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Introductory Microbiology > Antimicrobials > Flashcards

Antimicrobials Flashcards

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1
Q

What is empiric therapy?

A
  • antimicrobial therapy targeting likely pathogens

- need to consider clinical presentation, patient risk factors, and pharmacokinetic factors

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2
Q

How do we assess clinical presentation for empiric therapy?

A
  • probable site of infection (lungs skin, blood)

- suspected organism based on disease state

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3
Q

What aspects of a patient history should be considered when determining risk factors?

A
  • demographics
  • past infection/colonization
  • contacts; people and animals
  • co-morbid conditions
  • antimicrobial use
  • prior hospitalizations
  • travel/new Canadian
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4
Q

What pharmacokinetic factors should be considered for empiric therapy?

A
  • Absorption: N/V, diarrhea, intact bowel
  • Distribution: suspected site of infection, underweight or obese
  • Metabolism: known enzyme deficiency
  • Excretion: hepatic or renal impairment
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5
Q

Cultures collected ____ starting antimicrobial therapy are most useful because…

A
  • before
  • collecting samples after even one dose of antibiotics can reduce likelihood of isolating pathogen
  • two blood culture sets from two separate sites if suspected bacteremia
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6
Q

What drug considerations are made for empiric therapy?

A
  • spectrum
  • mechanism of action
  • pharmacokinetics and pharmacodynamics
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7
Q

What are pharmacokinetics and pharmacodynamics?

A

Pharmacokinetics: what the body does to the drug, ADME

Pharmacodynamics: how the drug acts on the body, influenced by spectrum, mechanism of action, and site of infection

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8
Q

What is broad spectrum vs narrow spectrum antimicrobials?

A

Broad spectrum: effective against many different types of pathogens, good for empiric therapy

Narrow spectrum: effective only against a few types of pathogens, good for targeted therapy

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9
Q

What is bactericidal vs. bacteriostatic?

A

Bactericidal: causes microbial death, required in serious infections

Bacteriostatic: inhibits microbial growth, requires a functioning immune system, used for less serious infections

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10
Q

What is concentration-dependent killing?

A
  • need a required concentration to minimum inhibitory concentration (MIC) ratio
  • targeting a specific concentration
  • dosed less frequently, often once per day
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11
Q

What is time-dependent killing?

A
  • longer time above minimum inhibitory concentration (MIC)
  • targeting a length of time above MIC
  • generally dosed multiple times a day
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12
Q

What are three ways that antimicrobials can be combined to improve empiric therapy?

A

1) Broaden spectrum of activity; can help to fill in the gaps in one drug’s spectrum
ex. adding metronidazole to a cephalosporin
2) Double coverage; two antimicrobials covering a similar spectrum
ex. Pseudomonas infection may be treated with a beta-lactam and aminoglycoside
3) Synergism; two antimicrobials provide a stronger effect together than on their own
ex. beta-lactam and aminoglycoside

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13
Q

How does the site of infection help to determine appropriate empiric therapy?

A

Helps to determine which antimicrobials are most appropriate based on:

  • common causative pathogens
  • localized or disseminated nature
  • “hard to reach” area such as brain, bone or biofilm
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14
Q

How does potential antimicrobial resistance help to determine appropriate empiric therapy?

A

The ability of certain microbes to develop tolerance to specific antimicrobials to which they were once susceptible; broad spectrum empiric therapy is optimal

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15
Q

What increases risk of resistance?

A
  • recent antibiotic use (3 months)
  • previous hospital admissions or from long term care
  • travel history and new Canadians
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16
Q

What are four mechanisms of resistance used by microbes?

A

1) Enzymes that deactivate the drug (ex. beta lactamase)
2) Alteration of drug binding target protein (ex. MRSA has altered penicillin binding protein)
3) Alteration of the structure or electrical charge of the membrane (ex. aminoglycoside resistance)
4) Efflux pumps to remove drug from the cell (ex. some gram negatives)

17
Q

What is efficacy?

A
  • improvement of presenting signs and symptoms
  • can take 2-5 days depending on severity of infection
  • important to inform team if patient is not improving
18
Q

What adverse effects should be monitored for?

A
  • nausea, vomiting, diarrhea, headache, rash

- allergic reaction: hives, SOB

19
Q

How do we monitor for therapeutic drug levels?

A
  • timing of drawing the level is key
  • trough level: lowest serum concentration, draw 30 min BEFORE antibiotic dose is given
  • peak level: highest serum concentration, draw AFTER antibiotic dose finishes infusing
  • important for vancomycin and aminoglycosides
20
Q

What targeted therapy?

A
  • antimicrobial therapy targeting known pathogens
  • reduces risk of resistance, C. difficile infections, and opportunistic infections
  • if pathogen not identified, broad spectrum therapy is continued for the entire duration
21
Q

What is prophylaxis therapy?

A
  • antimicrobial agent given to prevent an infection
  • given after exposure to certain pathogens (ex. N. meningitidis)
  • given for immunocompromised patients (HIV, cancer, etc.)
22
Q

What are 6 types of antibiotic targets?

