are the patient factors?

141
Q

For empiric therapy, what are the drug factors?

142
Q

What is a culture and sensitivity?

143
Q

When it comes to monitoring, what are things that you need to do or look for?

144
Q

When should you convert IV to PO?

Pharmacology (14 decks)

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