A

1) Cell wall synthesis
2) Cell membrane
3) Folate synthesis
4) DNA
5) Protein synthesis
6) Multiple targets

23
Q

Why do antibiotics target cell wall synthesis?

A
  • selective toxicity toward bacterial cells (prokaryotic)
  • preventing proper cell wall formation leads to weak cell walls
  • cell unable to withstand osmotic pressure
  • cell ruptures and dies
24
Q

What is the mechanism of action of beta lactams?

A
  • peptidoglycan is the major component of bacterial cell walls
  • transpeptidation requires penicillin binding protein (PBP)
  • beta lactams bind to active site of PBPs, inhibiting peptidoglycan synthesis and thus cell wall formation
  • leads to cell rupture
  • bactericidal to growing cells; time-dependent killing
25
Q

What are the three types of beta lactams?

A

1) Penicillins (ex. penicillin G, cloxacillin, amoxicillin, ampicillin)
2) Cephalosporins (ex. cefazolin, cephalexin, ceftriaxone)
3) Carbapenems (ex. ertapenem, meropenem)

All beta-lactams have the common “beta lactam ring”

26
Q

What are penicillins?

A
  • narrow spectrum; covers gram positives more than gram-negatives
  • commonly used for otitis media, skin infections, strep throat
  • common AEs: GI upset, rash
  • uncommon AEs: anaphylaxis, seizures, neutropenia, anemia, thrombocytopenia
  • avoid if previous anaphylactic reaction to beta-lactams
27
Q

Only 10-20% of reported penicillin allergies are ___ allergies.

A

True

28
Q

What are type I and type IV beta-lactam allergies?

A

Type I: anaphylaxis and hives, avoid all beta lactams
Type IV: macular-papular rash, can be re-challenged with another beta-lactam agent with a different side chain
- often outgrow childhood allergies

29
Q

Cross-reactivity between beta-lactam agents is based on…

A

Side chains, not the beta-lactam ring

30
Q

What are cephalosporins?

A
  • mid to broad spectrum, covers gram positives and increasing gram negative coverage w/ higher generations
  • 1st and 2nd generation commonly used for skin and soft tissue infections and surgical prophylaxis
  • 3rd generation commonly used for pneumonia, intra-abdominal infections, and septic shock
  • AEs: GI upset, rash, seizures
  • increased risk of resistance and CDI with higher generations
  • avoid if previous anaphylactic reaction to beta lactams
31
Q

What are carbapenems?

A
  • broad spectrum, covers gram positive, gram negative, oral and gut anaerobes, and meropenem covers Pseudomonas aeruginosa
  • only used for severe infections caused by MDROs (ex. ESBL)
  • only given IV
  • AEs: GI upset, eosinophilia, seizures resistance, increased risk of CDI
32
Q

In what ways can bacteria become resistant to beta lactams?

A

1) Inactivation by beta-lactamase
2) Modification of PBP structure (ex. MRSA)
3) Impaired penetration through porins
4) Drug efflux

33
Q

What is beta lactamase?

A
  • an enzyme produced by some bacteria that cleaves the beta-lactam ring, rendering the drug inactive
  • ex. S. aureus, H. influenzae, E. coli, P. aeruginosa, enterobacter spp.
  • carbapenems are resistant to beta lactamase - why they are used to treat ESBL
34
Q

What are beta lactamase inhibitors?

A
  • allow extended spectrum to many beta lactamase producing gram negative bacteria
  • increased risk of resistance and CDI
  • amoxicillin-clavulanic acid (Clavulin)
  • piperacillin-tazobactam (Tazocin)
35
Q

What are the 3 clinical considerations for beta-lactams?

A

1) Penicillin allergies: always clarify allergies and update documentation
2) CDI: communicate with team about increased risk, report diarrhea, consider switch to narrow coverage, and ensure stop dates are in place
3) IV to PO step-down: if patient is improving and able to tolerate enteral feeds

36
Q

What is the mechanism of action of vancomycin?

A
  • binds to D-Ala-D-Ala terminus of peptidoglycan peptide
  • inhibits cell wall synthesis by preventing peptidoglycan cross-linking
  • leads to weak cell wall and cell lysis
  • bactericidal, concentration-dependent killing
37
Q

How can bacteria become resistant to vancomycin?

A
  • modified binding site (VRE and VRSA)

- thickened peptidoglycan layer with more D-Ala-D-Ala residues, which act as distractors for vancomycin (VRSA)

38
Q

What is vancomycin?

A
  • covers gram positives only, including MRSA
  • given IV for MRSA infections, endocarditis, and meningitis
  • only given PO for CDIs
  • AEs: ototoxicity, nephrotoxicity, Red Man Syndrome, irritation and injection site reactions
39
Q

What is Red Man Syndrome?

A
  • caused by vancomycin
  • symptoms: pruritus, flushing, erythema (face, upper torso)
  • due to histamine release from activated mast cells
  • reaction is RATE-related
  • prevent by limiting infusion rate to a maximum of 1000 mg over 1 hour

Introductory Microbiology (11 decks)

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